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Is Alzheimer’s Disease Detectable by Finger Prick Test?

Is Alzheimer’s Disease Detectable by Finger Prick Test?

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The ability to diagnose and monitor Alzheimer’s disease remotely may be possible with finger prick tests, according to research.

In contrast to primary care physicians, who only have about 55% accuracy, a different study indicated that blood tests have over 85% accuracy in diagnosing Alzheimer’s disease.

The accuracy and accessibility of diagnosing and managing Alzheimer’s disease may potentially be improved by blood tests.

The number of Americans who have Alzheimer’s disease is currently at 6 million. This number is expected to rise to about 13 million by the year 2050.

Even though there is presently no cure for Alzheimer’s, research have shown that early detection and treatment are essential for postponing the disease’s onset.

Magnetic resonance imaging (MRI), cognitive testing, and physical examinations are currently used as diagnostic techniques. However, access to them is limited because it calls for going to a clinic with knowledgeable staff and involved sample delivery and storage processes.

These tests’ degree of accuracy vary as well. According to a research, almost 25% of people who received a lifetime clinical diagnosis of likely Alzheimer’s had no signs of the disease when they were autopsied.

Furthermore, according to research, up to 50% of dementia sufferers never receive a formal diagnosis while they are still living.

The capacity to detect Alzheimer’s disease earlier and administer treatments that may slow disease development could be aided by increasing the reliability and accessibility of Alzheimer’s testing.

A method for analysing finger prick tests for Alzheimer’s that may be performed at home without a doctor’s supervision was recently developed by researchers.

In contrast to conventional physical examinations, which only accurately diagnose patients with Alzheimer’s disease about 55% of the time, blood tests can detect the disease with a rate of over 85% accuracy.

Alzheimer’s blood tests you can do at home

77 patients from a Barcelona, Spain, memory clinic were involved in the study. All participants gave blood samples from their veins and finger pricks, as well as taking cognitive tests.

For overnight delivery to the University of Gothenburg in Sweden, blood samples were either spotted and dried on “dry blood spot” (DBS) cards or preserved using an anticoagulant called ethylenediamine tetraacetic acid (EDTA).

DBS cards are simpler to carry than EDTA blood samples because they just need to be protected from humidity and moisture. Additionally, centrifugation—the mechanical separation of fluids based on their density—must be performed on EDTA samples before they can be studied, but not on DBS samples.

The blood samples were then examined in Sweden for indicators of Alzheimer’s disease, such as phosphorylated tau, glial fibrillary acidic protein (GFAP), and neurofilament light (NfL).

They noticed that all of the blood samples contained indicators for Alzheimer’s disease. As a result, they claimed, Alzheimer’s biomarkers may be measured with finger prick collection, and DBS might facilitate routine monitoring of patients with possible neurological problems.

How precise are Alzheimer’s blood tests?

Dr. Sebastian Palqvist, Ph.D., associate professor at Lund University in Sweden, and colleagues compared the effectiveness of blood-based biomarkers for detecting Alzheimer’s disease with examinations from primary care physicians in a second study that will also be presented at the Alzheimer’s Association International Conference.

They had 307 patients, ranging in age from middle-aged to old, with a mean age of 76. Cognitive evaluations and a CT or MRI scan were part of primary care examinations. Additionally, participants donated a sample of venous blood, which was examined to evaluate the levels of beta-amyloid and phosphorylated tau.

Blood tests accurately detected Alzheimer’s more than 85% of the time, whereas primary care doctors only correctly identified alterations associated with Alzheimer’s 55% of the time.

According to a news release from Dr. Palmqvist, primary care physicians may find it challenging to diagnose Alzheimer’s due to a lack of precise diagnostic equipment.

This too frequently results in misdiagnosis and ineffective therapy. Alzheimer’s blood tests have enormous promise for increasing diagnostic precision and providing patients with the best care possible. In the near future, as new medications that slow the disease in its early stages become more widely accessible, these tests might become even more crucial.

A faster, less expensive method of diagnosis

“We see these new tools improving our ability to recognise the earliest changes of Alzheimer’s and ultimately speeding our ability to prevent or delay the onset of memory decline,” said Dr. Jeffrey Burns, neurologist and co-director of the University of Kansas Medical Center’s Alzheimer’s Disease Research Centre, who was not involved in the study.

“The general public will soon have access to these instruments. We anticipate the FDA approving blood tests for Alzheimer’s within the next one to two years”. Dr. Jeffrey Burns stated, “We are entering a new and exciting era of Alzheimer’s disease with novel diagnostic and treatment options that will significantly alter how we practise.“

Psychiatrist and director of the Pacific Brain Health Centre at the Pacific Neuroscience Institute in Santa Monica, California, Dr. David Merrill, Ph.D., who was not involved in the study, said that there is currently a shortage of specialists who can perform the extensive testing required to diagnose Alzheimer’s.

“Lumbar puncture tests and radioactive brain scans are riskier, more expensive, and require specialised medical care. Even today’s blood tests require specialist processing and handling to prevent results from being tainted,” he said.

