Middle Age Sexual Satisfaction: A Potential Early Sign of Cognitive Decline

During my marriage sexual satisfaction was nil but that is not going to give me cognitive decline.

You doctor is responsible for getting you fucking again post stroke.

With all the benefits of sex I bet your doctor doesn't know or do a damn thing for your sex life.  I'll have to add this one: Among them are delayed onset of dementia

All this is why you need to be doing lots of sex, why the hell can't your doctor get you fucking again? In fact you should be doing it in the hospital.

Sexual Frequency Predicts Greater Well-Being, But More is Not Always Better

 

Sex after stroke

 

Sex linked to better brain power in older age

Sex: The Ultimate Full Body Workout

 

Better Memory From This Extremely Pleasurable Activity - Sex

 

WHY SEX IS BETTER FOR YOUR BRAIN THAN SUDOKU 

 

Sex linked to better brain power in older age  (Put this in here twice because it's so important!)

 

Good News About Sex- It Doesn't Cause a Stroke

 

Sex Does Not Increase Heart Attack Risk - What about stroke?

 

Frequent orgasms may protect against heart attacks

 

An orgasm a day keeps the doctor away!

In case you don't have a partner she could prescribe this.

Electrosex

And the benefits of marijuana for sex here:

Sex, Marijuana and Baby Booms

 

And how is your doctor ensuring you get enough sex while in the hospital?

The latest here:

 Middle Age Sexual Satisfaction: A Potential Early Sign of Cognitive Decline

Summary: Researchers found lower sexual satisfaction in middle age may be a warning sign of future cognitive decline.

The study examined associations between erectile function, sexual satisfaction, and cognition in hundreds of middle-aged men, discovering a correlation between declines in sexual satisfaction and future memory loss.

This study tracks sexual satisfaction, sexual health, and cognition over time, revealing a novel potential risk factor for cognitive decline. While the causality remains uncertain, this relationship suggests that improving sexual satisfaction might positively affect memory function.

Key Facts:

1. The study found that in middle-aged men, decreases in sexual satisfaction and erectile function correlated with future memory decline.
2. The researchers utilized survey data from 818 men over a 12-year span, using neuropsychological tests and self-reported assessments for male sexual health.
3. This study is the first to longitudinally track the changes in sexual satisfaction in conjunction with sexual health and cognition.

Source: Penn State

Low sexual satisfaction in middle age may serve as an early warning sign for future cognitive decline, according to a new study led by Penn State researchers.

The study, which tracked associations between erectile function, sexual satisfaction and cognition in hundreds of men aged 56 through 68, found that declines in sexual satisfaction and erectile function were correlated with future memory loss.

The study, published in the latest issue of the journal Gerontologist, is the first to longitudinally track sexual satisfaction in tandem with sexual health and cognition, the researchers state, and its findings point to a potential novel risk factor for cognitive decline.

“What was unique about our approach is that we measured memory function and sexual function at each point in the longitudinal study, so we could look at how they changed together over time,” said Martin Sliwinski, professor of human development and family studies at Penn State and co-author on the study.

They examined the shifts starting in middle age because it represents a transition period where declines in erectile function, cognition and sexual satisfaction begin to emerge. Credit: Neuroscience News

“What we found connects to what scientists are beginning to understand about the link between life satisfaction and cognitive performance.”

The study explored the relationship between physical changes like the microvascular changes relevant for erectile function, and psychological changes, such as lower sexual satisfaction, to determine how the changes relate to cognition.

They examined the shifts starting in middle age because it represents a transition period where declines in erectile function, cognition and sexual satisfaction begin to emerge.

Sliwinski added that while the team discovered a strong correlation between the three health factors, they can only speculate as to the cause.

“Scientists have found that if you have low satisfaction generally, you are at a higher risk for health problems like dementia, Alzheimer’s disease, cardiovascular disease and other stress-related issues that can lead to cognitive decline,” he said.

“Improvements in sexual satisfaction may actually spark improvement in memory function. We tell people they should get more exercise and eat better foods. We’re showing that sexual satisfaction also has importance for our health and general quality of life.”

For the study, the researchers used survey data from 818 men who participated in the Vietnam Era Twin Study of Aging. Through neuropsychological tests, such as tests of memory and processing speed, they examined cognitive changes of participants over the 12-year span from age 56 to 68, adjusting for participants’ cognitive ability in young adulthood.

