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CRISPR gene therapy: Can it cure Alzheimer’s disease?

CRISPR gene therapy: Can it cure Alzheimer’s disease?

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During the Alzheimer’s Association International Conference (AAIC) 2023 in Amsterdam, two cutting-edge CRISPR-based therapy strategies for Alzheimer’s disease were disclosed.

One strategy is to lessen the impact of the APOE-e4 gene, a substantial genetic risk factor for Alzheimer’s. The second strategy is to lessen the amount of beta-amyloid, a damaging protein linked to the illness.

These innovations offer hope to people who are impacted by Alzheimer’s and have the potential to advance treatment options.

Scientists modify genes using the CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) mechanism. Similar to a pair of tiny molecular scissors, CRISPR makes a precise cut in a particular spot in a DNA sequence.

Once the DNA has been sliced, researchers can eliminate undesirable genes, replace defective genes with healthy ones, or even add new genes entirely.

CRISPR has the potential to advance our understanding of genetic disorders, and aid in the creation of fresh therapies. Also, it hastens the discovery of new therapeutic targets and eventually speed up the drug discovery process.

At the Alzheimer’s Association International Conference (AAIC) 2023, which was recently held in Amsterdam, researchers announced two new CRISPR-based therapeutic strategies to cure and prevent Alzheimer’s.

Decreased synthesis of amyloid beta after CRISPR

As part of the initial investigation, scientists at the University of California, San Diego, created a CRISPR-based gene-editing method. It selectively targets the amyloid precursor protein (APP), a key component of Alzheimer’s disease.

The APP gene generates a variety of byproducts, some of which are pathological (beta-amyloid, sAPPa), while others are protective (sAPPa).

This strategy seeks to increase neuroprotective effects while reducing beta-amyloid formation. The researchers experimented on mice with Alzheimer’s disease to see how well their plan worked.

They discovered that beta-amyloid plaques decreased with CRISPR therapy, as did brain inflammatory indicators, and neuroprotective APP products increased. Also, behavioral and nervous system performance improved.

Importantly, CRISPR editing did not have any unfavourable impacts in mice that were in good health.

According to study, lead author Dr. Brent Aulston, a postdoctoral researcher at the Altman Clinical and Translational Research Institute at UC San Diego, “the idea of our therapeutic is to utilize CRISPR to introduce a change in the patient’s genome that is protective against Alzheimer’s disease.”

“So far, we have tried this strategy in rats that exhibit the same disease symptoms as do human Alzheimer’s patients, and we have discovered that our medication lowers disease markers. Additionally, no unfavorable side effects have been noticed,” he added.

Our CRISPR therapy was developed to treat both familial and sporadic varieties of Alzheimer’s disease, according to the authors. Dr. Brent Aulston stated, “We are currently working on transferring this strategy from the lab to the clinic with the hope that our CRISPR-based gene therapy will someday be a treatment option for the illness”.

The APOE gene’s expression may be reduced via CRISPR.

In a different study, a group of scientists from Duke University created a potential therapeutic strategy utilizing CRISPR to target APOE-e4, a genetic risk factor for Alzheimer’s disease.

It is more likely to get Alzheimer’s if you inherit this gene; one copy of APOE-e4 enhances the risk by two to three times, and two copies further magnify the risk by about eight to twelve times.

To reduce the levels of APOE-e4, the researchers used an epigenome treatment platform based on the CRISPR/dCas9-editing technique.

In human induced pluripotent stem cell-derived miniature brains from an Alzheimer’s patient as well as in humanized mice models, their lead candidate showed notable efficacy in lowering APOE-e4 levels.

It’s significant that this strategy had no impact on the levels of other APOE variants thought to have a protective or neutral effect.

The most powerful genetic risk factor for Alzheimer’s is APOE.

As a senior co-author of the study and professor at the Duke University Medical Center’s Alzheimer’s Disease Research Centre and Centre for Genomic and Computational Biology, Dr. Ornit Chiba-Falek stated that they have created this innovative therapeutic platform for Alzheimer’s based on gene editing technology.

“The platform reduces the expression of APOE, the strongest genetic risk factor for Alzheimer’s disease, by closing the genomic region surrounding the gene making it less accessible for the transcriptional machinery,” explained Dr. Chiba-Falek.

“This study provides proof-of-concept for our therapeutic strategy in both human-based cellular and rodent models, demonstrating the efficacy and beneficial effects related to Alzheimer’s pathology,” the researcher continued.

A newly discovered therapeutic target for Alzheimer’s disease is APOE. Dr. Ornit Chiba-Falek stated, “The findings of this study pave the way for gene therapy in Alzheimer’s disease and lay the groundwork for the advancement of this APOE-targeted epigenome therapy towards clinical studies and ultimately precision medicine in Alzheimer’s.”

Proof-of-concept, therefore more study is required

The chief medical officer and CEO of INmune Bio, Raymond J. Tesi, MD, told MNT that “this technology is fascinating and promising.” However, Dr. Tesi noted that at this time, Alzheimer’s disease might not be the optimal condition to use CRISPR.

“Using CRISPR to treat [Alzheimer’s patients] and stop the production of new amyloid is a confused approach. According to what I understand, CRISPR therapy will prevent the creation of amyloid but will not eliminate it for people with [Alzheimer’s]. Is not removing amyloid from the brain the goal of amyloid-targeted therapy? Does eliminating amyloid from the brain have the same advantages as preventing its production? I’m not sure,” he replied.

“Is this outcome sufficient to conduct a clinical trial? To think that stopping more amyloid synthesis will have the same therapeutic advantages as eliminating amyloid from the brain strikes me as naive. Dr. Raymond J. Tesi remarked, “I either need more information or more research on this therapeutic approach.”

Dr. Tesi stated that while thinking about the second strategy, “60% of Alzheimer’s patients exhibit ApoE4. Unfortunately, we are unsure of which ApoE4 patients may ultimately get [the condition].

“In addition, we don’t know what ApoE4 does. In other words, does ApoE4 contribute to the pathology that results in [Alzheimer’s] or does ApoE4 itself contribute to cognitive decline? Before we apply it to humans, in my opinion, more research needs to be done to better understand the impact of’silencing’ ApoE4,” he said.

“I think it’s time to broaden our efforts beyond the amyloid-targeting therapy approaches; we know how effective they are,” Dr. Raymond J. Tesi declared that ApoE4 is an intriguing target that merits more investigation.

There are a lot of other targets worth considering. We favour neuroinflammation and have evidence to back up that therapeutic approach, said Dr. Tesi.

Another aspect to take into account is cost.

Dr. Tesi also emphasised the significance of taking into account cost while planning gene therapies. All currently accessible gene therapies cost millions of dollars.

The lecanemab (Leqembi) community considers its $26,500 annual cost to be prohibitive. Anti-amyloid CRISPR therapies are anticipated to cost significantly more than antibody-based therapies.

Patients, payers, and governments are all impacted by this issue in practice because therapies, especially preventative ones, should be less expensive than treatments.

It will be crucial to strike a balance between the attractiveness of new technology and its actual use.

Ultimately, more research is required because many therapeutic approaches are only at the proof-of-concept stage.

In addition to continuing to research potential treatment targets, it is important to take into account the logistical and financial difficulties involved in actually providing these kinds of therapy.

REFERENCES:

For Alzheimer’s disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?therapy=31

Do reading and puzzle-solving fade away dementia?

Do reading and puzzle-solving fade away dementia?

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Dementia is a chronic neurological disease that affects memory and thought processes and affects millions of individuals worldwide. The most prevalent type of dementia is Alzheimer’s.

There are various medications available to help manage dementia symptoms, but there is no known treatment for the illness.

Significant research is being done to find out more about the pathophysiology of dementia and to create therapies, but it is also being done to find out how lifestyle changes may affect dementia risk and cognition.

This study looks at the effects of reading and crossword puzzles and other cognitively stimulating activities on dementia risk and cognition.

High levels of cognitive activity, such as reading, playing games like checkers and puzzles, and writing letters, can delay the start of Alzheimer’s disease by five years in those 80 years and older, according to a study published in Neurology in 2021.