“If this method is validated, it could increase the number of patients screened for Alzheimer’s and may help catch the disease early, when interventions can have a greater impact,” said Dr. Jennifer Bramen, Ph.D., a senior research scientist at the Pacific Neuroscience Institute in Santa Monica, California, who was also not involved in the study.

“A simple finger prick of blood put onto a card that can be shipped directly from a patient’s home at room temperature simplifies the process of getting tested for Alzheimer’s,” explained Dr. David Merrill.

Why only a blood test may not be sufficient?

Dr. Bramen pointed out that the findings were limited by the fact that it was a tiny pilot study and that the research procedures and conclusions had not yet undergone peer review.

Detecting amyloid is not the same as diagnosing Alzheimer’s, Dr. Burns continued. It will be crucial to discover the optimal ways to use these technologies in clinical practise, he added.

A neuropsychologist at Baptist Health Marcus Neuroscience Institute named Dr. Raphael Wald, Psy.D., who was not engaged in the study, was also consulted by experts. Although the test may be helpful in corroboration of an Alzheimer’s diagnosis, he pointed out that it does not reveal the severity of an individual’s impairment.

“Some persons can manage their daily lives quite well despite having Alzheimer’s disease as determined by other testing. Others are severely damaged and show no indications of Alzheimer’s,” he said.

Dr. Merrill added that while blood testing might be more accurate than just gathering medical histories, physicians must also think about the care that would follow.

Will confirmatory testing be easily accessible? Who will pay for the test’s repeatability and how often can or should it be performed? Will blood spot testing be recognised as a starting point for therapies, or will additional testing be necessary? How will newly diagnosed patients be supported? Alzheimer’s disease diagnosis can be a heartbreaking event. Before making this test available to the entire public, there are still many details to be resolved,” he said.

REFERENCES:

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

Alzheimer’s disease and protein imbalance in middle age.

Alzheimer’s disease and protein imbalance in middle age.

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Even though Alzheimer’s disease is the most prevalent form of dementia, it is not a natural part of ageing and affects an increasing number of people.

The hunt for early disease markers is ongoing because early diagnosis and treatments help both dementia patients and their carers.

Now, 32 proteins have been related to the later development of Alzheimer’s disease in middle-aged persons after a lengthy investigation. The researchers advise more investigation into these proteins as potential indicators of Alzheimer’s disease.

The most prevalent type of dementia, Alzheimer’s disease, affects more than 6 million people in the United States. According to the World Health Organisation, Alzheimer’s disease is to blame for 70 percent of the 55 million cases of dementia globally.

Alzheimer’s symptoms can be treated, but there is currently no known cure for the condition. Trials of new drugs, however, are encouraging.

Donanemab, lecanemab, and aducanumab, novel monoclonal antibody medications that remove amyloid proteins from the brain, appear in clinical trials to delay the onset of disease symptoms.

Early diagnosis is essential to successful therapy because studies have shown that these drugs work best when administered during the early stages of the disease. Donanemab trial data recently made public indicate that the medication dramatically slows the clinical course of Alzheimer’s when taken soon after symptoms first occur.

Proteins that are connected to the later development of Alzheimer’s have been found in a recent study of adults between the ages of 45 and 65.

What is the disease Alzheimer’s?

A form of dementia that progresses is Alzheimer’s disease. A condition that adversely impacts memory, thinking, and behavior is referred to as dementia. The modifications make daily life more difficult. There are numerous possible causes of dementia, including diseases and brain traumas. Sometimes there is no known cause.

The Alzheimer’s Association estimates that 60 to 80 percent of dementia cases are caused by Alzheimer’s disease. The condition is typically diagnosed in patients over the age of 65. Alzheimer’s disease is typically described as having an “early onset” or “younger onset” if it is discovered earlier.

Alzheimer’s has no known cure, but some medications can halt the disease’s growth.

A 32 protein biomarker imbalance

The goal of this study was to find proteins that are improperly expressed in middle-aged persons (defined as those between the ages of 45 and 65) who later experience dementia.

Researchers collected blood samples from 10,981 individuals with a mean age of 60 at the beginning of the trial, between 1993 and 1995. Then, using the blood samples, they examined more than 4,800 plasma proteins.

1,874 patients (17%) had dementia diagnoses over the course of the 25-year follow-up period.

32 plasma proteins were discovered by the researchers to be linked to dementia risk. GDF15, a protein involved in inflammation, oxidative stress, and metabolic and immunoregulatory regulation, showed the highest correlation.

They next looked into whether proteins were linked to dementia risk in the short-term (within 15 years of protein measurement) and long-term (beyond 15 years following protein measurement).

Seven midlife proteins, including GDF15 and others related in immunology, growth factor binding, protein breakdown, and nerve and synaptic function, were linked to a higher chance of developing near-term dementia.

Along with six other proteins that were not prominent at the 15-year mark, GDF15 was also linked to a risk of long-term dementia, indicating that the molecular pathways underlying the risk of dementia evolve with time.

Early warning signs of Alzheimer’s disease

The proteins were also discovered in some of the brain tissue. However, GDF15, which was linked to both short- and long-term risks of dementia, was not found by the researchers in the brain tissue.

