The Vitamin Deficiency That’s Putting Your Mental Health At Risk - Vitamin D

Is your doctor testing for this and getting it corrected?  Or is s/he blaming your depression on stroke using Occam's razor but not testing for the real reason? The answer to that will define your doctor's competence.

Don't do the following, practicing medicine without a license:

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The Vitamin Deficiency That’s Putting Your Mental Health At Risk

The deficiency is linked to depression and poorer brain function, lower verbal fluency and even dementia.

Vitamin D deficiency is linked to depressive symptoms and more negative thoughts, research finds.

Vitamin D deficiency is also linked to cognitive impairments in young people.

Foods that have high levels of vitamin D include oily fish and eggs but most people get their vitamin D from the action of sunlight on the skin.

That is why levels are typically lower in the body through the winter months in more Northern climes.

The research was carried out on 225 patients being treated for psychotic disorders and 159 well people.

Among people with psychosis, higher levels of negative symptoms and depression were found in those with low vitamin D levels.

Problems with processing speed and verbal fluency were also found among young people with low levels of vitamin D.

The findings fit in with previous research that low vitamin D levels are linked to depression.

The vitamin is also thought to play a role in regulating serotonin, a neurotransmitter important for mood.

Vitamin D deficiency has even been linked to dementia.

The study’s authors conclude:

“In a clinical setting, this could support vitamin D as adjuvant therapy in treating co-morbid depressions in psychotic disorders

The associations between low vitamin D levels and increased negative and depressive symptoms, and decreased processing speed and verbal fluency are good arguments for planning large scale randomised controlled studies in target populations, in order to reach conclusions about vitamin D’s potential beneficial effect in psychotic disorders.”

The study was published in the journal Schizophrenia Research (Nerhus et al., 2016).

Can CV Fat Predict Cognitive Function in Women in Midlife?

Maybe you want your doctor to test for this to identify your reason for cognitive decline rather than using Occam's razor to immediately assign the cause to your stroke. It just might require a different solution to reverse that cognitive decline.

Can CV Fat Predict Cognitive Function in Women in Midlife?

Quality of fat, not quantity, was tied to working memory, researchers say

by Amanda D'Ambrosio, Enterprise & Investigative Writer, MedPage Today September 26, 2021

The quality of cardiovascular (CV) fat in midlife women may predict their cognitive function later on in life, a researcher found.

High radiodensity of perivascular adipose tissue (PVAT) around the descending aorta among women in their middle years (average age around 51) was significantly associated with worse working memory in the future (P=0.01), reported Meiyuzhen Qi, MPH, of the University of Pittsburgh (Pitt).

Each unit increase of PVAT was associated with a 0.29 unit decrease in working memory, Qi said in a presentation at the North American Menopause Society (NAMS) virtual meeting.

While Qi and colleagues group found that the quality of fat around the blood vessels was significantly associated with cognitive function later in life, fat volume was not significant. The quantity and quality of lower epicardial and total heart fat tissue were not related to memory.

"The fat around the descending aorta had a relationship with working memory for our participants," said co-author Samar El Khoudary, PhD, MPH, also of Pitt.

"What is novel here is that we found the quality of the fat around the vessels, rather than the quantity, could be a marker of cognitive decline in midlife women," she told MedPage Today.

Higher radiodensity of fat around the blood vessels may indicate an increase in inflammatory markers to the brain, El Khoudary stated. While this could be a potential mechanism of cognitive decline, she emphasized that future research should look further into pathophysiology.

In this study, Qi's group used data from the Study of Women's Health Across the Nation (SWAN) to assess the volume and radiodensity of CV fat among midlife women, as well as the relation to cognitive function.

Researchers collected data on the volume and radiodensity of lower epicardial adipose tissue, total heart adipose tissue, and PVAT surrounding the descending aorta, which were measured by a CT scan at one visit during the course of the SWAN study. Working memory, verbal episodic memory immediate and delayed recall, and processing speed were measured repeatedly throughout the study starting at the fourth visit.