Their erectile function and sexual satisfaction were measured alongside cognition, using the International Index of Erectile Function, a self-reported assessment for male sexual health. The researchers then built a statistical model to understand how the three variables changed as individuals aged.

“Research on sexual health has historically focused on quantifiable facets of sexuality like number of sexual partners or frequency of sexual activity,” said Riki Slayday, a doctoral candidate at Penn State and lead author on the study.

“What we were interested in is the perception of that activity, how someone feels about their sex life, and how that influences cognitive function, because multiple people could be in the same situation physically but experience completely different levels of satisfaction.”

The study found that decreases in erectile function and sexual satisfaction were both associated with memory decline, which the researchers say points to a connection between psychological and physical health.

“When we mapped the relationship over time, we found increases or decreases in erectile function and sexual satisfaction were associated with concurrent increases or decreases in cognitive function,” Slayday said.

“These associations survived adjustment for demographic and health factors, which tells us there is a clear connection between our sex lives and our cognition.”

Prior studies have found a link between microvascular changes and changes in erectile function over time. In fact, the active ingredient in Viagra (Sildenafil) was originally developed to treat cardiovascular problems, Sliwinski explained, so the connection between vascular health and erectile function is well understood.

How erectile function connects to other aspects of health should be an area of focus for future research, he added.

Increasing the assessment and monitoring of erectile function as a vital sign of health may help identify those at risk of cognitive decline before their 70s, he said.

The researchers note that the older adult population in the U.S. is expected to double over the next 30 years, which means twice as many people will likely enter their 60s and experience declines in erectile function and sexual satisfaction.

“We already have a pill for treating erectile dysfunction. What we don’t have is an effective treatment for memory loss,” Sliwinski said.

“Instead of the conversation being about treating ED, we should see that as a leading indicator for other health problems and also focus on improving sexual satisfaction and overall well-being, not just treating the symptom.”

Other co-authors on the paper are Tyler Bell, Teresa Warren, William Kremen and Carol Franz of the University of California San Diego; and Michael Lyons, Rosemary Toomey and Richard Vandiver of Boston University.

Funding: The work was supported the National Institute on Aging at the National Institutes of Health.

About this aging and cognition research news

Author: Adrienne Berard
Source: Penn State
Contact: Adrienne Berard – Penn State
Image: The image is credited to Neuroscience News

Examining first treatment for strokes linked to dementia

Since you already have dementia when you get this stroke you'll have to hope like hell that your doctors are up-to-date on this treatment because you won't be able to inform them of this. Or better yet ask your doctor now to follow this since results are not expected for 5 years.

Examining first treatment for strokes linked to dementia

People who experience a type of stroke linked with nearly half of all dementias could be treated for the first time by repurposing two cheap and common drugs, a trial shows.

Researchers found that isosorbide mononitrate and cilostazol, which are already used to treat other heart and circulatory diseases, can safely improve the debilitating outcomes people experience after lacunar stroke.

The two drugs, which were found to be even more effective when used in combination, could be available as a treatment for lacunar strokes within five years, if the results are confirmed in further trials, experts say.

Lacunar strokes affect at least 35,000 people in the UK each year. They are caused by cerebral small vessel disease, where small blood vessels deep within the brain become damaged and stop working properly. Small vessel disease is also a common cause of cognitive impairment and dementia.

The strokes can be distressing as people may develop problems with their thinking and memory, movement, and even dementia. There are currently no specific effective treatments.

The trial, led by the Universities of Edinburgh and Nottingham and the UK Dementia Research Institute, involved 363 people who had experienced a lacunar stroke.

As well as their standard stroke prevention treatment, for one year participants took either isosorbide mononitrate or cilostazol individually, both drugs together, or neither.

The trial, funded by the British Heart Foundation, investigated cilostazol and isosorbide mononitrate as they possibly improve the function of the inner lining of blood vessels, which researchers believe play a role in small vessel disease.

Participants that took both drugs were nearly 20 per cent less likely to have problems with their thinking and memory compared to the group that did not take either drug. They were also more independent and reported a better quality of life.