Another study indicated that more time spent engaging in cognitively passive activities, like watching TV, is associated with an increased risk of dementia, whereas more time engaged in cognitively active activities, like using a computer, is associated with a decreased risk of dementia.

Five experts were interviewed to learn more about themes such as how cognitively stimulating activities lower the risk of dementia, what else lowers the risk of dementia, and what action should be taken in light of the research.

Engaging pursuits increase mental capacity

Dr. Joyce Gomes-Osman, vice president of interventional therapy at Linus Health and a volunteer assistant professor of neurology at the University of Miami Miller School of Medicine, was the first person the experts spoke with.

She claimed that engaging in intellectually demanding activities, like reading and crossword puzzles, increases one’s cognitive reserve, which she compared to the amount of one’s mental library and lowers the chance of developing dementia, and improves cognition.

Every knowledge we acquire is like a book on a shelf. The library keeps expanding as more books are added. You might wonder why this matters, though. Building a library of knowledge in your brain, then, acts as a buffer against memory loss, she explained.

She said, “When your library is large, even if many volumes are checked out, there will still be plenty of other books on the shelves, serving as alternatives and maintaining the library in good condition.”

She outlined how education and experiences in life, particularly those that are difficult and require thought, help people grow their cognitive reserves over the course of their lives.

Research

Researchers looked into the effects of early cognitive development, educational attainment, and leisure activities on cognitive reserve in a recent study that was published in 2022 in Neurology.

From their early years up until the age of 69, they monitored 1,184 persons from the United Kingdom. At that age, the participants underwent a cognitive test with a possible score of 100.

Ultimately, the researchers discovered that those with a bachelor’s degree or more typically scored 1.22 points higher than those with no formal schooling. In comparison to individuals who participated in only four of these activities, those who participated in six or more leisure activities such as educational classes, volunteer work, and social activities scored an average of 1.53 points more.

Meanwhile, those with professional or intermediate-level jobs outperformed those with partially skilled or unskilled jobs by 1.5 points or more on average. Additionally, they discovered that those with better reading skills exhibited a slower rate of cognitive deterioration than those with worse reading skills.

The brain is exercised in several ways during mental exercises.

Dr. David Hunter, an assistant professor of neurology at McGovern Medical School at UTHealth Houston, was also interviewed by experts. Research, he said, has shown that even people with advanced dementia can benefit from what he refers to as “mental exercise”—anything that simultaneously stimulates various sections of the brain.

Just a few examples are reading, crosswords, painting, conversation, gaming, and work. The sole restriction, in reality, is that watching TV all day doesn’t count.

He noted that if patients are unable to engage in their previous interests, other options include colouring books, music, word searches, and simple chat.

Does the cognitive reserve have a limit?

Even if specialists concur that a person’s cognitive reserve is crucial in assisting them in maintaining their thinking abilities, they also point out that there are limits to how much we can improve this reserve through “mental exercises.”

Raphael Wald, a board-certified neuropsychologist with a doctorate in psychology from Baptist Health Marcus Neuroscience Institute, stated to experts:

“Because they have more cognitive reserve, people with high IQs typically fare better with dementia”. However, once dementia has developed, cognitive activities like crossword puzzles cannot stop the degenerative process. But it might make things go more slowly.

We also had a conversation with Dr. Karen D. Lincoln, a professor at the University of California, Irvine’s Department of Environmental and Occupational Health.

While some research indicates that mental workouts like crossword puzzles or word games reduce cognitive deterioration in those with mild cognitive impairment, the research is still ambiguous, she observed.

Puzzles alone may not always enhance cognitive ability or reduce the incidence of dementia, but these kinds of mental tasks are crucial for brain stimulation. Instead of breaking our circulatory system down into discrete sections, we must take it all into account.

Dr. Gomes-Osman concurred that focusing just on mentally stimulating activities is insufficient for lowering the risk of dementia. She pointed out that the “cutting-edge” research in the subject demonstrates that various healthy behaviours are most effective at reducing dementia risk and improving thinking abilities.

What are the 12 modifiable dementia risk factors?

Dr. Gomes-Osman used the Lancet Commission’s 2020 report on dementia prevention, intervention, and care when discussing which behaviours to focus on.

The study identified 12 risk factors for dementia, which together account for 40% of dementia cases.

  • The education level of a person
  • their degree of interpersonal ties
  • unsound hearing
  • workout regimen
  • depression indications
  • using alcohol
  • adult obesity
  • pollution from the air exposure
  • smoking customs
  • head trauma
  • High blood pressure, or hypertension
  • diabetes

According to the report’s authors, addressing these factors can lower the risk of dementia by lowering neuropathological damage. This includes accumulation of tau protein and inflammation, and by either boosting or maintaining cognitive reserve.

Dr. Gomes-Osman stated, “Just to give you an idea, if we all took these steps today, we would reduce dementia cases by over a third next year.”

How to lower the risk of dementia?

It’s crucial to stress that learning something new can strengthen your brain even if you’re already suffering from memory loss. Learning something new will sharpen your memory, focus, and thinking processes while also enhancing your quality of life, according to Dr. Gomes-Osman.

She continued by saying that having fresh, joyful experiences and taking in new sights could both benefit brain function.

Picking something that is neither too easy nor too difficult is crucial in this situation since our brains respond positively to novelty, she explained.

“Change the place where you perform your favorite activities. Going to new areas can boost your outlook on life and strengthen your brain“, according to Dr. Gomes-Osman.

Try walking somewhere new if you typically go for a walk, for instance. Additionally, you might choose a different route to get to work or a different grocery store. Even locating the milk aisle in several stores will need you to use creative problem-solving techniques. Don’t let a day pass without getting out and seeing something new, advised Dr. Joyce Gomes-Osman.

“A special note for African Americans,” Dr. Lincoln said, “who have the highest risk of dementia and Alzheimer’s disease in the United States.”

If you enjoy playing bid whist, dominoes, or spades, you are truly exercising your brain, he claimed. “The games are played with others, not necessarily because they are difficult or need good recall. Social interaction benefits the brain.

REFERENCES:

For Mental disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_478

Importance of Intense exercise for Parkinson’s symptoms.

Importance of Intense exercise for Parkinson’s symptoms.

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According to a recent study, vigorous exercise may help reduce the progression of Parkinson’s disease.

Nearly 90,000 people in the United States receive a new diagnosis of Parkinson’s disease each year. The second most prevalent neurological disease worldwide is Parkinson’s.

Recent findings from an international team of researchers suggest that a vigorous exercise regimen may possibly halt the progression of Parkinson’s disease, opening the door for non-pharmaceutical methods of relieving symptoms and treating the condition.

According to the Parkinson’s Foundation, almost 90,000 people in the United States receive a new diagnosis of Parkinson’s disease each year. Right now, there is no remedy.

Clinical researchers from all over the world are working to manage symptoms and better understand how to do so in addition to trying to find a cure.

Parkinson’s disease, which has been afflicting people for many years, is the second most prevalent neurological ailment in the world after Alzheimer’s disease.

However, because many of the symptoms appear years after the damage begins, it can be challenging to understand this disorder in its early stages.

This rat study looked at whether strenuous exercise could alter the brain abnormalities shown in a Parkinson’s disease experiment.

Physical activity and Parkinson’s

Data showing that vigorous exercise reduces both the motor and cognitive symptoms connected with Parkinson’s disease were published on July 14 in the journal Science Advances by a team of neuroscientists from the Faculty of Medicine of the Catholic University, Rome Campus with the A. Gemelli IRCCS Polyclinic Foundation.

They have gained a better understanding of how this works thanks to their research.

As a neurologist treating Parkinson’s disease patients in the early stages, Paolo Calabresi, Full Professor of Neurology in the Department of Neuroscience at Catholic University of the Sacred Heart in Rome, Italy, said: “I noticed that some of them had a better course of the disease when they were routinely actively doing aerobic exercise.”

How is exercising beneficial?

Exercise, according to experts, is essential to sustaining a healthy lifestyle in general. They also think it can lessen some of the more noticeable symptoms of some illnesses, like Parkinson’s.