Researchers adjusted for education level, race, age, menopausal status, HDL cholesterol, waist circumference, systolic blood pressure, as well as other confounding factors.

There were 487 women included in the study, approximately 31% of which were postmenopausal. Black women made up around 36% of the study population. CV fat was measured an average of 3 years before the first cognitive test.

The radiodensity of PVAT was associated with worse working memory, but not other measures of cognitive function. The researchers also found that higher PVAT radiodensity was linked with lower future performance in verbal episodic memory delayed recall among Black women, but researchers emphasized that future studies should confirm this finding.

El Khoudary stated the research was limited by its small sample size. As there was a small number of Black women, it was difficult for the researchers to measure racial disparities in these outcomes. Additionally, this study relied on CT scans to measure quality, and future studies may use biopsies to further investigate how the quality of CV fat impacts cognitive outcomes, she stated.

• Amanda D'Ambrosio is a reporter on MedPage Today’s enterprise & investigative team. She covers obstetrics-gynecology and other clinical news, and writes features about the U.S. healthcare system. Follow

Disclosures

The study was supported by AHA Great River Affiliation Clinical Research Program, Department of Health and Human Services, NIH, the National Heart, Lung, and Blood Institute, the National Institute on Aging, the National Institute of Nursing Research, and the Office of Research on Women's Health.

Primary Source

North American Menopause Society

Source Reference: Qi M, et al "Longitudinal association between cardiovascular fat and cognitive function among midlife women: The Study of Women's Health Across the Nation (SWAN) Cardiovascular Fat Ancillary Study" NAMS 2021; Abstract S-11.

 

The Structural and Functional Neuroanatomy of Post-Stroke Depression and Executive Dysfunction: A Review of Neuroimaging Findings and Implications for Treatment

I can explain post stroke depression in two words. NO PROTOCOLS! If you had rehab protocols survivors wouldn't have time to be depressed, they would be counting reps and exercising all day long to get to recovery. Are you that fucking clueless that you are ignoring Occam's razor? And you came up with NO protocols for executive dysfunction. Useless.

The Structural and Functional Neuroanatomy of Post-Stroke Depression and Executive Dysfunction: A Review of Neuroimaging Findings and Implications for Treatment

Show all authors

Abhishek Jaywant, PhD, Larissa DelPonte, BA, Dora Kanellopoulos, PhD, ...

First Published October 19, 2020 Review Article Find in PubMed 

https://doi.org/10.1177/0891988720968270

Article information

Abstract

Post-stroke depression and executive dysfunction co-occur and are highly debilitating. Few treatments alleviate both depression and executive dysfunction after stroke. Understanding the brain network changes underlying post-stroke depression with executive dysfunction can inform the development of targeted and efficacious treatment. In this review, we synthesize neuroimaging findings in post-stroke depression and post-stroke executive dysfunction and highlight the network commonalities that may underlie this comorbidity. Structural and functional alterations in the cognitive control network, salience network, and default mode network are associated with depression and executive dysfunction after stroke. Specifically, post-stroke depression and executive dysfunction are both linked to changes in intrinsic functional connectivity within resting state networks, functional over-connectivity between the default mode and salience/cognitive control networks, and reduced cross-hemispheric frontoparietal functional connectivity. Cognitive training and noninvasive brain stimulation targeted at these brain network abnormalities and specific clinical phenotypes may help advance treatment for post-stroke depression with executive dysfunction.

Keywords cerebrovascular disease, neuroimaging, magnetic resonance imaging, cognitive control, default mode network

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Utilization of Medications With Cognitive Impairment Side Effects and the Implications for Older Adults’ Cognitive Function

Is your doctor analyzing your medications to make sure your cognitive impairment is correctly diagnosed and fixed properly? Without immediately using Occam's razor to assign blame to your stroke? And without telling us what these problematic medications are, we can't tell our doctors what needs to be done.

