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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

Can a daily brief walk could help with depression?

Can a daily brief walk could help with depression?

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Exercise can enhance brain health, lower disease risk, build bones and muscles, and manage weight.

There is mounting evidence that it can also reduce the signs and symptoms of depression, the main disorder connected to mental health. However, opinions on how much exercise is necessary to have a positive impact vary.

Now, a 10-year research in Ireland has discovered that even little quantities of exercise, like a daily 20-minute stroll, can help older persons experience less despair.

Depression, one of the most prevalent mental health illnesses, is characterized by a persistent sense of emptiness, sadness, or an inability to experience a pleasure. The World Health Organisation (WHO) estimates that it affects about 5% of adults globally.

In 2020, there were 21 million individuals in the United States (8.4% of all adults), and women were more likely than males to experience serious depressive episodes.

According to official government figures, one in six adults in the United Kingdom reported having depressed symptoms in 2021–2022.

Depending on the type of depression a person is dealing with, there are several treatments available, such as antidepressants, psychotherapy like cognitive behavioural therapy (CBT), or a combination of therapy and medicine. Many people find them to be helpful, but once treatment is discontinued, depression may recur.

A little exercise can make a big difference.

There is mounting evidence that altering one’s lifestyle helps lessen depression symptoms. A diet rich in fruit, vegetables, seafood, and whole grains may be linked to a lower incidence of depression, according to a 2014 analysis of 21 research. Additionally, a 2022 analysis of studies revealed that exercise reduced the symptoms of depression.

How much exercise is necessary to reduce depression, however, has not been the subject of many studies.

Now, a ten-year study has discovered that even little exercise helps lessen depression in older persons, defined as those who are 50 years of age and older.

The Health Research Board (HRB) Ireland-funded study, which is published in JAMA Network Open, discovered that a 20-minute brisk walk five times a week dramatically decreased the incidence of depression.

The University of Limerick in Ireland’s Dr. Eamon Laird, the study’s author, explained why the group conducted the investigation:

“Unfortunately, depression is becoming more common in older adults and is linked to a higher risk of developing chronic illnesses like cardiovascular disease (CVD), cognitive decline, death, and suicide. Previous studies have linked physical activity to a lower risk of depression, but no one has ever looked into the absolute minimum amount of physical activity that might be beneficial.

Exercise in general lessens depression

The Irish Longitudinal Study on Ageing (TILDA), a sizable longitudinal study with the goal of enhancing Irish citizens’ ageing experiences, provided the researchers with 4,016 participants. They gathered information between October 2009 and December 2018 at five different intervals.

The researchers used self-completed questionnaires, nurse health assessments, or interviews to gather thorough data on demographic, health, lifestyle, and social aspects at each time point.

The Centre for Epidemiological Studies Depression (CES-D) short form was used to evaluate depressive symptoms. Using this information, they defined major depression as either having a CES-D score more than or equal to nine and/or experiencing a major depressive episode at any moment throughout the data collection process.

Participants self-reported their physical activity over the previous seven days at each data point. They were to keep track of the days they engaged in vigorous, moderate, and walking activities as well as the duration of those activities.

After estimating each person’s weekly total of MET minutes, the researchers divided them into three groups based on their level of physical activity: low, moderate, and high.

Dr. Laird informed us, “We found that older adults who engaged in as little as 20 minutes of moderate to vigorous physical activity (MVPA) per day (for five days a week) had a 16% lower risk of depressive symptoms and a 43% lower odds of depression than those engaging in no exercise.”

The benefits grew as the researchers’ exercise levels rose in each of the three exercise categories. The most active people had a 20% lower chance of developing depression than the least active people.

Even individuals who exercised infrequently had a 16% lower risk of depression than those who did not exercise at all.

Exercise, chronic illness, and depression

Dr. Laird noted that exercise reduced the probability of both depressive symptoms and major depression in people with chronic diseases, and that the benefit grew with increased activity levels.

The WHO standards threshold of 30 minutes a day [per] 5 days [a] week for depressed symptoms was met by participants, specifically for those with chronic conditions, albeit the biggest decreases came with increasing exercise dose, according to the study.

He continued, “In essence, those with chronic diseases may find more benefits. It might be several pathways, including anti-inflammatory, immunological function, heart-brain communication, enhanced muscle performance, etc.”