They contend that rather than being an Alzheimer’s disease-specific protein, it is connected to the neuroinflammation that is linked to aging-related disease.

However, they think they have “identified several pathway-specific plasma proteins that may be relevant in the earliest phase of Alzheimer’s and related dementias.” The researchers did not discover any direct causal links between proteins and Alzheimer’s.

Do new Alzheimer’s tests result from this?

“Although the dementia-associated proteins alone did not provide a highly accurate prediction of 25-year dementia risk, these proteins, in combination, did add modest predictive value to a group of demographic and clinical variables which are themselves strong predictors of dementia risk,” the study’s authors stated.

The proteins that have been discovered, according to the researchers, ought to serve as the starting point for additional study because they might be dementia risk factors.

Additionally, they assert that their findings might shed light on pertinent biological pathways and make it easier to uncover illness early signs and molecular triggers.

Therefore, with more study, these proteins might be helpful in determining a person’s risk of dementia. We will have to wait and see if they contribute to the development of new dementia diagnostic tests.

REFERENCES:

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

Superagers: Why resistant to age-related memory decline?

Superagers: Why resistant to age-related memory decline?

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An observational study investigated whether age-related memory decline may not affect superagers, or those 80 years and older who possess the cognitive abilities of people who are decades younger.

In comparison to older persons with cognitive deterioration, the octogenarians with strong memory retention moved more quickly and experienced lower levels of worry and depression. Additionally, MRI scans revealed that certain memory-related brain regions had increased grey matter in super-agers.

Superagers are people over the age of 80 whose recollections of their past are just as clear as those of others who are 20 or 30 years younger. Scientific research is becoming increasingly interested in the mechanisms of superaging.

According to a recent study, older persons with cognitive decline had higher rates of anxiety and despair compared to octogenarians with strong memory retention. They also do better on movement tests.

The researchers speculate that such superagers may also have more grey matter in their brains.

In a press release, the study’s first author Marta Garo-Pascual, a Ph.D. candidate at the Technical University of Madrid in Spain who studies healthy memory ageing, stated:

“We are now getting closer to answering one of the most important outstanding concerns about superchargers: whether they are actually resistant to age-related memory decline or whether they have coping mechanisms that allow them to outperform their contemporaries in overcoming this decline. Although the specific causes of super agers resistance to these processes are still unknown, our data suggest they do. We may be able to learn vital information about the mechanisms underlying the maintenance of memory function well into old life by investigating the connections between superaging and movement speed in more detail.”

Superagers: Exercise promotes the health of the brain

For the study, 55 typical older persons and 64 superagers who were identified by a memory test used in a prior study on Alzheimer’s disease were compared. The average age of research participants was 79.5 years or higher.

The Timed Up and Go Test, which assesses mobility, and a finger-tapping test, which gauges fine motor function, revealed that the superagers outperformed the general population.

Even when super agers reported no appreciable change in exercise levels from the older people in the control group, the findings persisted.

The study’s principal author, Dr. Bryan Strange, a neurologist at the Technical University of Denmark, noted that although superagers report similar activity levels to average older adults, it’s possible that they engage in more physically taxing hobbies like gardening or stair climbing.

“There are many direct and indirect benefits of being physically active that may contribute to improved cognitive abilities in old age, from lower blood pressure and obesity levels to increased blood flow to the brain,” stated Dr. Bryan Strange.

It’s also plausible that the reason superagers move more quickly is because their brains are in greater health to begin with, according to Strange.

The amount of grey matter in superagers brains is higher.

The results also supported earlier studies that found super-agers have more grey matter in the brain regions linked to memory.

Researchers Dr. Alexandra Touroutoglous, Dr. Bonnie Wong, and Dr. Joseph M Andreano of Harvard Medical School wrote in an editorial statement that accompanied the article that this discovery predominantly focused on the medial temporal lobe of the brain, “which is consistent with previous research.”

The comments pointed out that previous studies on the anterior mid-cingulate cortex, another crucial area of the brain, reported more cortical thickness and stronger functional connectivity among super-agers, who in turn had greater memory performance.

The attention, memory, executive function, and motivation are just a few of the processes that the anterior mid-cingulate cortex is involved in.

The researchers concluded that “[the] greater performance of super agers relative to typical older adults may not only reflect differences in motivation, executive function, and persistence in the face of difficulty, which suggests that super-agers have a higher level of tenacity than typical older adults.”

Compared to other older individuals, superagers age differently.

According to the University of Madrid study, there were no discernible differences between superagers and other adults of a similar age in terms of biomarkers or genetic risk factors for neurological illness. This suggests that another protective mechanism may be at play.

Similar levels of dementia blood biomarkers were found in both the superager and standard older adult groups, the researchers said, “suggesting that group differences reflect inherent superager resistance to typical age-related memory loss.”

The study’s large sample size, according to Dr. S. Jay Olshansky, a professor in the Division of Epidemiology and Biostatistics at the University of Illinois at Chicago School of Public Health, makes the results an essential addition to the field of “geroscience,” the research of mechanisms that cause aging.