Utilization of Medications With Cognitive Impairment Side Effects and the Implications for Older Adults’ Cognitive Function

Duy Do MS, Jason Schnittker, PhD

First Published January 6, 2020 Research Article

https://doi.org/10.1177/0898264319895842

Article information

Abstract

Objectives:
Many medications have cognitive impairment, memory loss, amnesia, or dementia as side effects (“cognitive side effects” hereafter), but little is known about trends in the prevalence of these medications or their implications for population-level cognitive impairment.  
Method:
We use data from the National Health and Nutrition Examination Survey (1999–2016) to describe trends in the use of medications with cognitive side effects among adults aged 60+ (N = 16,937) and their implications for cognitive functioning (measured using word learning and recall, animal fluency, and digit symbol substitution assessments).  
Results:
Between 1999 to 2000 and 2015 to 2016, the prevalence of older adults taking one, two, and at least three medications with cognitive side effects increased by 10.2%, 57.3%, and 298.7%, respectively. Compared to non-users, respondents who simultaneously used three or more medications with cognitive side effects scored 0.22 to 0.27 standard deviations lower in word learning and recall (p = .02), digit symbol substitution (p < .01), and the average standardized score of the three assessments (p < .001).  
Limitation:
Dosage of medications associated with cognitive side effects was not measured.  
Discussion:
Concurrent use of medications with cognitive side effects among older adults has increased dramatically over the past two decades. The use of such medications is associated with cognitive impairment and may explain for disparities in cognitive function across subgroups. These findings highlight the need for cognitive screenings among patients who consume medications with cognitive side effects. They also highlight the synergic effects of polypharmacy and potential drug-drug interactions that result in cognitive deficits.

Keywords medications, cognitive function, dementia, chronic conditions

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Think declining mental sharpness ‘just comes with age’? Think again

Is your doctor assigning your cognitive decline immediately to your stroke because of lazily invoking Occam's razor rather than figuring out the true reason and getting a stroke protocol to correct that decline?  I expect our doctors to completely know their stuff and deliver correct interventions for every disability we have. If your doctor writes E. T.(Evaluate and Treat) prescriptions, she knows absolutely nothing about getting you recovered, fire her. 

Think declining mental sharpness ‘just comes with age’? Think again

FeaturedNeurologyNeuroscienceOpen Neuroscience Articles5 min read

Summary: Age-related diseases and not age itself contributes to cognitive decline.
Source: American Geriatrics Society
Declining mental sharpness “just comes with age,” right? Not so fast, say geriatrics researchers and clinicians gathered at a prestigious 2018 conference hosted by the American Geriatrics Society (AGS) with support from the National Institute on Aging (NIA). In a report published in the Journal of the American Geriatrics Society (JAGS), attendees of a conference for the NIA’s Grants for Early Medical/Surgical Specialists Transition into Aging Research (GEMSSTAR) program describe how increasing evidence shows age-related diseases–rather than age itself–may be the key cause of cognitive decline. And while old age remains a primary risk factor for cognitive impairment, researchers believe future research–and sustained funding–could illuminate more complex, nuanced connections between cognitive health, overall health, and how we approach age.
“We’ve long been taught that cognitive issues are ‘just part of aging,'” explains Christopher R. Carpenter, MD, MSc, who helped coordinate the conference. “But contemporary medical research shows how bodily changes that lead to diseases like dementia appear long before the symptoms we associate with ‘old age.’ This begs the question: Is it really age that causes cognitive decline, or is it ultimately the diseases we now associate with age–in large part because we see them with increasing frequency now that we live longer? That’s what we wanted to tackle coming together for this meeting.”
Hosted by the AGS and NIA in 2018 as the third conference in a three-part series for GEMSSTAR scholars, the NIA “U13” conference brought together NIA experts and more than 100 scholars, researchers, and leaders representing 13 medical specialties to explore experiences with cognitive impairment across health care. Conference findings, published in JAGS (DOI: 10.1111/jgs.16093), detail early thinking on the two-way relationship between cognitive health and the health of other organ systems, as well as opportunities for moving science and practice forward.

And while old age remains a primary risk factor for cognitive impairment, researchers believe future research–and sustained funding–could illuminate more complex, nuanced connections between cognitive health, overall health, and how we approach age. The image is in the public domain.