The study’s non-participant, Dr. Thomas MacLaren, a consultant psychiatrist at Re: Cognition Health, applauded the results.

Chronic health conditions are known to worsen depression and may possibly increase one’s likelihood of getting depressed. The study’s conclusion that there was a dose-dependent association for this group is really positive and shows that adding more brisk walking to your daily routine will help you feel better, he said.

The benefits of exercise for mental health.

Exercise may lower the chance of getting depression or lessen depressive symptoms for a number of reasons.

Exercise improves blood flow to the brain, lowers stress reactivity, and stimulates the hypothalamic-pituitary-adrenal (HPA) axis, which affects motivation and mood. Endorphins, the body’s natural pain and stress relievers, are also produced in greater quantities.

As Dr. MacLaren noted, the impacts go beyond the physical.

Exercise raises fitness levels and encourages the body to release endorphins. Your mood can be elevated naturally by these advantageous consequences. Additionally, it may indirectly improve your daily routine and increase social contact, both of which are crucial in the fight against depression.

Dr. Laird concurred, pointing out that for maximum effect, exercise should be a component of a healthy lifestyle.

“Try to incorporate [exercise] into a routine with hobbies or activities that you enjoy, and we would recommend doing it with others as social interactions, particularly with activity, can also have additional benefits for your mental health,” he advised.

“Remember that it is one component and that nutrition and a healthy lifestyle will also give additive benefits in addition to the physical activity,” said Dr. Laird.

REFERENCES:

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

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

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

Short sleep may cancel mental benefits gained from exercise

Short sleep may cancel mental benefits gained from exercise

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In 8,958 persons in England who were 50 years of age and older, researchers examined cognitive function over a period of ten years.

According to the study, persons who get between 6 and 8 hours of sleep each night and who exercise more frequently had superior cognitive function.

Even if they engaged in higher levels of physical activity, people who slept for fewer than 6 hours per night exhibited a more rapid deterioration in cognitive function over ten years.

The advantages of higher levels of physical activity on cognitive function appeared to be preserved among participants aged 70 and older regardless of the quantity of sleep.

Physical activity appears to be good for the brain and may help prevent the onset of neurodegenerative diseases including dementia and Parkinson’s disease, according to existing research. A recent study discovered that sleep deprivation can lessen the advantages of exercising.

According to a 2022 nationally representative survey on the prevalence of cognitive impairment, 22% of Americans aged 65 and older have mild cognitive impairment and about 10% have dementia.

Numerous studies have revealed that exercise may lower the risk of dementia. More research continues to link a lack of sleep to a higher risk of dementia.

“Physical activity and sleep are factors that are thought to independently contribute to cognitive function, but they are also interrelated, where more physical activity is correlated with better quality sleep and physical activity may also regulate circadian rhythms,” said Mikaela Bloomberg, Ph.D.

Few studies that examined the effects of physical activity and sleep on cognitive function have been conducted, according to a team of UCL academics led by Bloomberg. Small and cross-sectional studies, which gather information from participants at a specific point in time, were the type of research they discovered.

Study is based on healthy people’ self-reported data.

Researchers from UCL analyzed longitudinal data from the English Longitudinal Study of Ageing (ELSA), which included 8,958 cognitively healthy people from England who were 50 years and older. The information was gathered from January 1, 2008, to July 31, 2019.

Every two years, participants provided reports on how much they moved and how long they slept.

Participants were asked how many hours they typically slept on a weeknight by researchers. The UCL researchers then classified sleep as “long” if it lasted longer than eight hours, “optimal” if it lasted between six and eight hours, and “short” if it lasted fewer than six hours.

Participants’ level of exercise was also questioned by researchers. Participants gave information about how often they engaged in light, moderate, and strenuous physical activity as well as whether they worked out more than once a week, once to three times a week, rarely, or never.

Using the immediate and delayed recall tests from the Consortium to Establish a Registry for Alzheimer’s disease, researchers evaluated the participants’ episodic memory. Participants were given a list of ten words by researchers, and they were asked to recall the terms both right away and a day later. The participants’ verbal fluency was also evaluated by the researchers using a test in which they had to name as many animals as they could in one minute.