Drug Discovery eBook Compilation of the top interviews, articles, and news in the last year. Download the latest edition

In addition, those who took isosorbide mononitrate were less likely to have had further strokes at one year than those who did not take the drug.

Taken on their own, isosorbide mononitrate also improved thinking and memory skills, and quality of life, while cilostazol improved independence and mood. These effects were strengthened when the two drugs were taken together, researchers say.

The team is now planning to test these drugs in a larger four-year clinical trial, which they hope to start by the end of 2023. They are also looking to test whether the drugs are effective in different conditions linked to small vessel disease, such as vascular cognitive impairment and dementia.

Now we understand more about what is triggering these small vessel strokes to attack the brain, we've been able to focus our efforts on treatments that can put a halt to this damage. We need to confirm these results in larger trials before either drug can be recommended as a treatment. However, as these drugs are already widely available for other circulatory disorders, and inexpensive, it shouldn't take too long to move our findings from research into everyday clinical practice."

Joanna Wardlaw, Professor and Chair, Applied Neuroimaging, University of Edinburgh

Professor Sir Nilesh Samani, Medical Director at the British Heart Foundation, said: "These promising findings provide a long-awaited positive step towards the first treatments becoming available for lacunar strokes, offering much needed hope for thousands of people. Lacunar strokes are not the only way that cerebral small vessel disease can affect someone. These findings also open new avenues of research into other conditions related to small vessel disease, such as vascular dementia."

Source:

University of Edinburgh

Journal reference:

Wardlaw, J. M., et al. (2023) The Lacunar Intervention Trial-2 (LACI-2) Randomized Clinical Trial. JAMA. doi.org/10.1001/jamaneurol.2023.1526.

Tracking changes in blood vessels may hold clues to early detection of neurodegenerative diseases

 

It is your doctor's responsibility to understand how to apply this knowledge to prevent MCI and dementia post stroke.

Your risk of dementia, has your doctor told you of this?  Your doctor is responsible for preventing this!

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here:

Tracking changes in blood vessels may hold clues to early detection of neurodegenerative diseases

While age-related brain disorders like Alzheimer's disease often develop slowly across an individual's lifetime, they usually aren't detected until symptoms have already started. With that in mind, teams of biomedical researchers led by Brown University scientists have been exploring for years whether devastating neurodegenerative diseases could be caught decades earlier -; perhaps through something as simple as a routine eye exam instead of a battery of diagnostic tests.

In a new study, one of the Brown-led teams describes early steps in making that a possibility. They show in Nature Communications that it is possible to track how blood vessels in the brains of mice change over long periods of time. The results begin to give biomedical researchers a tool to identify and study biomarkers in these blood vessels that may hold pivotal clues to early detection of progressive neurodegenerative diseases like Alzheimer's, Parkinson's, Huntington's disease and multiple sclerosis.

The hope is that they can next use their method to image the retina in mice to look for these biomarkers, and from there scale up to imaging the retina of humans to study and track how the blood vessels change. The work is among a number of research efforts by Brown scientists to catch Alzheimer's early by peeking into the eyes.

In this paper, we show that using our imaging technology we can image the brain of the same animal over and over again repeatedly for almost one year, measuring the properties of blood vessels of the brain. The results potentially open a path to being able to predict when someone is at risk for developing these neurodegenerative diseases and for doctors prescribing early treatments for them."

Jonghwan Lee, senior study author, assistant professor in Brown's School of Engineering and Carney Institute for Brain Science

Tracking how cerebral blood vessels change over extended periods of time in people who develop age-related neurodegenerative diseases, compared to what normal change looks like, has long been a goal for scientists. It's thought that cerebral blood vessels in people who develop brain diseases show signs of degradation and decline decades before symptoms from the disease begin.

"If we can detect the change in the blood vessels in the brain, or in the retina, for long periods of time, it has long been considered to be possible to predict the onset of these kinds of diseases," Lee said.

Challenges in current microscopic methods have made this type of longitudinal tracking extremely arduous, however, requiring various workarounds. The research team -; which also included scientists from Brown's Warren Alpert Medical School and School of Public Health -; set out to find a more direct approach.

The novel method they created combines advanced imaging techniques and AI algorithms to track changes in the dynamics and anatomy of blood vessels of the brain. The researchers used the method to measure these changes in 25 different mice for more than seven months.