Tremors, a shuffling stride, and general slowness of physical movement are some of the early signs of Parkinson’s disease. Harvard Health Letter claims that one of the best methods to treat the illness is through exercise.

How does it assist?

It has been demonstrated that physical activity increases the production of neurotrophic factors including brain-derived neurotrophic factor (BDNF). These elements are essential for the development, maintenance, and survival of neurons. These are essential for the development of new neurons, the preservation of existing neurons, and the improvement of synaptic connections, according to Jennifer Prescott, RN, MSN, CDP, the study’s lead author.

Exercise has been demonstrated to enhance mitochondrial function and encourage mitochondrial biogenesis. For the generation of energy and overall brain health, healthy mitochondria are essential, according to Prescott.

Dr. Daniel Truong, a neurologist and the medical director of The Parkinson’s and Movement Disorder Institute at MemorialCare Orange Coast Medical Centre in California, claims that there are more ways exercise benefits people with Parkinson’s disease.

For us, Truong provided the following examples:

Reduced Alpha-Synuclein Aggregates: The spread of pathogenic alpha-synuclein aggregates in the brain is inhibited by intense exercise. These aggregates, which are a defining feature of Parkinson’s disease, cause neuronal malfunction and death.

Exercise May Help Preserve Motor Control and Visuospatial Learning: According to research, Parkinson’s disease frequently results in a decline in motor control and visuospatial learning because of the degradation of particular brain regions (the substantia nigra pars compacta and the striatum).

The study found that the neurotransmitter glutamate, which is important in learning and memory, interacts with the NMDA receptor for BDNF, whose levels rise with exercise. Through this interaction, neurons in the striatum can react to stimuli more quickly, which offers advantages that go beyond exercise practice.

Exercise has been shown to have anti-inflammatory effects, which may help treat Parkinson’s disease.

Which workouts are most beneficial for Parkinson’s disease

Dr. Andrew Feigin, the executive director of the Marlene and Paolo Fresco Institute for Parkinson’s and Movement Disorders at NYU Langone Health in New York stated that regular exercise helps maintain motor function in [Parkinson’s] patients and may reduce the advancement of the disease.

“We frequently advise all of our Parkinson’s patients to engage in regular exercise. However, we do urge activity,” Feigin said. “Of course, patients have varying capacities for exercise depending on a variety of things, including the severity of Parkinson’s.

“In the past, exercise advice might have been ambiguous, such as ‘taking a walk occasionally. With a better understanding of the advantages of exercise, we are offering more specific advice: this study and others that came before it emphasizes the need for high-intensity exercise, with earlier research suggesting that this intensity should achieve 80 to 85 percent of maximum heart rate for 30 minutes, three to four times per week.

Power walking, swimming, water aerobics, exercise cycles, and other activities with little to no impact but high intensity are frequently recommended to patients, said Petrossian. Additionally, in line with earlier studies, we suggested strength training twice a week using progressive resistance exercises with heavier weights or repetitions. Additionally, we offer our patients advice on stretching, balance training, core strengthening, and skill-based exercises like Pilates, yoga, dance, boxing, and ping pong.

“Exercise can help reduce the symptoms of [Parkinson’s] in the short term, improve energy, lengthen strides and balance, prevent falls, improve sleep and mood, and improve cognition,” she added. In addition to the recent study indicating decreased alpha-synuclein propagation, BDNF release is neuroprotective. Through angiogenesis, exercise can also increase cerebral blood flow.

In advanced Parkinson’s disease, exercise can help

The researchers examined exercise in the new trial and found distinct and significant advantages when the disease was in its early stages.

According to experts, exercise may also be advantageous later on and have other goals.

“In the later stages of Parkinson’s disease, the primary benefits of exercise could potentially shift towards the maintenance of mobility, strength, balance, and flexibility, as well as improvement in quality of life,” added Truong. “As we all know, exercise can help control symptoms like constipation and can also enhance mood and sleep. Falls are less likely when you exercise your balance.

Truong stated that it’s crucial to keep in mind that patients with Parkinson’s disease in its latter stages frequently experience more severe symptoms and may have additional medical problems. “Therefore, any exercise programme must be carefully designed to ensure safety and effectiveness for the individual’s specific condition and needs.”

Summary

Intense exercise may help people with Parkinson’s disease lessen their symptoms, according to a recent study. Exercise preserved the aggregates that cause Parkinson’s disease and prevented their spread, according to research done on rats. They discovered that exercise reduced the symptoms and slowed the disease’s progress as a result.

REFERENCES:

For Parkinson’s disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?therapy=64

Depression: High blood sugar and lower grey matter links.

Depression: High blood sugar and lower grey matter links.

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Around the world, 5% of adults are thought to be depressed. A known risk factor for depression is fluctuations in a person’s blood sugar levels.

The relationship between blood sugar levels and the likelihood of developing depression, according to Sun Yat-sen University researchers, may be mediated by decreased grey matter volume in the brain.

About 5% of the adult population worldwide suffers from depression, a mental illness that makes a person feel incredibly depressed and hopeless to the point where they are unable to enjoy their daily activities.

Variations in glycemia, or a person’s blood sugar levels, are one of the many risk factors for depression.

According to earlier research, people with diabetes, a disorder in which a person struggles to maintain adequate blood sugar levels, are two to three times more likely to experience depression.

The relationship between blood sugar levels and depression may now have a precise biological cause. This is according to researchers from Sun Yat-sen University in Guangzhou, China.

According to research, the association between blood sugar levels and the risk of depression may be mediated by a decreased grey matter volume in the brain.

Depression, blood sugar, and brain structure

According to Dr. Hualiang Lin, a professor in the Department of Epidemiology at Sun Yat-sen University and the study’s corresponding author, they chose to investigate the effect of blood sugar on the risk of developing depression. Earlier research has established a link between changes in blood sugar levels and the development of depression.

Also, a lot of research has shown a clear connection between depression development and changes in brain structure and function. As a result, the information that is now available strongly supports that brain anatomy may play a moderating role in the co-morbidity of diabetes and depression. As a result, we carried out this research to learn more about this connection, said Dr. Lin.

Changes in the amount of grey matter in the brain have been linked in the past to depression. According to a 2019 study, particular changes in gray-matter volume were linked to lifetime major depressive illness.

Additionally, a study conducted in 2022 discovered that individuals with significant depression, bipolar illness, and schizophrenia spectrum disorders frequently have lower hippocampus grey matter volume.

Examining brain’s grey matter

Dr. Lin and his team gathered information from more than 500,000 UK Biobank individuals between the ages of 40 and 69 for this observational study.

Researchers examined the data and discovered a “significant correlation” between sadness, decreased grey matter volume, and raised levels of HbA1c, or glycosylated hemoglobin.

A quick test called HbA1c determines a person’s blood sugar levels during the previous three months, or glycosylated hemoglobin.

In comparison to study participants with or without diabetes, researchers found that a reduced grey matter volume was associated with depression. This association was particularly pronounced in study participants with prediabetes.

Even if the outcome supports our hypothesis, Dr. Lin stated, “We are still very excited about it.”

Previous studies on the specific brain regions connected to depression have been rather scarce, frequently concentrating on well-established clinical regions such the hippocampus or prefrontal cortex. Contrarily, we were able to more thoroughly analyse and identify probable grey matter regions that may be connected to depression in our study since it made use of MRI data from hundreds of different brain areas,” he said.

Age as a risk factor for increased risk

Furthermore, participants in the study who were 60 years of age or older had the strongest correlation between decreased grey matter volume and depression.

According to Dr. Lin, “This finding has important public health implications, particularly for the neurological health of older individuals.”

In particular, the findings indicate that in older people compared to younger people, the decline in grey matter volume is more pronounced for every one unit increase in HbA1c. The difference can be more than twice as great in some brain regions, according to Dr. Hualiang Lin.

This study shows that we may soon face increased dangers to brain health and mental well-being, he said, “given the global trend of population aging and the rising risk of diabetes.”

What does a normal blood sugar level mean?