Dr. Olshansky stated, “We do a lot of things to shorten our lives by adopting unhealthy lifestyles,” and many superchargers and centenarians people who live past 100 live longer and have better cognitive health because they age differently from the general population.

Do super-agers have a hereditary propensity for aging?

The appearance of some children of superchargers, Dr. Olshansky recalled, supported the idea that some people’s “biological time clock ticks at a slower rate” due to genetic factors. This is said to also explain why the superchargers in the Spanish study also performed better on movement tests.

Even though they have completed 80 orbits around the sun, he claimed that they are not biologically 80 years old.

“Asking superagers for their key to longevity is therefore ludicrous because they have no idea. They recently emerged as the birth genetic lottery winner.

The latest study, according to Dr. Olshansky, attempts to better understand why some people age differently than others and determine whether the process may be changed.

He said, “Start with not shortening your life,” in the meanwhile. “We will still age and pass away, even if you control all the risk factors,” he stated. We are at the mercy of our genes, but we have some power over those genes.

REFERENCES:

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

Hearing aids may almost 50% lower the risk of dementia.

Hearing aids may almost 50% lower the risk of dementia.

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The effect of hearing aids on slowing cognitive decline was studied in the largest clinical research to date.

Researchers discovered a 48% decrease in risk among those who were at an increased risk of dementia. The findings contribute to the body of knowledge on the relationship between hearing loss and cognitive decline.

According to the National Institute on Ageing, someone worldwide gets dementia, a group of illnesses that damage the brain. Also, result in cognitive decline and memory loss, every three seconds.

Alzheimer’s disease (AD) is the most prevalent form of dementia.

Dementia can occur for a variety of reasons, and there are a number of risk factors for dementia as well. Hearing loss is one of them. Hearing loss and a higher risk of dementia have been linked in previous studies.

The largest clinical experiment to look into whether a hearing loss therapy intervention can lessen a person’s risk for cognitive decline has now been completed. The results have been published by researchers from the Ageing and Cognitive Health Evaluation in Elders (ACHIEVE) study.

Researchers showed that using a hearing aid and getting support and counselling from an audiologist significantly reduced cognitive deterioration in individuals in a higher-risk subgroup by 48%.

Recognising those who use hearing aids

The study discovered differences in hearing aid usage based on geography, gender, and ethnicity.

Nearly 115,000 adults over the age of 66 who had hearing loss and insurance coverage from a significant. Also, private insurance firm between 2008 and 2016 were studied using data from these individuals.

Participants were followed up on by the team 3 years after their diagnosis and one year prior.

Men were more likely to use hearing aids if they had hearing loss. In actuality, 13.3 percent of men and 11.3 percent of women purchased hearing aids.

Additionally, 13.6% of white persons, 9.8% of African Americans, and 6.5 % of those of Latino descent received a hearing aid.

Nearly 37% of hearing-impaired Americans who wore hearing aids resided in the north-central region of the nation, compared to 5.9% of persons in the mountain states.

Those who wore hearing aids had an 18% decreased chance of receiving a dementia diagnosis within three years of a hearing loss diagnosis (including Alzheimer’s disease).

Hearing aid users had a 13 percent lower likelihood of receiving treatment for injuries sustained from falls and an 11 percent lower risk of receiving a diagnosis of depression or anxiety by the end of the three-year period.

The study’s findings, ACHIEVE

Participants in the ACHIEVE study range in age from 70 to 84, have mild to moderate hearing loss that is untreated, and do not have significant cognitive impairment. Four American locations were used to carry out the study.

977 individuals in all were recruited for the study. About 740 of them were recently recruited healthy community participants. The Atherosclerosis Risk in Communities (ARIC) study has about 240 participants.

Researchers found that participants in the ARIC group had more cognitive risk factors, poorer baseline cognitive scores, and a faster rate of cognitive deterioration over the course of the study’s three years than the other participants.

One group of participants underwent a three-year intervention that included receiving hearing aids, a self-management “toolkit” for hearing loss, and regular training and counselling with an audiologist.

Only speaking sessions with a health educator to address the prevention of chronic diseases were provided to the control group.

After three years, researchers discovered that ARIC study participants who received hearing aids and intervention had decreased the rate of their cognitive loss by 48%.

The ACHIEVE study’s co-principal investigator, Dr. Frank Lin, a professor at the Bloomberg School of Public Health and the Johns Hopkins University School of Medicine, said, “A 48% reduction in cognitive deterioration is significant, and we were happy to learn that the benefit was so big.”

How are hearing loss and cognitive deterioration related?

Dr. Lin claims that it has been well established for more than ten years by researchers that hearing loss significantly increases the risk of dementia and cognitive decline.

But he continued, “We didn’t know if treating hearing loss may actually slow cognitive deterioration and perhaps even cut the likelihood of dementia.”

Dr. Lin outlined three key factors that shed light on why dementia and hearing loss may be linked:

“First, hearing loss causes speech and sound to be muddled before they reach the brain, which makes it harder for the brain to understand the signals coming from the ear. The brain’s capacity to sustain thinking and memory is therefore reduced.”