Participants who disclosed receiving a dementia diagnosis during the follow-up period as well as those whose test results indicated some degree of cognitive impairment were excluded by the UCL researchers. Researchers also took into account information like whether participants had previously taken the same cognitive test when adjusting their analyses.

How do sleep duration and activity affect cognitive scores?

1,525 participants (50%) of the 3,069 participants who were assigned to the “higher physical activity category” said they exercised lightly, moderately, or vigorously more frequently than once per week. Another 1,161 individuals (37.8%) said they exercised lightly and moderately more frequently than once per week and vigorously once or twice per week.

2,384 (40.5%) of the 5,889 participants in the lower physical activity category said they did no vigorous exercise but did more than weekly mild and moderate exercise. Another 1,511 people (25.7%) said they did no vigorous exercise, just light exercise more than once a week, and only moderate exercise once or less frequently.

Participants who exercised more frequently were more likely to get 6 to 8 hours of sleep each night. In addition, they had higher levels of education and affluence than those in the lower physical activity group, and they were more likely to be male, younger at baseline, married, or living with a partner. In comparison to individuals in the lower physical activity group, those in the greater physical activity group were more likely to not smoke, had lower body mass indices (BMI), fewer diagnoses of all chronic illnesses, and fewer depressive symptoms.

The long-term cognitive benefits of sound sleep

Regardless of how much sleep they had, participants from the higher physical activity group often had the highest baseline cognitive scores.

“However, for ages 50 and 60 years, those with higher physical activity and short sleep declined more rapidly such that after 10 years of follow-up, they had cognitive scores similar to those in the lower physical activity groups,” the UCL researchers wrote in their study report.

“We were surprised to see that the cognitive benefits associated with physical activity were reduced when participants had insufficient sleep duration, but these findings are certainly in line with previous research pointing to an important role of sleep in cognitive and physical recovery,” said Dr Bloomberg.

The cognitive advantages of exercise seemed to persist even in older participants (age 70 and above) who had trouble sleeping.

Dr. Vernon Williams, a sports neurologist, pain management expert, and founding director of the Cedars-Sinai Kerlan-Jobe Institute in Los Angeles’ Centre for Sports Neurology and Pain Medicine, told us he was glad to see research showing the value of sleep for long-term advantages in cognitive function.

The idea that sustaining physical health in the absence of optimum sleep health lowers the cognitive benefits of physical activity, along with evidence showing both exercise AND sleep are key elements for maintaining cognitive health, is convincing, according to Dr. Williams.

More study is required to determine how exercise and sleep affect brain function.

Ryan Glatt, a senior brain health coach and the FitBrain Program’s director at the Pacific Neuroscience Institute in Santa Monica, California, told CNN that he thought the study was “very interesting” but pointed out its shortcomings.

The accuracy of self-reported physical activity and sleep length may have problems, and Glatt noted that the potential presence of sleep disorders or the effects of specific medications were not taken into account.

Dr. Bloomberg thinks there might be a way to carry out this study without depending on the participants’ honesty.

“An interesting next step would be to use objective measures of sleep and physical activity—for example, using wrist-worn accelerometers—to see whether we observe similar results,” she said.

The UCL researchers hope to see a similar study conducted on a wider range of populations in the future. Dr. Bloomberg further stated that she would like “to extend the results to dementia.”

To increase the likelihood that the impacts of sleep on cognition and not the other way around, Dr. Bloomberg said, “We purposefully excluded those with dementia and those whose cognitive scores suggested cognitive impairment.” Future studies ought to look into how physical activity and sleep patterns affect dementia risk.

REFERENCES:

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

Resistance training reduces Alzheimer’s signs in mice model

Resistance training reduces Alzheimer’s signs in mice model

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Exercise is known to help older persons think more clearly and lower their risk of developing dementia.

The underlying process is unclear, and the majority of study focuses on how aerobic exercise, which raises heart and breathing rates, affects the body.

Brazilian researchers have now examined how resistance training, such as lifting weights, affects cognition in male mouse models.

According to the Centres for Disease Control and Prevention (CDC), exercise is already known to be associated with better bone and muscular health, a lower risk of disease and obesity, and better mental health.

According to the World Health Organisation (WHO), physical activity is associated with better cognition in children, adolescents, and adults. There is also evidence that older persons who engage in more physical activity have reduced rates of dementia.