Glucose, sometimes referred to as blood sugar, is crucial for numerous bodily processes. It is the body’s main source of energy, to start. And glucose is what “feeds” the brain, keeping it active and maintaining connections amongst its associated nerve cells.

The food you eat, especially carbohydrates like starchy vegetables, whole grains, and fruits, provides the body with blood sugar. Glucose is released into the bloodstream as these nutrients are broken down by the body through the digestive tract.

The pancreas starts to secrete insulin as soon as blood glucose levels increase. To give the body’s cells with the energy they require, insulin aids glucose absorption.

An individual with diabetes or one who is at risk for getting it may have high fasting blood sugar levels:

  • A good fasting blood sugar level is one that is 99 mg/dL or lower.
  • Prediabetes is indicated by a fasting blood sugar level between 100 and 125 mg/dL.
  • One has diabetes if their fasting blood sugar level is 126 mg/dL or greater.

Hyperglycemia, or having too much glucose in the bloodstream, can cause the following symptoms:

Could controlling blood sugar lessen depression?

Dr. Daniel Pompa, a cellular health expert, author of the “Cellular Healing Diet,” and host of a weekly Cellular Healing TV podcast and YouTube show. He stated after reviewing this study that it has long been known that blood sugar levels have a significant impact on brain health. Also, this study only serves to further that understanding.

High glucose levels cause brain inflammation, which lowers cognitive function and emotional control. According to Dr. Daniel Pompa, long-term exposure to elevated glucose levels has been related to altered brain circuits that raise the chance of developing depression.

In those with prediabetes and type 2 diabetes, higher levels of glycosylated hemoglobin (HbA1c) are associated with a reduction in brain capacity. Elevated HbA1c is linked to decreased grey matter sizes in regions including the hippocampus, thalamus, and prefrontal cortex. This is according to several other research that have supported this, Dr. Pompa continued.

As a strategy to treat type 2 diabetes, Dr. Pompa said he would like to see further research on the impact of lifestyle modifications and fasting. It also brain scans to measure these people’s grey matter volume.

In particular, he asked, “Can reducing type 2 diabetes symptoms stop or even reverse the loss of grey matter and lower rates of depression?”

Dr. Matthew J. Freeby, director of the Gonda Diabetes Centre and associate director of diabetes clinical programmes at the David Geffen UCLA School of Medicine, said: “Unfortunately, depression is quite common in people living with diabetes, and there’s not much known as to the connection. For a better understanding of the problem’s causes and potential treatments, more research is urgently needed.

Although this research makes an interesting observation, Dr. Freeby stated that he did not believe we could yet identify physical changes in grey matter volume as the explanation.

REFERENCES:

For Depression medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_478

Brain’s unique “pain fingerprint” may help pain management

Brain’s unique “pain fingerprint” may help pain management

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When nerve cells notice damage, they experience pain and send signals to the brain for interpretation.

Because everyone experiences pain differently, it is difficult for doctors to identify and manage it.

Gamma oscillations and brain waves associated with pain perception have variable timing, frequencies, and locations in various individuals, according to a recent study that used brain scans to gather its data.

This discovery might result in pain management strategies based on these unique “pain fingerprints.”

When nociceptors, which are nerve endings in the skin, notice damage and send messages to the brain, people experience pain. The pain may be chronic, lasting for a considerably longer time and being more difficult to treat, or acute, abrupt onset, typically short-lived, and manageable by addressing the source of the pain.

However, not everyone experiences pain in the same way, making it challenging for medical professionals to gauge how much someone is hurting.

They frequently employ a number scale, with zero denoting no pain at all and ten denoting the most excruciating suffering possible. Other strategies include:

  • The doctor uses a verbal descriptor scale to specify the type of pain by asking several descriptive questions.
  • short pain inventory: a written questionnaire that aids medical professionals in determining the impact of a patient’s pain and tracking changes in pain to look for patterns.
  • Respondents to the McGill Pain Questionnaire (MPQ) select three main categories of word descriptors (sensory, affective, and evaluative) to describe their subjective pain experience.
  • Faces scale: This is mostly used for kids. The doctor displays a range of emotive faces, from sad to pleased, and the kids use them to convey how much pain they are in.

How does the brain register pain?

Senior lecturer at the University of Essex’s Centre for Brain Science and lead author Dr. Elia Valentini said the following to us:

The sense of pain may be mediated by these fast brain oscillations known as gamma, according to previous research. Our research shows that, despite the fact that we all experience pain to a similar degree, some of us will exhibit these gamma oscillations in response to painful stimuli while others won’t.

In essence, he said, “we propose that gamma oscillations are not necessary for pain, but that they constitute a stable and repeatable property of the individual when present.

What reactions does the brain have to pain?

Seventy volunteers underwent pain testing for the researchers. The average age of those who participated in the study was 24, and they were all in good health. Males made up the majority.

They kept track of the outcomes of two independent studies. In the first, there were 22, and there were 48 in the second.

In the first experiment, subjects were repeatedly exposed to touch and pain stimuli on the right hand’s back twice, two weeks apart. A Tm: YAG laser produced the pain stimuli. Participants graded both stimuli on a scale of 0 to 10.

In the second experiment, a Nd: YAG laser used to deliver high- and low-intensity pain stimuli to subjects. Each subject was exposed to 80 stimuli of high and 80 of low intensity. On a scale of zero for no discomfort to one hundred for the most manageable pain, they were asked to rate them.

In all studies, individuals wore an electrode cap while being exposed to the stimuli, which produced electroencephalogram (EEG) data from which the gamma responses were analysed.

How is pain quantified?

Dr. Vernon Williams, a sports neurologist and pain management expert who founded the Cedars-Sinai Kerlan-Jobe Institute’s Centre for Sports Neurology and Pain Medicine who was not engaged in this study, provided the following explanation to us:

“An unpleasant sensory or emotional experience connected to, or similar to, actual or potential tissue injury is referred to as pain. It is a “experience,” not a “sensation.” As a result, it is always unique, subjective, and personal. The fact that gamma oscillations differ greatly from person to person is therefore not surprising.

In addition to the fact that the pattern of gamma oscillations varied between individuals, the researchers also discovered that it did not change for each person who underwent the repeat trial.

“Our work demonstrates that there is a remarkable stability: Participants with high/low gamma activity and high/low pain ratings in the previous recording had high/low gamma activity and high/low pain ratings two weeks later,” said Dr. Valentini.

This could be beneficial for pain management, according to Dr. Williams: “Interestingly, the findings are reproducible within an individual, and that may have future implications regarding objective measures of pain and objective measures to assess pain interventions/treatments, particularly in the short term.”

Dr. Valentini cautioned, nonetheless, that the significance of gamma oscillations for pain processing may be greatly exaggerated. It serves as a timely warning that, even when a large group-level association is replicated by multiple research, we might still be duped into interpreting the results as causative.

Do the results have any clinical application?

Dr. Valentini summarised the findings by saying, “In a nutshell, we suggest that gamma oscillations are not necessary for pain, but when present, they are a stable and repeatable feature of the individual.”

As Dr. Valentini said, “Our work resonates with the idea of personalized medicine whereby clinicians may focus on the specific individual’s biological patterns to achieve faster and better diagnosis or treatment.” Their findings may result in more personalized pain management.

Despite the fact that there are no obvious therapeutic implications of our findings, he explained that they “pave the way to a more precise assessment of neural responses mediating the experience of pain.”

Dr. Williams concurred that there was cause for hope. He explained to us that “reproducible” in the trials indicated that subjects’ results were consistent across tests conducted two weeks apart.

That might not be the case if tests are conducted two months or two years apart, or if social, psychological, or biological circumstances have changed in the interim. Dr. Williams continued, “If changes take place under various circumstances, that might imply that the person’s ‘fingerprint’ can change over time (or if circumstances change).”

“That gives us cause for hope because it implies that their experience—the pain they feel—can be diminished, enhanced, or completely erased with the proper mix of therapies. He said, “Chronic pain does not have to last ‘forever’.

Dr. Valentini intends to conduct additional research because, in his words, “my colleagues and I believe that gamma and other brain oscillations are an important area of investigation for pain neuroscience. Maybe some of us will be able to repeat similar studies in individuals with acute or chronic pain, better addressing the therapeutic applicability of our research.