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According to the study, the research team focused on a non-invasive imaging test called optical coherence tomography. OCT uses light waves to look through the retina and image blood vessels that surround the optic nerve. The team adapted multiple OCT techniques to image brain blood vessels like pial vessels, cortical vessels and capillary network. They then integrated the OCT methods with image processing algorithms to search for patterns in the data they collected from normal mice and Alzheimer's disease model mice.

Analyzing the data, they noticed differences between normal age-related changes and vascular changes brought on by disease.

"We found several candidate biomarkers like large blood vessels getting thinner and blood flow getting lower, and, more interestingly, the network pattern of vessels significantly altering, compared to the normal aging animals," Lee said.

The ultimate goal is to fine-tune the method and gather enough data so that the group's algorithms can analyze and predict through regular eye exams the chance of a person developing neurodegenerative diseases years before they do. The team is a long way off from this goal but is off to a strong start with the proof of concept in mice, which act as model organisms. In the coming years they plan to look closer at the biomarkers they found and identify more. The next step is imaging blood vessels in the retinas of mice.

The work was co-led by Warren Alpert Medical School student Konrad W. Walek, while he was an undergraduate in Brown's Department of Neuroscience, and Sabina Stefan, while she was a graduate student at Brown's School of Engineering. Both worked in Lee's lab. Other Brown authors include Jang-Hoon Lee, Anna H. Kim, Seong Wook Park, Tao Liu, Yu-Wen Alvin Huang and Christopher Moore.

The work was supported by the National Institute on Aging.

Source:

Brown University

Journal reference:

Walek, K.W., et al. (2023) Near-lifespan longitudinal tracking of brain microvascular morphology, topology, and flow in male mice. Nature Communications. doi.org/10.1038/s41467-023-38609-z.

New research shows astrocytes are key to swaying the pendulum in Alzheimer's disease progression

It is your doctor's responsibility to understand how to apply this knowledge to prevent MCI and dementia post stroke.

Your risk of dementia, has your doctor told you of this?  Your doctor is responsible for preventing this!

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here:

 

New research shows astrocytes are key to swaying the pendulum in Alzheimer's disease progression

Why do some people develop Alzheimer's disease while others don't? And, even more puzzlingly, why do many individuals whose brains are chock-full of toxic amyloid aggregates-;a telltale sign of Alzheimer's brain pathology-;never go on to develop Alzheimer's-associated dementias?

University of Pittsburgh School of Medicine researchers appear to have found the answer. Star-shaped brain cells called astrocytes are key to swaying the pendulum in Alzheimer's disease progression, shows new game-changing research published today in Nature Medicine.

By testing the blood of more than 1,000 cognitively unimpaired elderly people with and without amyloid pathology, the Pitt-led research team found that only those who had a combination of amyloid burden and blood markers of abnormal astrocyte activation, or reactivity, would progress to symptomatic Alzheimer's in the future, a critical discovery for drug development aimed at halting progression.

Our study argues that testing for the presence of brain amyloid along with blood biomarkers of astrocyte reactivity is the optimal screening to identify patients who are most at risk for progressing to Alzheimer's disease. This puts astrocytes at the center as key regulators of disease progression, challenging the notion that amyloid is enough to trigger Alzheimer's disease."

Tharick Pascoal, M.D., Ph.D., senior author, associate professor of psychiatry and neurology at Pitt

Alzheimer's disease is a neurodegenerative condition that causes progressive memory loss and dementia, robbing patients of many productive years of life. At the tissue level, the hallmark of Alzheimer's disease is an accumulation of amyloid plaques-;protein aggregates lodged between nerve cells of the brain-;and clumps of disordered protein fibers, called tau tangles, forming inside the neurons.

For many decades brain scientists believed that an accumulation of amyloid plaques and tau tangles is not only a sign of Alzheimer's disease but also its direct culprit. This assumption also led drug manufacturers to heavily invest into molecules targeting amyloid and tau, overlooking the contribution of other brain processes, such as the neuroimmune system.

Recent discoveries by groups like Pascoal's suggest that the disruption of other brain processes, such as heightened brain inflammation, might be just as important as amyloid burden itself in starting the pathological cascade of neuronal death that causes rapid cognitive decline.