Both clinical trials and evaluations of the existing research have demonstrated that exercise helps older persons’ cognition.

This may be due to the anti-inflammatory effects of exercise. Myokines, which are chemicals released from the muscles as they contract, may be the cause of this in elderly people.

This suggests that in addition to aerobic activity, resistance training could potentially have a positive impact on health.

Strength training may improve cognitive functions

Researchers from the Federal University of Sao Paulo and the University of Sao Paulo in Brazil examined the effects of resistance training on male mice to learn more about the connection between cognitive health and exercise.

This study’s findings have been published in Frontiers of Science.

The study’s mouse model had a mutation that led to beta-amyloid plaques accumulating in the brain, thus researchers used that model in their investigation. The emergence of dementia is frequently linked to beta-amyloid plaques.

A third group of mice, which did have the mutation, were instructed to follow an exercise regimen that resembled strength training in humans whereas one group of mice with the mutation and a control group did not exercise.

The workout routine required the mice to climb a ladder over one meter tall that sloped at an inclination of 80 degrees while carrying burdens that were equal to 75%, 90%, and 100% of their body weight on their tails.

The mice were dissected after death to examine the development of beta-amyloid plaques.

The mice that had engaged in resistance training for four weeks not only had fewer amyloid plaques on the hippocampus, a part of the brain that is frequently affected by Alzheimer’s disease but also had more microglial cells, an immune cell type that helps to clear these plaques.

As Nancy Mitchell, a registered nurse with experience in geriatric care who was not involved in the study, explained to us, “According to this study, resistance training may aid in preventing or controlling Alzheimer’s disease by regulating the formation of the protein deposits (or plaques) on the hippocampus the part of the brain which controls memory and some thought processing.”

How do agitation and stress play a role?

Resistance exercise decreased stress, according to the findings. The hormone corticosterone, which in mice is the equivalent of cortisol in humans, was detected in the mice’s blood after four weeks of exercise.

Humans with high cortisol levels have an increased risk of developing Alzheimer’s disease. The levels of this hormone were discovered to be normal in the study mice, even though corticostfactorserone and cortisol can be released in response to exercise.

This was a startling discovery, according to Prof. Henning Ulrich, professor of biochemistry at the University of So Paulo and corresponding author of the study:

“We wanted to see if this kind of exercise would have any stressful effects. To our amazement, we discovered that it not only did not have any stressful effects, but it even lowered stress when compared to the inactive group! More significantly, exercise was also able to lower the amount of beta-amyloid that was present in the hippocampus, and in a different study conducted by our team, the amount of anti-inflammatory cytokines also helped to lower neuroinflammation.”

Before postmortem, mice were measured for movement to see whether they were agitated or restless because agitation is a hallmark of Alzheimer’s disease.

Resistance-trained mice were found to move less in their environment, which may have indicated that they were less disturbed.

Trials on humans have already started.

Although the results show a potential function for resistance training in Alzheimer’s mouse models, it should be highlighted that the study’s mice were all male.

They were adults but not typical of the senior population because they were also 6-7 months old. Prof. Ulrich stated, “We are preparing new experimental groups with female animals and the idea is to compare the results of males and females.”

He added that he and his colleagues also hoped that younger mice may be used in the tests.

When the first signs appeared, Prof. Ulrich said, “We already started an exercise routine with younger animals, to see if we can prevent the quick advance, or reduce the evolution of the disease when commencing physical activity in young individuals. This is comparable to a young person who engages in regular physical activity and does so into their later years.“

Furthermore, he added, some human study had already begun:

Additionally, we’ve started looking into how resistance training affects patients with mild cognitive impairment in collaboration with another UNIFESP study team. The effort is already underway, and we anticipate being able to present encouraging findings soon.

The benefits of exercise for brain health

There is growing evidence that physical activity has a protective effect against Alzheimer’s disease, according to an email from geneticist and Parkinson’s disease researcher Dr. Sumeet Kumar.

According to research, those who are active have a lesser probability of contracting this illness than those who are inactive, he continued.

Dr. Kumar cited a review that revealed the bulk of studies in this field focused on the impact of aerobic exercise, such as tai chi and yoga.

The reasons why exercise has this beneficial effect on older adults’ brain health are unclear, but current knowledge points to improved growth and differentiation of brain nerve cells, decreased inflammation, improved blood vessel function, and hormonal regulation as the likely causes.