REFERENCES:

For Pain relief medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=23

Epilepsy risk is 2.5 times higher in hypertensive people.

Epilepsy risk is 2.5 times higher in hypertensive people.

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Researchers looked into the connection between epilepsy and high blood pressure. They discovered that taking antihypertensive drugs lowers the risk of epilepsy. This is increased by high blood pressure by about 2.5 times.

They come to the conclusion that while high blood pressure is a risk factor for epilepsy, further research is required to fully understand the mechanisms that underlie the association.

Ablestock

After stroke and dementia, epilepsy is the third most prevalent neurological illness that affects elderly individuals.

According to research, late-onset epilepsy has increased in prevalence over the past 20 years. As the population ages, the prevalence of the disorder will undoubtedly continue to climb. This makes epilepsy a substantial public health concern.

Despite this, 32-48% of cases of epilepsy have unknown underlying causes. According to several studies, vascular risk factors may raise the chance of developing late-onset epilepsy. According to another study, epilepsy may be caused by vascular risk factors starting in a person’s 30s.

Policymakers may be better able to develop public health initiatives and preventive actions to lower and manage rates of the condition if they have a better understanding of the involvement of vascular risk factors in late-onset epilepsy.

A recent investigation of the relationship between vascular risk factors and the start of epilepsy was conducted by researchers in the United States under the direction of the Boston University School of Medicine.

They discovered a connection between hypertension and a nearly 2-fold increased incidence of late-onset epilepsy. For those who did not use medication to control their blood pressure, this risk was significantly larger.

Data evaluation

Data from the Framingham Heart Study (FHS), an ongoing, community-based study that started in 1948, was used by the researchers. Through health exams every four years, the Offspring Cohort follows the health outcomes of 5,124 of the children of the original participants.

The researchers combined data from 2,986 individuals who underwent their fifth checkup between 1991 and 1995, were at least 45 years old at the time, and whose health records contained information on vascular risk factors.

Systolic and diastolic blood pressure were measured as vascular risk factors. The researchers defined high blood pressure as having a systolic pressure of at least 140 millimeters of mercury (mm Hg) and a diastolic pressure of at least 90 mm Hg, as well as taking antihypertensive drugs.

Additionally, the researchers looked for:

  • diabetes
  • cholesterin amounts
  • smoking history
  • a cardiovascular condition
  • stroke
  • BMI, or body mass index

The ICD-9 codes associated with epilepsy or seizures, self-reported seizures, routine chart reviews for neurological diseases, and antiepileptic medication use were utilised by the researchers to screen participants for epilepsy or seizures.

To identify cases of epilepsy, the researchers also analysed electroencephalography (EEG), cardiac, and other pertinent data, as well as brain imaging.

The study found 55 cases of epilepsy in the group, of which 26 were confirmed, 15 were likely, and 14 were suspected. The average age of the subjects at the time of a possible diagnosis was 73.8 years old.

The study’s findings revealed a nearly 2-fold increased risk of epilepsy in people with hypertension. The other risk variables, however, were unrelated to epilepsy.

They also discovered that the probability of having epilepsy increased by 17% for every 10 mm Hg change in systolic blood pressure.

Underlying processes

The connection between epilepsy and hypertension is explained by several theories. The renin-angiotensin system (RAS), which controls blood pressure, may be one mechanism.

According to research, rats who have had repeated seizures had 2.6–8.2 times the RAS components of seizure-free mice. Antihypertensive medications that decreased RAS component levels postponed the start of seizures and decreased their frequency.

More investigation is required, though, as other studies indicate the system may only have a modest impact on the relationship between epilepsy and hypertension.

Small vascular disease (SVD), a disorder in which the walls of small arteries and capillaries are damaged and do not adequately convey oxygen-rich blood to numerous organs, is another potential underlying mechanism, claim the researchers. According to a recent study, the duration of high blood pressure is a reliable indicator of developing SVD in later life.

The researchers also mention that temporal lobe epilepsy and SVD are related. Cortical microinfarcts, tiny lesions in the cortical tissue, and the disruption of U fibers are a few potential explanations. These conditions may cause excessive excitability and hence seizures. U fibers link adjacent regions of the cerebral cortex.

The researchers draw the conclusion that hypertension is a standalone predictor of late-onset epilepsy and carries a 2-fold chance of getting seizures after 45 years.

They do acknowledge that their study has some limitations. It might not accurately represent all races and ethnicities because it was mostly made up of white people. The study’s observational design, according to the researchers, precludes the ability to establish causality.

Dr. Jason Hauptman, a neurosurgeon at Seattle Children’s Hospital, told us that these findings were particularly intriguing because there has been debate over whether elevated blood pressure (hypertension) is a standalone risk factor for stroke.

living with high blood pressure and epilepsy

A healthy blood pressure reading is less than 120/80 mmHg; if you are unsure of your current blood pressure, ask your doctor. High blood pressure is closely linked to a variety of health risks, including cardiac arrest, so it is important to try and maintain this level. The good news is that there are lots of easy lifestyle adjustments you can make to lower your blood pressure, like:

  • healthy eating
  • not a smoker
  • controlling stress
  • lowering the consumption of alcohol
  • Exercising
  • consuming less salt

Speak to your doctor if you have concerns about your epilepsy and high blood pressure. They can assist you in creating a management strategy to lower your blood pressure through dietary and activity modifications. while also making sure that you are controlling your seizures.

REFERENCES:

For Epilepsy disease treatments that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?therapy=49

New brain imaging techniques for the treatment of epilepsy.

New brain imaging techniques for the treatment of epilepsy.

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In a recent study, researchers identified a brain circuit that can be targeted with brain stimulation by mapping abnormalities in the brain linked to epilepsy.

They stated that they hoped their discoveries could lessen the symptoms that come along with seizures.

They stated that the brain mapping method might also aid in predicting whether stroke survivors will experience seizures.

According to a recent study published in the journal JAMA Neurology, deep brain circuit stimulation may be able to identify whether people who have had a stroke may eventually acquire the disease and assist treat epilepsy.

Scientists from Brigham and Women’s Hospital in Massachusetts examined five datasets that had more than 1,500 individuals with brain injuries for their study.

The lesions have several diverse causes, such as tumors, trauma, and stroke.

The ability to explore across many brain regions and forms of brain injury for common network connections associated with epilepsy as a result allowed researchers to do so.

Brain mapping: What is it?

There are specific functions for each region of the brain. The surgeon wants to comprehend how the brain regions close to the seizure onset operate before doing any type of brain surgery, including epilepsy surgery. This enables your team to determine how much of the seizure focus can be safely removed.

The process of brain mapping can be used to pinpoint the functions of various brain areas.

Different people have different locations for different bodily processes (such as movement, voice, vision, and more). Tumours, seizures, or other brain abnormalities may alter which regions of the brain are in charge of a certain function. Sometimes general laws don’t apply.

By activating particular brain regions, one can create a “map” of each person’s brain. The map reveals to medical professionals which regions of the brain are in charge of vital processes like speech, sensation, or movement.

Brain mapping for epilepsy

The sites of brain damage in epilepsy patients and those without the condition were compared by the researchers.

According to the researchers, the brain was filled with lesions connected to epilepsy. They did, however, have a common network.

The researchers pointed out that epilepsy may be brought on by disruption of brain connections rather than the site of the damage. The basal ganglia and cerebellum, two deep-brain regions, were the locations of the linkages.

According to the researchers, identifying lesions in a brain network may aid in determining whether or not a person may experience epilepsy following a stroke. They claimed that common brain pathways could connect various damages and result in epilepsy.

The researchers point out that earlier studies have linked deep brain regions to modifying and regulating seizures in epilepsy-prone animals. They might have a braking effect on the brain.

How have scientists used deep brain stimulation?

The researchers examined the deep brain stimulation results in 30 patients with drug-resistant epilepsy.

If the stimulation was linked to the same brain network they discovered when mapping brain lesions, they claimed that the benefit would be greater.