According to attendees, several themes emerged:

• Researchers and clinicians from across health care noted the critical relationship between two of their top concerns: Dementia and delirium (the medical term for abrupt, rapid-onset confusion or an altered mental state, which affects millions of older adults annually). Research now suggests delirium and dementia are mutually inclusive risk factors, with cases of one prompting risks for the other. Thus, prevention of delirium may offer the unprecedented opportunity to prevent or lessen future cognitive decline.
• Still, as one of the conference attendees noted, “[T]he brain is not an island.” Because the conference focused on the impact of cognitive impairment across specialties, a critical focal point for scholars was the complex, bi-directional relationship between cognition and the rest of the body. Cognitive impairments can serve as indicators or influencers in the course of other diseases and conditions. For example, cognitive impairment is perhaps “the strongest independent predictor” of hospital readmission and mortality for older people living with heart failure.
• As the field progresses, however, a major barrier remains: A dearth of research owing to the exclusion of potential study participants who are cognitively impaired. Though obtaining informed consent (the term used to describe a person’s willingness to participate in a study after confirming they understand all the possible risks and benefits) remains challenging, researchers pointed to data that willingness to participate remains high. Coupled with suggestions for tailoring consent safeguards to the types of studies and potential participants thus holds promise for protecting against exploitation while continuing to move cutting-edge care principles forward.

As the GEMSSTAR conference attendees concluded, “The aging of the U.S. population and the growing burden of dementia make this an area of critical research focus…[U]nderstanding and addressing cognitive health and its relationship with the health of other organ systems will require multidisciplinary team science…[and new] study designs…”
Funding: Funding for this conference was provided in part by the National Institutes of Health (NIH, Award Number U13AG048721). The information and views expressed in conference materials and this release are solely the responsibility of the authors do not necessarily represent the official views of the NIA and/or the NIH.

About this neuroscience research article

Source:
American Geriatrics Society
Media Contacts:
Daniel Trucil – American Geriatrics Society
Image Source:
The image is in the public domain.
Original Research: Open access
“Impact of Cognitive Impairment Across Specialties: Summary of a Report From the U13 Conference Series”. Christopher R. Carpenter et al.
Journal of the American Geriatrics Society. doi:10.1111/jgs.16093
Abstract
Impact of Cognitive Impairment Across Specialties: Summary of a Report From the U13 Conference Series
Although declines in cognitive capacity are assumed to be a characteristic of aging, increasing evidence shows that it is age‐related disease, rather than age itself, that causes cognitive impairment. Even so, older age is a primary risk factor for cognitive decline, and with individuals living longer as a result of medical advances, cognitive impairment and dementia are increasing in prevalence. On March 26 to 27, 2018, the American Geriatrics Society convened a conference in Bethesda, MD, to explore cognitive impairment across the subspecialties. Bringing together representatives from several subspecialties, this was the third of three conferences, supported by a U13 grant from the National Institute on Aging, to aid recipients of Grants for Early Medical/Surgical Specialists’ Transition to Aging Research (GEMSSTAR) in integrating geriatrics into their subspecialties. Scientific sessions focused on the impact of cognitive impairment, sensory contributors, comorbidities, links between delirium and dementia, and issues of informed consent in cognitively impaired populations. Discussions highlighted the complexity not only of cognitive health itself, but also of the bidirectional relationship between cognitive health and the health of other organ systems. Thus, conference participants noted the importance of multidisciplinary team science in future aging research. This article summarizes the full conference report, “The Impact of Cognitive Impairment Across Specialties,” and notes areas where GEMSSTAR scholars can contribute to progress as they embark on their careers in aging research.

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There won’t be a cure for Alzheimer’s disease in our lifetime

Well I'll be trying this. Haven't you heard of it? 

The End of Alzheimer's: The First Program to Prevent and Reverse Cognitive Decline by Dale Bredesen

There won’t be a cure for Alzheimer’s disease in our lifetime

A century of research later, and we’re still not sure what causes it

Norman A. Paradis May 19, 2019 6:00PM (UTC)

This story originally appeared on Massive Science, an editorial partner site that publishes science stories by scientists. Subscribe to their newsletter to get even more science sent straight to you.