Second, hearing loss depletes the areas of the brain that are normally activated by speech and sound, which can result in atrophy and modifications to the brain’s structure and function.

Thirdly, communication difficulties brought on by hearing loss might result in social isolation, another dementia risk factor, according to Dr. Frank Lin, co-principal investigator of the ACHIEVE project.

This is not the first study to look into the relationship between dementia, hearing loss, and hearing aids.

According to a 2022 study, wearing hearing aids may slow the cognitive impairment brought on by hearing loss.

Additionally, an observational study released in April 2023 discovered hearing loss was linked to a higher risk of dementia, and that utilising hearing aids may potentially help reduce that risk.

Additional proof that treating hearing loss enhances cognitive

Dr. Courtney Voelker, a board-certified neurotologist and the director of the Adult & Paediatric Cochlear Implant Programme at the Pacific Neuroscience Institute at Providence Saint John’s Health Centre in Santa Monica, California, commented on the study after reading it and said that it is an exciting study that provides additional proof that not only is hearing loss connected to cognitive decline as we age, but that we can also take action to prevent it.

According to her, there is growing evidence, which includes this study, that treating hearing loss aggressively can enhance cognition. This treatment may include cochlear implants or hearing aids, depending on the severity of the hearing loss. And it’s really exciting.

Dr. Voelker claimed that when discussing cognitive decline with her patients, she emphasises the significance of maintaining brain neuron activation and stimulation.

“And it’s very interesting patients really respond to this,” she added. “People who may have initially been reluctant to adopt hearing aids take the possibility of developing cognitive dementia very seriously when making their choice.” He also explains to patients why we allow people to go without hearing aids even though we would never allow someone to go without glasses if they had vision problems. Additionally, patients appear to connect with that parallel. According to neurotologist Dr. Courtney Voelker, “We want our hearing to be as crisp and clear as our vision is with glasses.”

Understanding hearing loss

The World Health Organisation (WHO) estimates that 20% of people worldwide have some form of hearing loss.

There are several reasons why someone could lose their hearing, including:

  • exposure over time to loud noises
  • hearing loss
  • destruction of the inner ear
  • a torn eardrum
  • a history of hearing loss in the family
  • some diseases, such meningitis, that raise the body’s temperature
  • a few medicines

Furthermore, hearing loss becomes more prevalent as we age, with the majority of cases typically happening beyond the age of 60.

Hearing loss can be either temporary or permanent, depending on the circumstances. There is currently no solution for age-related hearing loss, and it may get worse with time.

REFERENCES:

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

Are Ketamine injections effective for resistant depression?

Are Ketamine injections effective for resistant depression?

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Participants in clinical trials with treatment-resistant depression got placebo or racemic ketamine injections twice weekly for a month.

With the use of ketamine, about one in five patients had all of their symptoms go, and nearly a third had at least a 50% improvement.

A total of six clinical mood disorder centers from Australia and one from New Zealand collaborated on the study.

More and more academics are investigating the use of psychedelics, a class of drugs that alter consciousness, as a potential depression cure. The drug ketamine, which has been used as an anesthetic for many years, is of particular interest to many.

A recent study comparing the effectiveness of racemic ketamine vs a placebo in easing the symptoms of treatment-resistant depression was published in the British Journal of Psychiatry.

Depression that does not improve after receiving two or more forms of treatment is referred to as treatment-resistant depression.

What variations of ketamine are there?

The commercially produced nasal spray Spravato (ketamine) was approved by the Food and Drug Administration (FDA) in 2019 for adults with treatment-resistant depression and for individuals with major depressive disorder who have acute suicidal ideation.

In the US, racemic ketamine is permitted for use as anaesthetic. In addition, doctors prescribe it “off-label”—that is, for a condition other than the one for which the FDA has given its approval—to treat depression.

Additionally less expensive than Spravato is racemic ketamine.

Participants in the current trial, which was directed by academics at the University of New South Wales Sydney (UNSW) and the associated Black Dog Institute, got injections of racemic ketamine or a placebo twice a week.

Largest clinical trial to date

According to Medical News Today, the trial’s principal investigator, Dr. Colleen Loo, a clinical psychiatrist and professor of psychiatry at UNSW, started examining ketamine’s effects on depression in 2011. She had previously researched how ketamine was used in anesthesia for electroconvulsive treatment (ECT).

She said that this research experiment, which compares racemic ketamine with placebo for treatment-resistant depression, is the largest of its kind.

Dr. Loo further emphasized that one-fourth of the subjects had previously undergone ECT treatment but had not shown improvement.

“ECT is a highly effective treatment for severe and treatment-resistant depression, so it means that these people had high-end treatment-resistant depression,” she argued.

Because it is extremely difficult to get any treatment to work once someone has received ECT and is still ill, this group is typically left out of the research. According to Dr. Colleen Loo, this study “provides evidence of the efficacy of ketamine, at least the racemic form, in treating depression with a high level of treatment resistance.”