Dr. Frederic Schaper, an assistant scientist at the Centre for Brain Circuit Therapeutics at Brigham and Women’s Hospital and an instructor of neurology at Harvard Medical School in Massachusetts, said, “In our study, we analysed existing data from patients that received deep brain stimulation for drug-resistant focal epilepsy.”

Although all patients had electrodes for deep brain stimulation implanted in the anterior thalamus, Schaper informed us that each patient’s precise electrode placement and stimulation sites varied slightly. “We found that patients with deeper brain stimulation sites that were more connected to deep brain regions in the cerebellum and basal ganglia had better seizure control than patients who were less connected to these regions.”

“This finding suggests an important role for brain networks distant from the anterior thalamic deep brain stimulation site in the mechanism of action of deep brain stimulation for epilepsy and seizure control,” he continued.

Deep brain stimulation principles

The American Association of Neurological Surgeons defines deep brain stimulation as a surgical procedure in which electrodes are placed in particular parts of the brain. Then, in order to assist manage aberrant brain activity, these electrodes transmit electrical impulses.

The amount of stimulation is managed via an implanted programmable device that resembles a pacemaker. The device is connected to the brain’s electrodes by a wire.

The full mechanism through which deep brain stimulation reduces seizure frequency is unknown, according to Schaper. “Previous research in people and animal models indicates that deep brain stimulation disturbs the brain networks responsible for seizures. It is uncertain, nevertheless, whose brain networks are in charge of [deep brain stimulation]-induced seizure control.”

Schaper mentioned that deep brain stimulation is a safe and efficient treatment for drug-resistant focal epilepsy and has received approval from federal regulators.

Improving epilepsy symptoms

In this investigation, brain networks were sought after. They claimed that deep brain stimulation can lessen epilepsy symptoms if it activates just one node in the network.

“This study is quite exciting,” said Dr. Jean-Philippe Langevin, a neurosurgeon and the director of the Restorative Neurosurgery and Deep Brain Stimulation Programme at the Pacific Neuroscience Institute at Providence Saint John’s Health Centre in California. He was not involved in the research.

“The scientists discovered that networks were more associated with epilepsy than brain lesions. “They could influence epilepsy symptoms if they could concentrate stimulation within the networks,” Langevin told us.

The roadways in the brain are called brain networks. The roadside stops are called lesions. The researchers discovered that the entire network was influenced when electrical currents were applied anywhere along a network of streets.

According to Langevin, “Deep brain stimulation works for other diseases.” These include essential tremors, Parkinson’s condition, dystonia, obsessive-compulsive disorder, and dystonia. For certain conditions, “working within a single network would also hold true.”

“This is exciting because, in the future, when patients come to us with seizures, a scan can look at how the network is connected, making it easier to use [deep brain stimulation],” continued Langevin. “The scans do exist, but we don’t typically use them in the study.”

Symptoms of a seizure

Different people experience different pre-seizure warning symptoms.

But there are a few widespread indications:

  • a sense of impending disaster
  • For every seizures, the same tone or sound is produced.
  • trouble generating ideas
  • having trouble finding the right words
  • Having underwater-like audio perception
  • experiencing déjà vu or believing that nothing is familiar
  • feeling queasy in the stomach
  • having the impression that everything is deformed, either larger or smaller than it should be.

It is suggested that you lay on your side if you are experiencing a seizure. Someone else should roll a seizure victim over if they are unable to move.

Additionally, a person experiencing a seizure ought to be relocated to a location where they won’t damage themselves. For instance, a space free of any furnishings.

Ensure that they are not wearing anything tight around their neck, such as a necktie, scarf, or button-up shirt. If so, you ought to take these things off.

Never abandon a person experiencing a seizure. Until the seizure is finished, be at their side.

REFERENCES:

For Epilepsy medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?therapy=49

High levels of lean muscle may help prevent Alzheimer.

High levels of lean muscle may help prevent Alzheimer.

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High quantities of lean muscle may help prevent Alzheimer’s disease, according to recent studies. To determine whether this connection is causal, more study is required.

Resistance training and a sufficient intake of protein in the diet are advised by experts as ways to build lean muscle mass. Previous studies have shown a link between obesity and an elevated risk of Alzheimer’s.

A recent study that was published in BMJ Medicine suggests that having a lot of lean muscle may prevent Alzheimer’s disease. The authors of the study pointed out that additional study is required to comprehend the biological mechanisms underlying it.

Researchers gathered data on 450,243 participants’ genetics, lean muscle mass, cognition, and health for this study from the U.K. Biobank. They next used a method known as Mendelian randomization to search for genetic relationships between lean muscle mass and genetic variants.

The quantity of lean muscle and fat tissue in the arms and legs was measured using bioimpedance, an electric current that moves through the body at varying speeds. The researchers next discovered 584 genetic variations related to lean muscle mass, but none of these were located in an area of the genome known to include genes connected to an elevated risk of Alzheimer’s disease.

The chance of developing Alzheimer’s disease did, however, appear to be reduced in individuals who had high amounts of lean muscle mass and associated genetic variations.

These results were confirmed by measuring the quantity of lean muscle mass and body fat tissue in a second cohort of 252,879 individuals without Alzheimer’s disease and 7,329 individuals with the condition.

The findings indicated that lean mass was associated with enhanced cognitive performance, but this association did not account for lean mass’s protective effect against the onset of Alzheimer’s disease.

The study’s objectives

The majority of the data utilized by the researchers came from the UK Biobank, a continuous database that collects health and genetic data on 500,000 people. The researchers used data from hundreds of thousands of people.

Mendelian randomization, which employs gene variations as a proxy for specific risk variables, was used to analyze the data.

Additionally, bioimpedance measurements which determine the speed at which an electrical current travels through the body based on its composition in terms of muscle and fat were used to calculate each person’s lean mass.

A total of 584 genetic variations were connected to lean muscle mass, but none of them were discovered in the region of the brain linked to Alzheimer’s susceptibility.

Participants’ chance of developing the disease was statistically significantly (12%) lower on average for those with higher amounts of (genetically proxied) lean muscle.

The analysis was performed using data from an additional 260,208 individuals, of whom 7,329 were identified as having Alzheimer’s disease, in order to confirm these findings. They measured lean muscle mass over the entire body, not only in the arms and legs.

Again, they discovered that having more lean muscle was linked to a lower risk of Alzheimer’s.

Unexpectedly, the analysis did not reveal a correlation between body fat and the probability of developing Alzheimer’s disease once lean mass was taken into account. Body fat was associated with inferior performance in cognitive activities.

The significant contrast between the protective effect of lean mass on dementia risk and the lack of an effect of fat mass on dementia risk, according to Daghlas, startled him.

How Alzheimer’s disease and lean muscle are related?

The fact that the processes underlying the association between lean muscle and Alzheimer’s disease are still unknown is another drawback of the study.

The researchers made brief speculations about possible connections. For instance, Alzheimer’s has long been linked to cardiovascular illness, though Daghlas cautioned that the connection is “complicated.”

According to Daghlas, heart disease problems like stroke and hypertension are what fuel vascular dementia. Though this is a contentious idea, he added, “the most recent causal evidence suggests weaker evidence for an effect of vascular risk factors on Alzheimer’s disease risk.”

Lean mass may very possibly lower the incidence of vascular dementia through lowering the risk of cardiovascular disease, according to Daghlas, however more research is needed in this area. “This can be looked into in upcoming studies.”

In the publication, the researchers also made the speculative claim that “new” processes, such as centrally acting myokines, may be at work.

Myokines are proteins that muscles produce that have an impact on other tissues, according to Daghlas. “Experimental studies have demonstrated that they are induced by exercise and have a positive impact on brain function.”

Other muscle-related issues, in addition to these, “may explain the larger picture,” according to Dr. Anna Nordvig, a neurologist at NewYork-Presbyterian and Weill Cornell Medicine who was not involved in the study. Examples include “bone hormones, cardio vs. strength training differences, sex hormones, glymphatic drainage depending on exercise, and sleep, to name a few.”

In the end, further clinical intervention studies are required to demonstrate the link between lean muscle and Alzheimer’s disease and the mechanisms underlying it.