Biogen recently announced that it was abandoning its late stage drug for Alzheimer’s, aducanumab, causing investors to lose billions of dollars.
They should not have been surprised.
Not only have there been more than 200 failed trials for Alzheimer’s, it’s been clear for some time that researchers are likely decades away from being able to treat this dreaded disease. Which leads me to a prediction: There will be no effective therapy for Alzheimer’s disease in my lifetime.
Clinically, I am an emergency physician. But my research interests include diagnostic biomarkers, which are molecular indicators of disease, and a diagnostic test for Alzheimer’s is something of a holy grail.
Alzheimer’s sits right at the confluence of a number unfortunate circumstances. Stick with me on this – it’s mostly bad news for anyone middle-aged or older, but there’s a reward of sorts at the end. If you understand why there won’t be much headway on Alzheimer’s, you’ll also understand a bit more why modern medicine has been having fewer breakthroughs on major diseases.
We don’t know what causes this disease

For decades it was widely believed that the cause of Alzheimer’s was the build-up of abnormal proteins called amyloid and Tau. These theories dominated the field and led some to believe we were on the verge of effective treatments – through preventing or removing these abnormal proteins. But had the theories been correct we would likely have had at least one or two positive clinical trials.
In retrospect, the multi-decade amyloid fixation looks like a mistake that could have been avoided. Although there is a correlation between amyloid and risk of Alzheimer’s, there are elderly people whose brains have significant amounts of the protein and yet are cognitively intact. Versions of this observation date back to at least the 1960s. That’s one reason why researchers have questioned the enthusiasm for this one hypothesis.
It was always possible that the classic plaques and tangles first seen by Alois Alzheimer, and now known to be made of abnormal proteins, were epiphenomena of aging and not the cause of the disease. Epiphenomena are characteristics that are associated with the disease but are not its cause.