Dr. Loo finds it significant that racemic ketamine injections were used in the trial rather than more costly and time-consuming infusions, demonstrating the efficacy of this less expensive option.

Study on ketamine for adult depression

The Ketamine for Adult Depression (KADS) research was a trial in which 184 patients with treatment-resistant depression participated. Six clinical mood disorder centres in Australia and one in New Zealand participated in the investigation.

Participants must have applied by April 2020, with the application period opening in August 2016.

Dr. Loo told that when the pandemic struck, researchers decided to stop recruiting new subjects for the trial. Originally, they had hoped to enroll more people.

Participants had a serious depressive disorder for at least three months and were 18 years of age or older. Furthermore, patients had to have received an inadequate response with at least two antidepressants.

Before beginning the trial, the participants had to have been taking the same dosage of their current antidepressant for at least four weeks. Additionally, they had to have a Montgomery-Sberg Rating Scale for Depression (MADRS) score of at least 20.

“Good safety profile” for injections of ketamine

Racemic ketamine or midazolam injections were given to participants at random. Midazolam is frequently used to assist patients unwind before surgery.

For four weeks, individuals received injections into their abdomen walls twice each week with at least three days in between each treatment.

According to Dr. Loo, the participants didn’t seem bothered by the abdominal injections.

“The injection used a very small needle to inject ketamine under the skin,” she claimed. “It can be done anywhere — arm, leg, abdomen — but we did it in the abdomen because there is usually more fat there under the skin, so it is more comfortable.”

Participants and researchers who administered the medication were unaware of who received racemic ketamine. Because midazolam also induces sleepiness, like ketamine, it was chosen as the placebo because it helped prevent participants from knowing which medication they would get.

Initially, a fixed dose of either 0.025 milligrammes per kilogramme of midazolam or 0.5 milligrammes per kilogramme of racemic ketamine was administered randomly to 73 subjects.

The authors of the study report that during a routine Data Safety Monitoring Board meeting, “a revisiting of drug dosage was recommended as no participants in the entire masked sample had remitted and the safety profile was good,”

As a result, the dosage was altered, and 108 individuals were randomly assigned to receive flexible doses of either midazolam or ketamine in a second group. Implementation of response-guided dosage. Racemic ketamine dosages were increased to 0.6 milligrammes per kilogramme, 0.75 milligrammes per kilogramme, and 0.9 milligrammes per kilogramme in sessions 2, 4, and 6 if patients had not improved by 50% from baseline scores. Elevated doses of midazolam were given to participants as well.

If they received at least one injection, they were considered for the trial, however, Most” people received all eight dosages.

Monitoring safety closely yields fruitful outcomes.

The majority of individuals in the flexible dosing group increased their racemic ketamine dosage to the maximum level. Dr. Loo claims that this aspect of the study turned out to be significant. “It showed that individual dose adjustment, up to the dose that each person requires for a response, is really important for getting the best outcomes,” the researcher added.

The Ketamine Side Effect Tool (KSET) was utilised by researchers to better understand the short- and long-term side effects of various racemic ketamine therapies.

Participants were checked on again four weeks following the last injection. The open-label therapy phase was open to participants who had relapsed; this means that they would be aware of the treatment they are getting.

“The study used a very detailed and comprehensive approach to safety monitoring, monitoring for cumulative effects between treatments, not just in the two hours after each treatment, or just enquiring at the end of the four weeks,” stated Dr. Loo.

The researchers state in the trial publication that “if ketamine treatment is halted after 4 weeks, the benefits are not sustained for all remitters and that ongoing treatment should be considered.”

According to the researchers, “most” individuals decided to start open-label treatment at the conclusion of the four weeks.

30% of subjects had a 50% improvement in symptoms

After a month of injections, 1 in 5 subjects getting flexible doses of racemic ketamine had completely recovered from their symptoms, compared to 2% of participants receiving placebos.

Compared to 4% of those who received a placebo, nearly 30% of those who received ketamine saw symptom improvements of at least 50%.

A 20% remission rate, which Dr. Loo deemed “quite good” for treatment-resistant depression, did not surprise her.

The outcomes are actually very positive, according to Dr. Loo. “Ketamine was still very effective, with an impressive 10 [times] difference compared to placebo,” according to the study. “Even in people with depression at the high end of treatment resistance excluded from most prior studies.”

The scientists want to develop the KSET further and run bigger, more extensive studies with generic ketamine in the future.

REFERENCES:

For Depression medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?therapy=6

Heart failure: An Important link with cognitive impairment.

Heart failure: An Important link with cognitive impairment.

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Heart failure affects more than 64 million people globally. One of the most frequent complications in heart failure patients is cognitive impairment.

Heart failure may cause cognitive decline because, according to Columbia University researchers, there is a little calcium leak inside the brain’s neurons.

Additionally, researchers have created an investigational medication that aims to ‘plug’ the calcium leak and halt the course of heart failure.

Heart failure, an incurable cardiovascular disorder where the heart cannot effectively pump blood throughout the body, affects about 64 million people globally.