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In his previous research, Pascoal and his group found that brain tissue inflammation triggers the spread of pathologically misfolded proteins in the brain and is a direct cause of eventual cognitive impairment in patients with Alzheimer's disease. Now, almost two years later, researchers revealed that the cognitive impairment can be predicted by a blood test.

Astrocytes are specialized cells abundant in the brain tissue. Just as other members of the glia-;resident immune cells of the brain-;astrocytes support neuronal cells by supplying them with nutrients and oxygen and protecting them from pathogens. But because glial cells don't conduct electricity and, at first, didn't seem to play a direct role in how neurons communicate with one another, their role in health and disease had been overlooked. The latest research from Pitt changes that.

"Astrocytes coordinate brain amyloid and tau relationship like a conductor directing the orchestra," said lead author of the study Bruna Bellaver, Ph.D., postdoctoral associate at Pitt. "This can be a game-changer to the field, since glial biomarkers in general are not considered in any main disease model."

Scientists tested blood samples from participants in three independent studies of cognitively unimpaired elderly people for biomarkers of astrocyte reactivity-;glial fibrillary acidic protein, or GFAP-;along with the presence of pathological tau. The study showed that only those who were positive for both amyloid and astrocyte reactivity showed evidence of progressively developing tau pathology, indicating predisposition to clinical symptoms of Alzheimer's disease.

The findings have direct implications for future clinical trials for Alzheimer's drug candidates. In aiming to halt disease progression sooner, trials are moving to earlier and earlier stages of pre-symptomatic disease, making correct early diagnosis of Alzheimer's risk critical for success. Because a significant percentage of amyloid-positive individuals will not progress to clinical forms of Alzheimer's, amyloid positivity alone is not enough to determine an individual's eligibility for a therapy.

Inclusion of astrocyte reactivity markers, such as GFAP, in the panel of diagnostic tests will allow for improved selection of patients who are likely to progress to later stages of Alzheimer's and, therefore, help fine-tune selection of candidates for therapeutic interventions who are more likely to benefit.

Source:

University of Pittsburgh

Journal reference:

Bellaver, B., et al. (2023). Astrocyte reactivity influences amyloid-β effects on tau pathology in preclinical Alzheimer’s disease. Nature Medicine. doi.org/10.1038/s41591-023-02380-x.

Insights into the direction and extent of gut microbiome dysbiosis in Alzheimer’s disease and mild cognitive impairment

 It is your doctor's responsibility to understand how to apply this knowledge to prevent MCI and dementia post stroke.

Your risk of dementia, has your doctor told you of this?  Your doctor is responsible for preventing this!

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here:

Insights into the direction and extent of gut microbiome dysbiosis in Alzheimer’s disease and mild cognitive impairment

In a recent study published in PLOS ONE, researchers performed a meta-analysis to determine the association between intestinal microbiota and Alzheimer’s disease (AD).

Study: Gut microbiome dysbiosis in Alzheimer’s disease and mild cognitive impairment: A systematic review and meta-analysis. Image Credit: Alpha Tauri 3D Graphics/Shutterstock.com

Background

The gut microbiota primarily impacts neurological function through the gut-brain axis, a means of interaction between the brain and the abdominal organs, through the nervous system and neuromodulator production. Neurodegeneration includes immunological activation through a defective gut barrier, neuroinflammation, and blood-brain barrier impairments.

AD, a neurodegenerative illness, is characterized by gradual cognitive decline and memory loss. The initial stage of AD is characterized by mild cognitive impairments (MCI). There is no definite cure for AD; however, studies have documented cognitive improvements using non-pharmacological treatments such as probiotics and fecal microbial transplantation (FMT) in the initial stages, indicating a potential role of gut microbiota in AD and MCI pathophysiology. However, the extent and direction of gut microbial imbalance among AD patients are not well-characterized.

About the study

In the present meta-analysis, researchers reported on the contribution of gut microbes to Alzheimer’s disease and associated mild cognitive impairments.

The team searched databases such as Cochrane, EBSCO, Scopus, and MEDLINE for case-control and interventional 16S and metagenomic studies on AD gut microbiota published in English between 1 January 2010 and 31 March 2022.