But even more convincing that researchers are closer to the beginning than the end in understanding the cause of Alzheimer’s is the long list of alternative theories. This now includes but is not limited to: infection, disordered inflammation, abnormal diabetes-likemetabolism and numerous environmental toxins.
And the past few years have seen more evidence for viral, bacterial and fungal infections. These viral and bacterial hypotheses were portrayed as eureka moments. But this begs the question: How did powerful tools of epidemiology miss associations with things like cold sores and gum disease?
Not one disease with one cause
When Occam’s razor – the principle that the simplest solution is often the best – is applied to this laundry list of possible causes, it leads to some profound implications. Either Alzheimer’s is not one disease, or many factors can contribute to triggering or promoting it.(See the Bredesen protocol above.) Some authorities have been trying to make such arguments for some time.
Either of these would be bad news, since we would need to develop multiple effective treatments, possibly in combination.
Unfortunately, our biomedical system is designed for the development and testing of one drug at at time. Combinations of drugs dramatically increase the number of clinical trials needed to test for efficacy and toxicity.
We’ve ignored the biology of aging
For 50 years after Alzheimer described the first patient, the disease was considered relatively rare. Called pre-senile dementia, it struck relatively early and sometimes ran in families. The much more common dementia of old age - senile dementia - was considered part of aging.
But here’s the thing – regardless of type, Alzheimer’s has a powerful age-related association. This is true even for patients with early-onset inherited form of Alzheimer’s. Give someone the worst possible genome for Alzheimer’s – including the dreaded APOE e4 gene that may be associated with a 10-fold increase in risk - and that person still needs to age a bit before developing the disease.
Combine the long list of risk factors with the powerful age association and Alzheimer’s comes into focus. Neurons may be the high-wire act of cell types, and the senescence of aging inexorably wears on them. Any one of many cellular insults may accelerate neurons toward earlier cell death. The worst of these may be a particularly bad gene you inherited from your parents, but all are additive to a greater or lesser degree.
If correct, this conception of the disease means we’re even further away from an effective treatment.
Aging is not disease. It is the normal arc of life and an ineluctable part of being human (“dust unto dust”). As such, the biology of aging didn’t get the attention that was bestowed on organ systems and diseases during the golden years of research funding.
In retrospect, I think this may have been a grave mistake. If you list the risk factors for the major diseases of modern life – heart disease, diabetes, dementia – the most powerful is almost always age.
Bottom line: We also lack an understanding of the basic science of Alzheimer’s most important risk factor.
We can’t even accurately diagnose this disease
While it is widely known that it is not possible to diagnose Alzheimer’s accurately during life, a dirty little secret of Alzheimer’s research is that a significant fraction of patients cannot be categorized even on autopsy. The classic plaques and tangles that Alois Alzheimer saw through his microscope may not be accurate biomarkers of this disease.
The single absolute requirement for the development of therapies is an accurate diagnostic. You can’t begin to develop a drug if you can’t accurately identify who has and does not have the disease. Alzheimer’s is the quintessential example of this, as it is very difficult to diagnose. In living patients, diseases like vascular dementia and Lewy body dementia can be indistinguishable from Alzheimer’s. Some of the newest technologies are actually based on imaging amyloid, which some studies show may not be a reliable diagnostic test.
Lead times for new therapies are longer than predicted
It takes a long time for the Food and Drug Administration to approve a drug. From the moment a possible drug is first conceived, it is often more than 10 years until it is available.
The brain has few if any repair mechanisms. So when we talk about Alzheimer’s treatments, we mean prevention not reversal.(Really?)
The natural history of Alzheimer’s is such that preventive therapy will need to be started early in the course of the disease. This will add years to the drug development cycle. A decade from discovery to bedside would be good news for an Alzheimer’s drug.
But history teaches us that the delays could be even worse. Shortly after the discovery of genetic engineering in the early 1980s, it was common to tell patients with diseases like sickle cell that a genetic cure was just a few years away. The sickle cell abnormality and its location in the genome had been known for some time. The organ system involved is easy to access. Thirty years later we have still not successfully cured diseases like sickle cell, and the hubris of those early predictions are painful memories for older physicians like myself.
The situation with Alzheimer’s looks much worse than sickle cell disease looked back in the 1980s. We don’t know the cause – which is likely multifactorial - and its in a hard to get at organ. And neurological diseases are a particular challenge because the brain is protected behind something called the blood-brain barrier. Even if you have a potentially effective drug, it may not reach its target.
Add all of these considerations together and the long road stretches out ahead.
But no drug for the foreseeable future does not mean there’s nothing to do. There is some indication that healthy lifestyle efforts may prevent Alzheimer’s. And even if they don’t, they’re likely effective in preventing vascular dementia, which is almost as common.

Is Memory Decline Associated With Inflammatory Response?

Now is your doctor testing for this or just lazily using Occam's Razor to blame poor memory on stroke and do nothing about it? Ask your doctor that question, you need to know their competency. Does your doctor understand Occam's Razor and the bias it introduces?

 

Is Memory Decline Associated With Inflammatory Response?

Amber M. Tetlow, BA, Ross Andel, PhD, Frank J. Infurna, PhD

First Published November 21, 2017 Research Article

https://doi.org/10.1177/0898264317742809

Article information

Abstract

Objective: To examine whether changes in memory over a 10-year period could predict a change in C-reactive protein (CRP) levels.  
Method: A mixed model analysis was first conducted to obtain the estimates for change in memory over the 10-year period using data from the Health and Retirement Study. Then a multivariate regression to determine whether a change in episodic memory could predict subsequent CRP levels was conducted. Furthermore, a general linear model was conducted to determine differences in CRP levels among different rates of change in episodic memory.  
Results: Greater declines in episodic memory were associated with higher levels of subsequent CRP (Estimate = −0.32, SE = 0.12, β = −.03, p = .008). The general linear model revealed that those with greater memory declines were more likely to have higher levels of CRP, F = 26.50, p < .001. Discussion: These results highlight the notion that memory decline and inflammation may be intertwined, and we discuss various avenues that warrant further investigation.