Complications include shortness of breath, arrhythmia, and kidney problems. Also, fluid retention in the lungs, belly, feet, and legs is more common in those with heart failure.

Additionally, one frequent complication in persons with heart disease is cognitive impairment.

A little calcium leak inside the brain’s neurons, according to Columbia University researchers, may be the reason heart failure can result in cognitive impairment.

In addition, researchers have created an experimental medication to “plug” the calcium leak and perhaps reduce the development of heart failure.

What is cognitive dysfunction?

Cognitive impairment is also known as mild cognitive impairment. It happens when a person struggles to perform routine tasks that call for mental abilities like memory and thought.

Cognitive disability examples include:

  • forgetfulness
  • missing events on the calendar
  • not knowing how to travel to frequented locations
  • difficulty understanding a talk
  • decision-making challenges
  • failure to follow through on commitments or directions

People who have modest cognitive impairment could also go through emotional changes like despair, anxiety, and rage.

Cognitive impairment can be brought on by a variety of conditions, including infections, prescription drugs, and other diseases.

A increased chance of developing other types of dementia, such as Alzheimer’s disease, exists in those with mild cognitive impairment.

How does brain dysfunction may affect cognition?

The team decided to investigate a potential link between heart failure and cognitive decline. Based on what they already knew about the ryanodine receptor type 2 (RyR2)/intracellular Ca2+ (calcium release channel), Dr. Andrew R. Marks, chair of the Department of Physiology & Cellular Biophysics at Columbia University Vagelos College of Physicians and Surgeons and lead researcher of this study explained.

Both the heart and the brain have the RyR2 channel, thus he said, “I reasoned that since the channel is leaky in the heart due to systemic stress of heart failure it might also be leaky in the brain.”

In heart muscle, there is an encoded protein called RyR2. It contributes to the delivery of that specific mineral to the cardiac muscles as a component of the intracellular calcium channel.

Calcium is essential for both heart and brain function, Dr. Marks noted. “Calcium is required to activate muscle contraction in the heart and for signaling in the brain.”

Testing the theory of the heart-brain relationship

Dr. Marks and his team tested their theory in this study using a mouse model. Researchers discovered that calcium leakage in the brain’s neurons caused cognitive impairment in rats with heart failure.

Scientists also looked at the brains of heart failure victims who had passed away. They looked at those brains and discovered leaky calcium channels, which may have contributed to cognitive impairment in those people.

Since heart failure is progressive, clinicians may want to closely examine their heart failure patients for cognitive impairment and keep track of this, according to Dr. Marks’ research. “The doctors could determine whether their patient’s cognitive impairment is affecting their capacity to comply with medical advice and take their medications.”

Are calcium leaks treatable by doctors?

Dr. Marks and his team discovered throughout the study that an investigational medication called Rycals created by Marks’ group. It could be used to “plug” the calcium leak and possibly delay the onset of heart failure.

“Rycals fix the leak in RyR channels and are in clinical trials at the Mayo Clinic and at the AMC in Amsterdam for an inherited form of exercise-induced sudden death,” stated Dr. Marks. In a year or two, depending on the outcome of this experiment, they might be available.

A broad unifying hypothesis?

About this study, Dr. Richard Wright, a cardiologist at Providence Saint John’s Health Centre in Santa Monica, California, who was not involved in the study, remarked.

He applauded the researchers for finally developing a comprehensive, all-encompassing theory of various disease states after years of research.

Dr. Wright said, “People with chronic heart failure are weak and have respiratory problems; this has long been known. As this article noted, they frequently exhibit cognitive impairment in comparison to their classmates.”

Here, Dr. Marks’ team is attempting to develop a unified theory to account for all these many changes that take place in heart failure patients, and I believe they have done so. Dr. Richard Wright stated, “I believe this idea that calcium excess is a unifying mechanism to explain not only the heart’s dysfunction but skeletal muscle dysfunction, diaphragm dysfunction, and as the article’s main thesis, brain dysfunction as well.”

The beginning of a new era is upon us.

Dr. Wright remarked that he was thrilled to learn of a substance created in the lab of the study team that has been demonstrated to favourably effect these alterations.

We are at the beginning of a new era, which I would refer to as the period of designer molecules, he remarked. “We’ve seen it in hypertrophic cardiomyopathy and amyloidosis already, where you can design molecules that change pathologic changes of proteins.”

They have compounds created in their lab to prevent alterations that help prevent calcium excess in neurons, heart cells, and skeletal muscle cells. This could have a significant impact on the results of our research.

Dr. Wright did point out that additional research is still required because the majority of the results in this article came from a mouse model.

Humans are not mice, he continued, so “sometimes we get misled.” However, they’ve done a great job of avoiding that and gone to the bother of using chunks of autopsied brains to support their claim, which I think is quite real.”

Other study limitations include the tiny number of human brains examined by the researchers and the fact that the study’s control group consisted of participants who were significantly younger than those who had suffered from heart failure and cognitive deterioration.

REFERENCES:

For Alzheimer’s disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_99

Abuse of alcohol and other substances alters the brain.

Abuse of alcohol and other substances alters the brain.