In addition, the included records’ references were searched, and data were extracted independently by two researchers on the location, sample size, mean age, female proportion, eligibility criteria, sequencing platforms, and bioinformatics tools used.

The primary study outcomes were altered alpha-diversity and microbial taxa abundance, analyzed by inverse variance-weighted random-effects modeling. The secondary study outcomes emphasized linear discriminant analysis effect sizes (LEfSe) and qualitative beta-diversity ordination. Bias risks were evaluated using suitable methods for the study types, and subgroups were analyzed in the case of considerable heterogeneity in the included studies.

Only studies assessing the gut microbiota profiles of AD patients by metagenomic sequencing and documenting outcomes such as alpha- and beta-diversity ordination, linear discriminant analysis effect sizes (LEfSe), and microbial taxa abundance were analyzed. AD was diagnosed using the National Institute on Aging and Alzheimer’s Association (NIA-AA) or Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria. Individuals who did not satisfy the AD criteria but reported cognitive decline and memory loss were grouped with individuals having MCI. Individuals consuming antibiotics within 14 days of specimen collection and those with a history of medical conditions such as genetic or neurological diseases, depression, or cancer were excluded from the analysis.

Results

In total, 2,235 records were identified initially, of which 42 underwent full-text screening, and 17 studies comprising 679 and 632 AD patients and controls, respectively, were considered for the final analysis. The mean age of the participants was 71 years, and 62% were female. The included studies of high quality with low risk of bias. An overall reduction in gut microbial richness was observed among AD patients, although Bacteroides species were consistently higher among United States (US) residents and lower among Chinese individuals.

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The findings indicated that location, lifestyle, and diet considerably impact the intestinal microflora and the pathogenesis of AD. Further, Phascolarctobacterium species increased significantly only in the initial stage of mild cognitive impairment. Among AD patients, a small but significant decrease occurred in alpha diversity, measured using the Simpson and Shannon index; however, the studies were significantly heterogeneous, and subgroup analysis yielded similar results for Chinese individuals.

In addition, a significant, moderate decrease occurred in Chao indices and species richness for AD patients. The LEfSe analysis showed an increased abundance of Actinobacteria, Proteobacteria, Bifidobacteriaceae, Clostridiaceae, Enterobacteriaceae, Lactobacilleae, Ruminococcaceae, and Akkermansia. On the contrary, the relative abundance of Bacteroidetes, Firmicutes, Bacteroidaceae, Lachnospireae, Prevotellaceae, Alistipes, and Anaerostipes decreased among AD patients.

Conclusions

Overall, the study findings showed that AD progression is related to more significant impacts on species richness than evenness in the intestinal microbiota and that regional differences in lifestyle and diet can affect the gut composition, especially Bacteroides abundance.

In addition, increased Phascolarctobacterium and decreased Bacteroides counts among individuals with MCI indicated that gut microbial dysbiosis commences in the MCI stage. Thus, gut microbiota studies can enable prompt diagnosis and early intervention in neurodegenerative diseases such as AD.

The LEfSe synthesis showed an increased abundance of propionate, lactate, and acetate producers such as Bifidobacterium, Lactobacillus, and Akkermansia, which have correlated negatively with clinical cognition indicators in previous studies. However, the findings must be interpreted with caution due to potential confounding by polypharmacy.

Journal reference:

• Jemimah, S. et al. (2023) "Gut microbiome dysbiosis in Alzheimer’s disease and mild cognitive impairment: A systematic review and meta-analysis", PLOS ONE, 18(5), p. e0285346. doi: 10.1371/journal.pone.0285346. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0285346

Diet low in flavanols linked to age-related memory loss

Is this enough for your competent doctor to have the dietician create diet protocols for all the needs post stroke?  For dementia prevention; for cognitive improvement; for cholesterol reduction; for plaque removal; for Parkinsons prevention; for inflammation reduction; etc.

 

Flavonols are a class of flavonoids that have the 3-hydroxyflavone backbone (IUPAC name : 3-hydroxy-2-phenylchromen-4-one). Their diversity stems from the different positions of the phenolic -OH groups. They are distinct from flavanols (with "a") such as catechin, another class of flavonoid

Diet low in flavanols linked to age-related memory loss

A large-scale study led by researchers at Columbia and Brigham and Women's Hospital/Harvard is the first to establish that a diet low in flavanols-;nutrients found in certain fruits and vegetables-;drives age-related memory loss.