REFERENCES:

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

The importance of the stomach in Parkinson’s research.

The importance of the stomach in Parkinson’s research.

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There is presently no cure for Parkinson’s disease, which affects millions of people worldwide. The specific etiology of this disorder is still unknown. Some academics are now focusing on the gut to comprehend the underlying mechanics. Why, and what might this study show? In this episode of our podcast In Conversation, we talk about how Parkinson’s disease may be influenced by gut health.

Parkinson’s disease is a neurological condition that affects mobility, balance, and muscle control in millions of people worldwide. However, it can also cause mood changes, digestive problems, a decline in memory and other cognitive abilities, and other symptoms.

The World Health Organisation (WHO) reports that the prevalence of Parkinson’s disease has doubled globally over the past 25 years and that the condition has caused “5.8 million disability-adjusted life years” globally.

Some of the current treatments for Parkinson’s disease include dopaminergic medications, deep brain stimulation, speech, and occupational therapy, but researchers are always looking for new and improved therapies.

Researchers are working to gain a better understanding of the mechanisms underlying Parkinson’s disease to pave the path for more effective treatments.

In the last 12 months, several research have concentrated on one specific element of Parkinson’s disease, particularly gut health. But why, and what insights may it provide into Parkinson’s, can gut health provide?

In the most recent episode of our In Conversation podcast, we welcomed two guests: Dr. Ayse Demirkan and Gary Shaughnessy, to learn more about the most recent research and how the disease can affect particular people.

Why trust your gut?

There has been a growing body of research over the past few years suggesting that the brain and the gut are capable of two-way communication. This is known as the gut-brain axis by researchers.

The gut-brain axis has been linked to a variety of brain-related illnesses, including depression and dementia. And while the relationship between the gut and the brain may be less obvious in other disorders, it is actually more evident in Parkinson’s disease, which is also sometimes accompanied by gastrointestinal symptoms like constipation.

The Braak hypothesis is one view on Parkinson’s disease. According to a reliable source, there are typically two ways for an unknown infection to enter the brain, one of which involves the gut.

The vagus nerve, the longest cranial nerve that connects the brain to, among other organs, the intestines, may be one route by which pathogens enter the body, travel through the gut, and then advance to the brain. Parkinson’s disease may then start to manifest as a result of this.

In our podcast, Dr. Demirkan recognized that it may initially seem strange to think about using your gut to learn more about Parkinson’s disease, but that the Braak hypothesis offers an intriguing lens through which to examine potential underlying mechanisms.

“Through the Braak hypothesis, there comes the idea that the disease actually starts in the intestines, and then through the vagus nerve, it spreads to the other tissues, and towards the brain,” she said.

She claims that for one straightforward reason alone, Parkinson’s disease is the neurological disorder that is most intriguing to examine regarding gut health because its gut microbiome stands out the most.

Parkinson’s disease has a distinct gut microbiota.

Dr. Demirkan and her colleagues recently discovered that people with Parkinson’s disease have unique gut microbiomes that were characterised by dysbiosis, the phenomenon of imbalance between so-called good and bad bacteria.

According to their research, those with Parkinson’s disease have gut flora that is different from those who do not have it by about 30%.

Dr. Demirkan stated in the podcast that “we found one-third of these microbes in the gut of people with Parkinson’s disease to be different.”

“As a result, this strongly suggests dysbiosis. Also different were the bacteria’s modes of operation and the types of genes they possessed. We observed a decrease in the number of short-chain fatty acid manufacturers, such as gut-friendly bacteria. Escherichia coli and other harmful bacteria were identified in greater numbers, and numerous bacterial pathways were disrupted, which may have an impact on the health of the neuronal tissues,” according to Dr. Ayse Demirkan.

In the guts of Parkinson’s disease patients, Dr. Demirkan and her colleagues discovered that levels of bacteria like Bifidobacterium dentium, which can result in infections like brain abscesses, were noticeably raised.

Desulfovibrio bacteria may be related to Parkinson’s disease, according to research from the University of Helsinki that was published in the May 2023 issue of Frontiers. These microorganisms release hydrogen sulfide, which can cause different types of inflammation.