The best way to build lean muscle mass

Having lean muscle mass has several health benefits in addition to possible advantages for the brain.

Resistance training using weights, bands, and pleiomorphic activities are advised by Dr. Joseph C. Maroon, clinical professor, vice chairman, and Heindl scholar in neuroscience at the Department of Neurosurgery at the University of Pittsburgh.

Additionally, he recommends supplementing with B-hydroxy B-methylbutyrate (myHMB), a good source of dietary protein.

This naturally occurring compound aids in the maintenance of a healthy weight and the development of lean muscle mass in humans. B-hydroxy helps muscles recover from hard activity, improves athletic performance, and enhances muscle and strength, according to him.

According to Dr. Sullivan, the best food, the best kind and frequency of exercise, the optimum amount of rest, and stress management are the primary factors that influence muscle growth.

These are the recommendations she makes:

Exercise: four to five quick strength-training sessions each week. In comparison to two or three longer aerobic exercises each week, this will produce greater lean muscle mass.

Diet: Put your attention on lowering insulin resistance by eating fewer carbohydrates and more protein, the building block of muscle.

Sleep: 8 to 9 hours of sleep per night are recommended if you want to recuperate from this kind of workout completely.

Stress management: With the rise in inflammation and blood sugar that stress hormones like cortisol induce, chronically high stress can sabotage any self-improvement effort. Long-term high cortisol levels can contribute to persistent muscle tension and lactic acid buildup, which can inhibit muscle growth. Moving your body more, going outside, eating more good foods, being an aggressive communicator, and finding your purpose are the simplest ways to relieve chronic stress.

How to lower your risk of developing Alzheimer’s?

Although there is no cure for Alzheimer’s, doctors think there are a number of steps you may take to lower your risk.

“Protect” and “stimulate” are the two categories that these fall under, according to Nordvig, and “physical activity falls into both of these.”

“Protect” includes monitoring factors like blood pressure, sugar levels, weight, nutrition, and sleep, she said. These are topics covered at a yearly checkup.

We should also work to safeguard ourselves from environmental risk factors associated to Alzheimer’s, according to Dr. Rena Sukhdeo Singh, a vascular neurologist at the University of Maryland Shore Regional Health.

The incidence of dementia has also been connected to fine particulate matter in air pollution.

According to Sukhdeo Singh, systemic inflammation also contributes to the development of Alzheimer’s disease. Numerous factors, including medications, a diet high in sugar and processed foods, smoking, and binge drinking, can contribute to chronic inflammation.

Optimising additional daily inputs that influence cognition is what “stimulate” entails. For instance, Sukhdeo Singh proposed, “learning a new skill, hobby, language, or instrument,” or taking part in shorter activities like “sudokus, puzzles, and number games.”

Unfortunately, there are some factors that we have no control over. Age, genetics, and sex are non-modifiable risk variables, she added.

Restrictions of this research

Researchers solely considered lean muscle mass for this investigation. However, there are other things to think about.

The protein amyloid, which is damaging to the functioning of the brain, is found in higher amounts in adipose tissue, but the researchers neglected to test these signs of inflammation and insulin resistance, according to Maroon. “This probably diminishes the significance of their findings.”

Furthermore, “while their positive finding was statistically significant, the effect size was modest in lean muscle mass reducing the risk of dementia and only explained 10% of the variance,” added Dr. Sullivan.

The link between more lean muscle mass and a lower incidence of Alzheimer’s disease has to be further investigated.

According to Nancy Mitchell, a registered nurse, “For now, people with lower muscle mass tend to be obese, which is a risk factor for type 2 diabetes.”

We refer to Alzheimer’s disease as “diabetes of the brain” because it has been hypothesized that high blood sugar harms the nerve endings in the regions of the brain that are most impacted by cognitive decline. Therefore, the link may actually be between a reduced risk of obesity and diabetes. This can be a study drawback in and of itself because greater specificity is still needed. Not all correlations indicate causation. Nancy Mitchell is a nurse practitioner.

REFERENCES:

For Alzheimer’s disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?therapy=31

Can Hormone therapy for menopause increase Dementia risk?

Can Hormone therapy for menopause increase Dementia risk?

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Menopausal hormone therapy is used by about 45% of all women to lessen menopause symptoms.

According to prior studies, some types of hormone replacement treatment may make women more susceptible to developing serious illnesses.

Menopausal hormone therapy is linked to an increased risk of dementia and Alzheimer’s disease, according to researchers from Copenhagen University Hospital, says Rigshospitalet.

These results go against earlier research that suggested HRT might reduce a woman’s risk of dementia.

Menopausal hormone therapy, often known as hormone replacement therapy (HRT), is used by about 45% of all women worldwide to cope with menopause symptoms.

HRT can cause adverse effects like nausea and migraines. According to earlier studies, women who use specific forms of HRT may be more susceptible to strokes, gallbladder problems, and malignancies including breast and endometrial.

Menopausal hormone therapy is now linked to a higher risk of dementia and Alzheimer’s disease, according to study from Copenhagen University Hospital, as per Rigshospitalet.

These results go against earlier research that suggested HRT might reduce a woman’s risk of dementia. The BMJ recently published an article based on this study.

What occurs throughout menopause?

Every woman experiences menopause, which is the end of the monthly cycle and the last time the ovaries release eggs.

Menopause usually begins in a person between the ages of 45 and 55. Perimenopause, often known as the menopausal transition, can persist between seven to fourteen years.

A woman who is beginning menopause may experience symptoms like:

  • a hot flash
  • morning sweats
  • irregular or absent
  • vulvar aridity
  • difficulty sleeping
  • mood swings like anxiousness and depression

Menopause is a natural part of ageing, but it comes with some changes that some people may desire to minimise. Menopause-related symptoms may be treated with the following methods:

  • HRT
  • hormonal birth control at a low dose
  • low-dose mood stabilisers
  • prescription or over-the-counter drugs for vaginal dryness

Additionally, several lifestyle modifications can assist in relieving some symptoms:

  • routine exercise
  • wholesome diet
  • meditation techniques
  • restricting alcohol
  • giving up smoking
  • counselling for mood changes
  • maintaining a healthy sleep routine

What is hormone therapy for menopause?

The purpose of HRT is to enhance and balance the levels of the female hormones progesterone and oestrogen in the body.

Although the body’s ovaries naturally produce both of these hormones, their production declines after menopause, leading to menopausal symptoms.

There are two primary types of menopausal hormone treatment that a doctor could recommend, depending on a woman’s situation and requirements:

  • treatment with just oestrogen
  • combined treatment utilising progesterone and oestrogen

HRT can be applied topically or vaginally, and comes in tablet, nasal spray, skin patch, and vaginal cream or suppositories forms.

The following are possible HRT adverse effects:

  • bloating
  • headaches
  • breast discomfort
  • nausea
  • acne
  • mood changes
  • uterine bleeding

How Does HRT Affect the Risk of Dementia?

Dr. Nelsan Pourhadi, the study’s lead author and a researcher at the Danish Cancer Society and the Danish Dementia Research Centre in the Department of Neurology at Copenhagen University Hospital – Rigshospitalet in Copenhagen, Denmark, claims that the study’s objectives were dual and based on understudied facets of the subject matter.

“First, we sought to look into whether menopausal hormone therapy use, as advised by guidelines, increased the incidence of dementia.” Second, he told us, “we were looking into continuous versus cyclic therapy regimes.”

Dr. Pourhadi and his team used data from a national registry database for this investigation. The study’s controls were about 56,000 age-matched women without a dementia diagnosis and approximately 5,600 women with dementia. Danish women between the ages of 50 and 60 in 2000 who had no history of dementia or any conditions that would exclude the use of HRT were included in the data, which covered the years 2000 to 2018.

The subjects’ average age at the time of dementia diagnosis was 70. In comparison to controls, 32% of women with dementia and 29% of controls had used estrogen-progestin therapy starting at an average age of 53 before receiving a diagnosis. For dementia-stricken women, therapy lasted an average of 3.8 years, compared to 3.6 years for males.