The study found that flavanol intake among older adults tracks with scores on tests designed to detect memory loss due to normal aging and that replenishing these bioactive dietary components in mildly flavanol-deficient adults over age 60 improves performance on these tests.

The improvement among study participants with low-flavanol diets was substantial and raises the possibility of using flavanol-rich diets or supplements to improve cognitive function in older adults."

Adam Brickman, PhD, professor of neuropsychology at Columbia University Vagelos College of Physicians and Surgeons and co-leader of the study

The finding also supports the emerging idea that the aging brain requires specific nutrients for optimal health, just as the developing brain requires specific nutrients for proper development.

"The identification of nutrients critical for the proper development of an infant's nervous system was a crowning achievement of 20^th century nutrition science," says the study's senior author, Scott Small, MD, the Boris and Rose Katz Professor of Neurology at Columbia University Vagelos College of Physicians and Surgeons.

"In this century, as we are living longer research is starting to reveal that different nutrients are needed to fortify our aging minds. Our study, which relies on biomarkers of flavanol consumption, can be used as a template by other researchers to identify additional, necessary nutrients."

Age-related memory loss linked to changes in hippocampus

The current study builds on over 15 years of research in Small's lab linking age-related memory loss to changes in the dentate gyrus, a specific area within the brain's hippocampus-;a region that is vital for learning new memories-;and showing that flavanols improved function in this brain region.

Additional research, in mice, found that flavanols-;particularly a bioactive substance in flavanols called epicatechin-;improved memory by enhancing the growth of neurons and blood vessels and in the hippocampus.

Next, Small's team tested flavanol supplements in people. One small study confirmed that the dentate gyrus is linked to cognitive aging. A second, larger trial showed that flavanols improved memory by acting selectively on this brain region and had the most impact on those starting out with a poor-quality diet.

In the new study, the Columbia team collaborated with researchers at Brigham and Women's Hospital studying the effects of flavanols and multivitamins in COSMOS (COcoa Supplements and Multivitamin Outcomes Study). The current study, COSMOS-Web, was designed to test the impact of flavanols in a much larger group and explore whether flavanol deficiency drives cognitive aging in this area of the brain.

Study methods

More than 3,500 healthy older adults were randomly assigned to receive a daily flavanol supplement (in pill form) or placebo pill for three years. The active supplement contained 500 mg of flavanols, including 80 mg epicatechins, an amount that adults are advised to get from food.

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At the beginning of the study, all participants completed a survey that assessed the quality of their diet, including foods known to be high in flavanols. Participants then performed a series of web-based activities in their own homes, designed and validated by Brickman, to assess the types of short-term memory governed by the hippocampus. The tests were repeated after years one, two, and three. Most of the participants identified themselves as non-Hispanic and white.

More than a third of the participants also supplied urine samples that allowed researchers to measure a biomarker for dietary flavanol levels, developed by co-study authors at Reading University in the UK, before and during the study. The biomarker gave the researchers a more precise way to determine if flavanol levels corresponded to performance on the cognitive tests and ensure that participants were sticking to their assigned regimen (compliance was high throughout the study). Flavanol levels varied moderately, though no participants were severely flavanol-deficient.

People with mild flavanol deficiency benefited from flavanol supplement

Memory scores improved only slightly for the entire group taking the daily flavanol supplement, most of whom were already eating a healthy diet with plenty of flavanols.

But at the end of the first year of taking the flavanol supplement, participants who reported consuming a poorer diet and had lower baseline levels of flavanols saw their memory scores increase by an average of 10.5% compared to placebo and 16% compared to their memory at baseline. Annual cognitive testing showed the improvement observed at one year was sustained for at least two more years.

The results strongly suggest that flavanol deficiency is a driver of age-related memory loss, the researchers say, because flavanol consumption correlated with memory scores and flavanol supplements improved memory in flavanol-deficient adults.

The findings of the new study are consistent with those of a recent study, which found that flavanol supplements did not improve memory in a group of people with a range of baseline flavanol levels. The previous study did not look at the effects of flavanol supplements on people with low and high flavanol levels separately.

"What both studies show is that flavanols have no effect on people who don't have a flavanol deficiency," Small says.