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Cognitive flexibility is the ability to adjust to changing conditions in order to get the best results.

Researchers are still trying to understand the interactions and alterations that take place when certain medications have an impact on cognitive flexibility.

The relationship between impaired cognitive flexibility and cocaine and alcohol usage was recently investigated.

The information provided a crucial understanding of the underlying neuronal networks underlying these alterations in the brain.

There is still much to learn about how the brain and some addictive chemicals interact. The complexity and distinct affected brain circuits are still a mystery to researchers.

A recent mouse study investigated the effects of cocaine and alcohol on particular brain circuits.

According to the study’s findings, cocaine and alcohol may block specific brain connections, making it harder to adjust to changing conditions.

Abuse of drugs impairs cognitive flexibility

People can change their behavior by adapting their ideas. This is referred to as cognitive flexibility. According to the authors of this study, cognitive flexibility enables individuals to modify their behaviour in response to their settings in order to obtain desirable results.

Ben Spielberg, a neuroscientist and the founder of Bespoke Treatment, elaborated on the significance of cognitive flexibility in his study:

The ability to change one’s mental focus and adjust to new challenges, objectives, and patterns is referred to as cognitive flexibility, a complicated phenomenon. Cognitive flexibility is defined as the capacity to think and act appropriately in response to changes in inputs, settings, and surprises. Our world is changing quickly, and if our thought patterns are rigid and unchanging, we can’t adjust to it. Cognitive flexibility is therefore vital.

The use of specific drugs and alcohol has been associated with a decrease in cognitive flexibility, according to the study’s authors.

The goal of this study, according to Dr. Jun Wang of the Texas A&M University School of Medicine, was to “examine why addictive substance use reduces cognitive flexibility.”

How do drugs and alcohol impact thinking?

In this study, mice and rats were used to examine the effects of cocaine and alcohol on cognitive flexibility and the underlying mechanisms at play.

Reversal learning tasks were employed by researchers to evaluate cognitive flexibility. This entails performing acts and tasks that are the opposite of what they were in the past.

They discovered that cocaine helps to inhibit particular neurons known as striatal cholinergic interneurons (CINs) by interfering with certain brain connections.

Previous research has shown that direct-pathway medium spiny neurons (MSN) are more active when exposed to addictive drugs over time. They discovered that exposure to cocaine seems to intensify the inhibitory signals that direct-pathway medium spiny neurons (MSN) send to striatal cholinergic interneurons (CINs). Their research provides additional evidence that alcohol has a similar effect.

The authors of the study also discovered that cocaine exposure reduced CIN firing to the dorsomedial striatum (DMS), a region of the brain. The ability to think creatively depends on this part of the brain.

The information sheds light on a few possible mechanisms by which addictive chemicals may limit cognitive flexibility. The identification of these mechanisms may aid in the creation of medications for the treatment of substance use disorders.

Dr. Wang provided some details regarding the team’s brain circuits, saying:

“It is unclear what mechanisms underlie the decrease in cognitive flexibility brought on by reinforcement. Through a collateral projection from dMSNs to CINs, this study discovered that dMSN activation by substance use decreases CIN function and flexibility. In other words, dMSN-to-midbrain mediates reinforcement, whereas dMSN-to-CIN lowers cognitive flexibility.”

According to Spielberg, drug abuse “is linked to impulsivity at initial stages (e.g., before physiological dependence kicks in). However, the brain switches to a compulsive pattern once one becomes dependent on the drug.”

The effects on the human brain require additional study.

The primary drawback of this study is that it was conducted on rodents, which means that it cannot be directly used to work with people.

To fully comprehend how alcohol and cocaine affect neural networks in the human brain, more research is required. For instance, it is unknown to what extent consuming alcohol or cocaine affects cognitive flexibility, Dr. Wang explained:

This study identifies an intrinsic circuit that mediates the cognitive flexibility brought on by reward. We haven’t yet looked at what dosages of alcohol or cocaine will make people less flexible cognitively. Alcohol or cocaine use disorder, which is defined as obsessive use of these substances despite negative effects, is widely thought to cause permanent alterations at dMSN-to-CIN.

Obtaining addiction therapy

This study adds to the body of research that shows how addictive chemicals affect people. Numerous alternatives are available to those who need assistance in reducing the possibly negative impacts of addiction.

Long-term management and learning new behaviors that challenge old patterns can both be part of addiction treatment.

Some drugs may be able to ease withdrawal symptoms and aid in the process of acclimating a person to life without a particular substance.

Therapy that enables people to alter their behaviors and way of thinking might be helpful to those seeking addiction treatment.

In his explanation of some facets of addiction treatment, Spielberg said:

“The current standard of care involves a community-based treatment programme such as a Partial Hospitalisation Programme (PHP) or Intensive Outpatient Programme (IOP). This is once a person has been medically detoxicated from substances. In addition to having a substance addiction disease, many persons also have other underlying mental health diagnoses that have to be treated. These diagnoses often include bipolar illness, PTSD, depression, anxiety, OCD, and ADHD.

REFERENCES:

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

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