Desulfovibrio was mentioned in another study from The Chinese University of Hong Kong that was published in Nature Communications in May 2023. This study found an “overabundance” of these bacteria in persons with REM sleep behavior disorder and early Parkinson’s disease indicators. The goal of the study was to find a way to diagnose Parkinson’s disease earlier.

What potential mechanisms exist?

The question that arises is: What mechanisms might mediate gut bacteria’s impact on neurological health, assuming that they do in fact contribute to Parkinson’s disease?

Given that some of the bacteria that are overabundant in this condition are pro-inflammatory, which means they can cause inflammation, one theory raised in the studies on the connection between the gut and the brain in Parkinson’s is that systemic inflammation may be one of the processes involved.

Research reveals that immunosuppressant medicine may reduce the chance of Parkinson’s disease, which raises the possibility that a medication of a similar kind may potentially assist manage the disease.

Parkinson’s disease is characterised by chronic brain inflammation, and some studies appear to suggest that systemic inflammation may exacerbate chronic brain inflammation and speed up the course of the disease.

In fact, some inflammatory disorders have been associated with an increased risk of Parkinson’s. For instance, a 2018 Danish study found that those with inflammatory bowel disease (IBD) had a 22% higher chance of developing Parkinson’s disease than their non-inflammatory counterparts.

In the podcast, Dr. Demirkan concurred that “bad” bacteria in the stomach may be the source of inflammation associated with Parkinson’s disease. She emphasised that more investigation is required before drawing clear conclusions because this proposed mechanism is not yet established.

Could nutrition help Parkinson’s patients with dysbiosis?

It could be logical to assume that nutrition could aid in the fight against gut dysbiosis and perhaps offer a simple option for symptom treatment if gut bacteria may play a role in Parkinson’s disease.

While there are certain dietary suggestions and nutritional supplements that may help some people with symptom alleviation, it’s still not clear how much food can actually do to change how this condition develops.

According to one study from 2022, diets rich in flavonoids, which are natural pigments present in many fruits, may be associated with a lower risk of mortality from Parkinson’s disease.

Additionally, an earlier study from 2018 suggested that a protein called parvalbumin, which is present in many types of fish, may help prevent Parkinson’s disease by preventing alpha-synuclein from clumping together in the brain, which occurs in the brains of people with Parkinson’s and disrupts signals between brain cells.

Dr. Demirkan did, however, show some scepticism when asked about the ability of food and vitamins to control gut flora in Parkinson’s patients.

She emphasised that it is challenging to provide generic advice that would truly be useful because different persons have various risk factors for Parkinson’s as well as varied forms of the disease.

“I find it very challenging to offer advice to anyone because each of us has a unique gut microbiota. Therefore, I believe that preventing the condition is one thing and that long-term maintenance, along with the various consequences of the disease, is another. I can’t really offer any advice because of this, although research indicates that consuming more sugar is problematic.

Can exercising treat Parkinson’s disease?

Nevertheless, some evidence suggests that exercising can help people with Parkinson’s disease manage their symptoms.

According to a study from 2022 that was published in Neurology, those with early-stage Parkinson’s disease may benefit from regular, moderate-to-vigorous exercise since it can delay the disease’s progression.

According to research published in 2017, doing at least 2.5 hours of exercise each week can assist Parkinson’s patients become more mobile while also delaying the onset of the disease.

Dr. Demirkan concurred that using exercise as a management tool for Parkinson’s disease can be beneficial. Exercise by itself is a fantastic technique to mould our brain and body, she claimed.

“There are some significant physiological consequences that we can consider in terms of reversing [Parkinson’s] disease. Your body must endure a lot of stress when you run a marathon, for instance. For instance, you may notice that your body temperature rises steadily and in a feverish manner. One thing is that there is a long-term rise in core heat, and it should unquestionably have a significant impact on the stomach,” she said.

In fact, some study indicates that the heat stress experienced during exercise may decrease intestinal blood flow, which may ultimately have an impact on the gut microbiota by allowing for the expansion of some bacteria while suppressing others.

In terms of the optimum type of exercise for persons with Parkinson’s disease, a Cochrane study that was released in January 2023 came to the conclusion that pretty much all types of exercise can assist those with this illness to live better lives. The authors of the review state that the available evidence “probably has a large beneficial effect” on the quality of life of aqua-based training.

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