It's also possible that the memory tests used in the previous study did not assess memory processes in the area of the hippocampus affected by flavanols. In the new study, flavanols only improved memory processes governed by the hippocampus and did not improve memory mediated by other areas of the brain.

Next steps

"We cannot yet definitively conclude that low dietary intake of flavanols alone causes poor memory performance, because we did not conduct the opposite experiment: depleting flavanol in people who are not deficient," Small says, adding that such an experiment might be considered unethical.

The next step needed to confirm flavanols' effect on the brain, Small says, is a clinical trial to restore flavanol levels in adults with severe flavanol deficiency.

"Age-related memory decline is thought to occur sooner or later in nearly everyone, though there is a great amount of variability," says Small. "If some of this variance is partly due to differences in dietary consumption of flavanols, then we would see an even more dramatic improvement in memory in people who replenish dietary flavanols when they're in their 40s and 50s."

Source:

Columbia University Irving Medical Center

Superior cognition in individuals who are 90+ associated with resilience to neurodegenerative pathologies

 My mom who is 94, still living alone in the old house, laundry still in basement is doing pretty good yet. Still drives locally, haven't convinced her yet to get a hearing aid so repeating sentences is required.  Dad however died at 92 with Parkinson's dementia the last three years. So I'm going to live a very long time with half my life being differently abled, stroke at age 50, I'm shooting for 100+ and going to get there.

Superior cognition in individuals who are 90+ associated with resilience to neurodegenerative pathologies

A University of California, Irvine-led team of researchers have discovered that the oldest-old, those who live to be 90+ and have superior cognitive skills, have similar levels of brain pathology as Alzheimer's patients, however, they also have less brain pathology of other neurodegenerative diseases that cause memory and thinking problems.

The study, "Superior Global Cognition in Oldest-Old is Associated with Resistance to Neurodegenerative Pathologies: Results from the 90+ Study," was published in the Journal of Alzheimer's Disease.

People who are 90+ and still have good memory and thinking abilities tend to have similar levels of Alzheimer's pathology in their brains. Our findings indicate that while Alzheimer's Disease neuropathological changes and vascular changes are common in their brains, these individuals are less susceptible to other types of neurodegenerative changes such as Lewy body disease."

Roshni Biswas, post-doctoral scholar with The 90+ Study

Age is the primary risk factor for cognitive issues, such as Alzheimer's, Lewy body disease and other related dementias. Over the past 30 years, the number of people aged 90 and older in the U.S. has nearly tripled, and this number is projected to quadruple in the next four decades.

With this rise in age, many people see increased problems with memory and brain function. However, little data is available on the changes in the brains of 90+ people who maintain superior cognitive abilities, despite their age.

The objective of the study was to examine the brain features of people without cognitive impairment and their relation to superior cognitive skills and reasoning in those that are 90+.

"There are some individuals who can maintain high levels of cognitive function well into advanced ages," said María M. Corrada, ScD, co-principal investigator of the study and professor in the Department of Neurology at UCI School of Medicine. "Further research into the factors that enable these individuals to maintain their cognitive function could provide insights into how to preserve cognitive health despite advanced age."

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The study results were derived by analyzing autopsy data from 102 cognitively normal individuals who died at a mean age of 97.6 years. They also used cognitive test scores from people taken between two to twelve months before death. The average age of study participants at the time of their last visit was 97.1 years of age.

"In our future research, we will examine how lifestyle habits and health conditions are associated with superior cognition in individuals who are 90+ and the factors that contribute to maintaining stable cognitive function over time," said Biswas.

The 90+ Study is a longitudinal study on aging and dementia that was initiated in 2003 to study the oldest-old population, which is the fastest growing age group in the United States.

With more than 2000 participants enrolled, it is now one of the largest studies of its kind in the world. The project has produced several significant findings regarding cognitive function, health and lifestyle habits in the oldest-old population information obtained during life.

This work was supported by the National Institutes of Health.

Source:

University of California - Irvine

Journal reference:

Biswas, R., et al. (2023) Superior Global Cognition in Oldest-Old is Associated with Resistance to Neurodegenerative Pathologies: Results from the 90+ Study. Journal of Alzheimer s Disease. doi.org/10.3233/JAD-221062.