Analysis revealed that women who got estrogen-progestin therapy had a 24% higher incidence of Alzheimer’s disease and all-cause dementia. Even ladies who started the treatment at age 55 or younger experienced this.

The Women’s Health Initiative Memory Study (WHIMS), the largest clinical experiment in the field, found similar results, according to Dr. Pourhadi.

Does HRT alter the risk of dementia?

Researchers have previously searched for a link between HRT and the risk of dementia.

Menopausal hormone therapy may aid in lowering a woman’s risk of dementia, according to earlier studies. Menopausal hormone therapy use was associated with a lower chance of developing all neurological disorders, including Alzheimer’s disease and dementia, according to a study released in May 2021.

Additionally, a study published in June 2022 discovered that women with depression who used HRT after menopause had a lower risk of developing Alzheimer’s disease and vascular dementia.

Several research have shown a connection between HRT use and an elevated risk of dementia. HRT was linked to a higher incidence of dementia, according to research released in September 2022.

And according to a study that was just released in April 2023, women who had HRT more than five years after the onset of menopause or who started menopause early had greater levels of tau protein in their brains, which is thought to be one of the main causes of Alzheimer’s disease.

When questioned why prior and current studies may have conflicting results, Dr. Pourhadi responded, “It is crucial to emphasise that our findings are in line with those of the largest clinical trial on the topic, WHIMS. The majority of prior clinical trials were hindered by issues like poor selection, limited sample sizes, brief follow-up periods, and results that were purely dependent on cognitive testing rather than a clinical evaluation of dementia.

Furthermore, earlier observational studies, particularly short-term ones, were unable to evaluate the use of menopausal hormone therapy close to menopause, the author continued. The discrepancies between the findings of those studies and those of our study “may be explained by these differences.”

Can HRT lead to dementia?

Dr. Pourhadi explained that because this study is an observational one and not a causal one, it is impossible to establish a link between menopause hormone therapy and dementia.

Therefore, more investigation is required to determine whether or not the observed link may be assumed to be causal. Additionally, it is important to distinguish between the various menopausal hormone therapy delivery methods such as tablets, patches, and gels,” he continued.

Dr. Mindy Pelz, a specialist in holistic medicine who specialises in women’s and hormonal health but was not part in this study, concurred.

It’s vital not to overestimate the results of this new observational study. Correlation does not imply causality, and prior research has shown that menopausal hormone therapy lowers the incidence of dementia, so it’s conceivable there’s a variable missing that we haven’t thought of yet, the researcher added.

She told us that many women go for hormone replacement medication to deal with their symptoms when they have cognitive deficiencies after menopause, which could be a sign of dementia in the future.

Dr. Jewel Kling, assistant director of women’s health internal medicine at the Mayo Clinic in Arizona and a non-participant in this study, informed us after reviewing the findings that because this was an observational study using data from a national registry, we could not draw any conclusions about the cause-and-effect relationship between menopausal hormone therapy and dementia risk.

The only way to conclude causation is through a randomised control design, which this wasn’t. “(We) can only claim that there was a relationship identified between the two in their data. According to the study’s design, there are numerous additional factors that could potentially explain this association, the researcher said.

REFERENCES:

For Mental disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_478

MS severity: Genetic markers may lead to better treatment.

MS severity: Genetic markers may lead to better treatment.

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Globally, 2.8 million people will have Multiple Sclerosis (MS) in 2020. The symptoms of MS can worsen over time and result in chronic problems, and the condition presently has no known cure.

The first genetic indicator of MS severity and progression has been identified by researchers at the University of California, San Francisco.

This discovery, according to scientists, may help in the creation of new medications that can delay the advancement of the illness.

Multiple sclerosis (MS), a condition of the central nervous system that affects mobility and vision, will impact roughly 2.8 million individuals worldwide by the year 2020.

MS presently has no known cure. Each person is uniquely affected by the illness, both in terms of when symptoms initially appear and how severe they are.

The severity of the illness can worsen as the body experiences a cycle of symptom flare-ups and remissions, resulting in persistent mobility problems, visual loss, and even partial or complete paralysis.

The first genetic signature connected to MS severity and progression has now been identified by researchers from the University of California, San Francisco.

This discovery, according to scientists, may help in the creation of new medications that can delay the advancement of the illness.

Research targets MS progression

The University of California, San Francisco’s Dr. Sergio Baranzini, professor of neurology and co-senior author of the study, explained that they chose to look for a genetic variation associated with faster MS progression because the disease develops differently in each patient after diagnosis.

“Neurological progression is a common feature in persons with MS, which is inexorable and independent of whether relapses are controlled or not,” he said.

“Some people have a very aggressive disease that can impact their mobility and neurological function in a few years, while others experience a much more benign course,” he said. We already knew that genetics has a significant influence on risk, but the wide range of outcomes revealed that genetics may also affect severity.

Data from The MultipleMS Consortium and The International Multiple Sclerosis Genetics Consortium (IMSGC), two sizable MS research consortiums, were used by Dr. Baranzini and his team.

For a genome-wide association study (GWAS), data from both groups were pooled to represent more than 12,500 MS patients.

From there, researchers combed through more than 7.5 million genetic variants before discovering one linked to accelerated disease progression in MS patients.

This particular mutation is situated between two genes named DYSF and ZNF638 that had no known association with MS. ZNF638 aids in the control of viral infections whereas DYSF aids in the restoration of damaged cells.

Possibility of new treatments for MS

Since there is currently no treatment for MS, doctors employ a variety of drugs to treat the symptoms, delay the disease’s course, and help avoid relapses.

The results of this study, according to Dr. Baranzini, will open the door for a new class of medicines that will treat progression and probably target the central nervous system.

Dr. Baranzini made the point that genetic information considerably reduces the risks associated with drug development because developing medicines represents a considerable risk for the pharmaceutical business, where only a tiny percentage of drugs reach the market.

“This discovery will set up several development programs that will target the unmet need of disease progression in MS,” he said.

“All relapse-controlling medications are immunomodulatory, which is consistent with the genetics of the more than 200 MS risk variations. The central nervous system should be the target of this new class of therapies, according to the genetics of illness severity.”

Dr. Baranzini explained that since it has been proven that genetics contribute to the severity of an illness, the IMSGC is currently preparing for a new genetic study including even more participants.

The researcher continued, “Our prior experience with disease susceptibility suggests that a larger study translates into more findings, and we are pleased to uncover new genetic variants that could aid in the development of more efficient treatments for MS.”

How is MS being treated right now?

The capacity to move, think, talk, and see clearly can all be significantly impacted by MS since it affects the brain and nerve system.

The majority of scientists concur that MS is caused by the body’s immune system wrongly attacking the central nervous system, even though the exact origin of MS is still unknown.

The myelin that wraps the nerve fibres in the brain and spinal cord is damaged by this onslaught. When myelin is destroyed, it is unable to protect the exposed nerve fibre, which prevents messages from travelling from the nerves to the brain.

Additional MS risk factors include:

  • age – between the ages of 20 and 50, most persons acquire a diagnosis
  • MS is more prevalent in women than in men.
  • an MS family history
  • smoking
  • a lack of vitamin B12 or vitamin D
  • exposure to specific viral illnesses, such as mononucleosis or the Epstein-Barr virus

Why the recent study is beneficial?

We discussed the significance of the study with Dr. Krupa Pandey, director of clinical research at the Neurosciences Institute in New Jersey, director of the Hackensack University Medical Centre MS Centre, and associate professor of neurology at the Hackensack Meridian School of Medicine who was not involved in the current investigation.

She said, “There are a few ways in which this study is helpful. Finding a connection between genes and the potential severity of a disease is a positive step.”

“It is also beneficial since it offers more proof that environmental variables, like smoking, truly do assist people with genetically susceptible diseases to get sicker. This is a fantastic illustration of how a disease may be affected by both nature and upbringing, said Dr. Pandey.

The expert went on to say that similar discoveries “may lead to future findings that can help us counsel patients on how to tailor not just medication regimens but modify lifestyle-related factors.”

“It is also helpful for companies looking at MS therapies [to] enroll patients with higher risks for progression to see if the drug is effective,” she said.

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