Keywords cognitive function, cognitive status, biomarkers

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Vol 31, Issue 5, 2019

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A Mental Sign Of Vitamin B12 Deficiency - poor memory

Now is your doctor testing for this or just lazily using Occam's Razor to blame poor memory on stroke and do nothing about it? Ask your doctor that question, you need to know their competency.

A Mental Sign Of Vitamin B12 Deficiency - poor memory

Around one-quarter of people may be deficient in vitamin B12.

A poor memory can be a sign of vitamin B12 deficiency, research finds.
People in the study with low levels of vitamin B12 had worse memory for both ideas and events in their lives.

→ Support PsyBlog for just $4 per month. Enables access to articles marked (M) and removes ads.

Low levels of vitamin B12 can contribute to brain shrinkage, the study also suggested.
Good sources of vitamin B12 include fish, poultry, eggs and low-fat milk.
Fortified breakfast cereals also contain vitamin B12.
People who may have difficulty getting enough vitamin B12 include vegetarians, older people and those with some digestive disorders, such as Crohn’s disease.
Dr Christine C. Tangney, the study’s first author, said:

“Our findings lend support for the contention that poor vitamin B12 status is a potential risk factor for brain atrophy and may contribute to cognitive impairment.”

For the study, 121 older people were given tests of memory and thinking and had their vitamin B12 levels measured.
Brain scans 4.5 years later revealed brain shrinkage in those who were deficient.
B12 deficiency was also linked to worse scores on cognitive tests.
Dr Tangney said:

“Our findings definitely deserve further examination.
It’s too early to say whether increasing vitamin B12 levels in older people through diet or supplements could prevent these problems, but it is an interesting question to explore.
Findings from a British trial with B vitamin supplementation are also supportive of these outcomes.”

Other, common signs of vitamin B12 deficiency include feeling tired, experiencing muscle weakness and being constipated.

About the author

Psychologist, Jeremy Dean, PhD is the founder and author of PsyBlog. He holds a doctorate in psychology from University College London and two other advanced degrees in psychology.
He has been writing about scientific research on PsyBlog since 2004. He is also the author of the book “Making Habits, Breaking Habits” (Da Capo, 2003) and several ebooks:

Association Between Programed Cell Death-1 and CD4+ T Cell Alterations in Different Phases of Ischemic Stroke Patients

If there is any useful information in here I don't understand it. Our fucking failures of stroke associations should be translating all stroke research into readable and actionable formats. A database of stroke research and stroke protocols would be the easy way to do this, but will never occur until survivors run everything. 

Association Between Programed Cell Death-1 and CD4+ T Cell Alterations in Different Phases of Ischemic Stroke Patients

Yi Zhang^1†, Li Wei^2†, Yupeng Du³, Yirui Xie², Wei Wu^2* and Yuan Yuan^4*

• ¹Department of Laboratory Medicine, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China
• ²State Key Laboratory of Diagnostic and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China
• ³Department of Rehabilitation, The Third Affiliated Hospital, Zhejiang University of Traditional Chinese Medicine, Hangzhou, China
• ⁴Department of Neurology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China

Objective: We aimed to analyze alterations in T cell subgroups during different post-ischemic stroke (IS) phases to explore the possible mechanisms underlying stroke-induced immune depression (SIID).
(Maybe depression occurs because survivors are given no way to get 100% recovered. Use Occam's razor.)

Methods: Sixty-four IS patients who met the entry criteria were divided into three groups: an acute phase group, a sub-acute phase group and a stable phase group. Fourteen healthy individuals were selected as normal controls. The phenotype distribution of T cells in patient peripheral blood was analyzed, and the immune checkpoint receptors programed cell death-1 (PD-1) and T cell immunoglobulin and mucin domain 3 (Tim-3) were detected in different T cell phenotypes.

Results: Compared with the control group, the absolute number of CD4⁺ T cells and CD4⁺ T central memory (TCM) cells was significantly increased in the acute phase group but decreased in the sub-acute phase and stable phase groups compared with that in the acute phase group. PD-1 expression in CD4⁺ T cells in the stable phase group showed a significant increase compared with that in the acute phase group. The expression of PD-1 on CD4⁺ TCM cells and CD4⁺ T effector memory (TEM) cells showed significant decreases in the acute phase compared with control cells; however, in the sub-acute phase and the stable phase, PD-1 expression was significantly increased compared with that in the acute phase.

Conclusions: T cell dysfunction, especially CD4⁺ T cell dysfunction, occurred during different IS phases. PD-1 was highly expressed in CD4⁺ T cells of different phenotypes after the acute phase and was associated with alterations in CD4⁺ T cells. Particularly, PD-1 was negatively correlated with the absolute number of TCM cells among different CD4⁺ T cell phenotypes, which may be one of the possible mechanisms of SIID.

Introduction

Stroke is a disease associated with high death and disability worldwide and results in permanent neurological damage to patients (Strong et al., 2007). Ischemic stroke (IS), which accounts for 80%–85% of stroke cases, is frequently induced by thromboembolic occlusion of the cerebral artery. In particular, infectious complications have been reported to occur in 23%–65% of stroke patients after stroke, which leads to poor recovery of patients (Chamorro et al., 2007).

The immune system is considered to play critical roles in patient outcomes following stroke, including in acute stroke events and long-term post-stroke recovery (Bravo-Alegria et al., 2017). In a mouse model, Prass et al. (2003) reported that stroke induced immunodeficiency, which increases susceptibility to bacterial infections. In a human study, impaired T cell responses and decreases in peripheral lymphocyte counts have been reported in stroke patients (Haeusler et al., 2008).

IS induces two immunological cascades: an autoimmune response to central nervous system (CNS) antigens that induces brain inflammation and stroke-induced immunodepression (SIID), which impairs resistance to bacterial infections, resulting in increased incidence of infection, particularly urinary tract infections and pneumonia (Vogelgesang and Dressel, 2011). However, the mechanisms leading to SIID remain unclear, which seriously affects prevention and control of infectious complications in the clinic.

T cell immunity is involved in IS. T cell, but not B cell, contributions to inflammatory and thrombogenic responses have been reported in mice IS (Yilmaz et al., 2006). Chamorro et al. (2005) reported that T cells shift from a Th1-type response to a Th2-type response post-stroke phase. Tregs have been reported to reduce the infarct volume in rats subjected to transient brain ischemia. Dolati et al. (2018) reported that increased Th17 cells and decreased Tregs might contribute to the pathogenesis of IS. Furthermore, accumulating evidence has shown that T cells play important roles in the stroke process (Ishibashi et al., 2002).

T cells are classified as naïve, effector, or memory cells according to the expression of CD45 isoforms and CCR7, a chemokine receptor that helps T cells home to lymph nodes (Ebert et al., 2005). Memory T cells in the context of persistent herpes virus infection contribute to relative control and immunosurveillance of active replication or viral reactivation (Torti and Oxenius, 2012). Effector T cells have a superior capacity to respond quickly to antigenic stimulation compared with naïve T cells (Sallusto and Lanzavecchia, 2009). However, the roles of effective/memory T cells in stroke currently remain unclear. Low numbers of T lymphocytes flow into the healthy brain; however, the role of these cells in stroke is not well understood but has increasingly attracted the attention of researchers (Gemechu and Bentivoglio, 2012).

Our research group previously reported that programed cell death-1 (PD-1) and T cell immunoglobulin and mucin domain 3 (Tim-3) are important cell surface markers that play key roles in immune responses. In addition, Zhao et al. (2011) reported that an increase in Tim-3 is positively correlated with IL-17 and TNF-α levels in IS. Ren et al. (2011) reported that the PD-1 pathway limited CNS inflammation and neurologic deficits in an animal stroke model. Therefore, we hypothesized that PD-1/Tim-3 may be associated with T cell alterations in stroke, which may be one of the mechanisms of SIID.

Therefore, to verify our hypothesis and explore the mechanisms underlying SIID, we investigated T cell alterations during different post-stroke phases and the correlations of PD-1 and Tim-3 with the T cell alterations.