Study links certain fatty acids in blood to decreased Alzheimer’s risk

You can ask your competent? doctor what should done with this research to vastly reduce your chances of dementia.

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

Study links certain fatty acids in blood to decreased Alzheimer’s risk

In a significant stride towards understanding Alzheimer’s disease, researchers have discovered that higher levels of certain fatty acids in the blood are associated with a lower risk of brain changes typical of the disease. This finding, published in The Journals of Gerontology: Series A, could pave the way for more effective early detection and management strategies for Alzheimer’s, a condition that affects millions worldwide.

Alzheimer’s disease is a progressive neurological disorder that primarily affects older adults, leading to memory loss, impaired reasoning, and changes in personality and behavior. It is the most common form of dementia, characterized by the accumulation of amyloid-beta proteins in the brain, forming plaques that disrupt cell function. Despite extensive research, Alzheimer’s remains incurable, and its exact cause is still not fully understood, making early detection and management strategies critical.“The incidence of dementia is increasing over time, impacting the persons affected, as well as their families and loved ones,” said study author Natasha A. Grande de França. “An earlier and more accurate diagnosis can help to prolong the quality of life; however, the diagnosis of dementia is still plenty biased and hard to do. For this reason, we were interested in finding blood biomarkers that could be used to help clinicians in the diagnosis of dementia, especially Alzheimer’s disease (the most common dementia).”concerns just overwhelming. Feelings it was It was hard to To carry out the study, the researchers employed a cross-sectional design, utilizing baseline measurements from a larger ongoing study named COGFRAIL. This study involved 317 older adults, aged 70 and above, who exhibited mild cognitive impairment but not severe dementia. The participants were chosen based on specific cognitive scores and were either prefrail or frail, meaning they showed signs of physical decline but were not entirely dependent on others for daily living. The study excluded individuals with severe psychological conditions or high dependency on others for basic activities. The final sample included a total of 177 individuals. França and her colleagues employed several measures to gather data. They used positron emission tomography (PET) scans to measure the levels of amyloid-beta, a protein that forms clumps in the brains of people with Alzheimer’s, in various brain regions. Blood samples were also collected and analyzed for various nutrients, including different types of fatty acids, vitamins, and an amino acid called homocysteine. The analysis of fatty acids was particularly comprehensive, examining their composition in red blood cell membranes. Over half of the participants (57.6%) were identified as having high amyloid-beta levels in their brains. The researchers found that higher concentrations of a fatty acid called clupanodonic acid were consistently associated with lower amyloid-beta load in the brain. This association was observed in almost all regions of the brain, except for the thalamus. “I was expecting that if any association would be significant, that would arise from the fatty acids omega-3 EPA and DHA,” França told PsyPost. “However, a more consistent result was observed with a metabolite of EPA, the clupanodonic acid. This suggests we should expand the look and the research to less well-known fatty acids, in particular the metabolites of the EPA and DHA as potential more precise biomarkers.” Furthermore, the study noted that linoleic acid showed a positive association with amyloid-beta load, while mead acid and adrenic acid were negatively associated, though less consistently than clupanodonic acid. Interestingly, the study did not find any significant associations between amyloid-beta load and blood vitamins or homocysteine, a common amino acid in the blood.“Our study found potential blood biomarkers to be used in the diagnosis of dementias associated with the aggregation of amyloid-beta in the brain – a peptide associated with the development of Alzheimer’s disease,” França told PsyPost. “However, this is just the first step that needs to be confirmed with other studies in other populations.” Like all scientific research, this study comes with its limitations. The cross-sectional nature of the research means that it can’t definitively establish cause and effect. Additionally, the sample consisted of older adults who were either prefrail or frail, which may not represent the broader population. “Our study has a cross-sectional design and was conducted with a very specific population (older adults with a light degree of cognitive impairment and who were at least pre-frail). So, some questions I can list include: has the association between clupanodonic acid and amyloid-beta happened by chance? Is this association true in populations in different conditions? What is the timing? – when does it start and when does it finish?” França explained. The study, “Associations Between Blood Nutritional Biomarkers and Cerebral Amyloid-β: Insights From the COGFRAIL Cohort Study“, was authored by Natasha A. Grande de França, Gustavo Díaz, Laetitia Lengelé, Gaëlle Soriano, Sylvie Caspar-Bauguil, Laure Saint-Aubert, Pierre Payoux, Laure Rouch, Bruno Vellas, Philipe de Souto Barreto, and Sandrine Sourdet.

Problem in the Recent American Heart Association Guideline on Secondary Stroke Prevention: B Vitamins to Lower Homocysteine Do Prevent Stroke

Have your doctor prove their well reasoned conclusion from this disagreement.

Problem in the Recent American Heart Association Guideline on Secondary Stroke Prevention: B Vitamins to Lower Homocysteine Do Prevent Stroke

J. David Spence

and

Graeme J. Hankey

Originally published24 Jun 2022https://doi.org/10.1161/STROKEAHA.122.038640Stroke. 2022;0:10.1161/STROKEAHA.122.038640

Abstract

In this article, we discuss a problem in the most recent American Heart Association guideline on secondary stroke prevention that apparently arose from the rules of evidence imposed on the guideline panel. We are told by the cochair of the panel that American Heart Association rules about guidelines for secondary prevention prohibited consideration of primary prevention studies and secondary analyses of secondary prevention studies. However, evidence-based medicine should consider all the best external evidence available and also clinical judgement. The most important problem in the guideline was the recommendation that B vitamins to lower homocysteine do not prevent recurrent stroke. When considering all the best external evidence, it is clear that B vitamins do prevent stroke, but in the early secondary stroke prevention studies, the benefit of B vitamins in participants with good renal function was apparently offset by harm from cyanocobalamin among participants with renal failure (level B-R evidence). We review the evidence that B vitamins should be used to prevent stroke, both in primary and secondary stroke prevention (class 2a recommendation). We also review issues in folate metabolism that require further study, with regard to the form of folate to be used for stroke prevention. We recommend that the guideline be revised to say that B vitamins to lower homocysteine prevent stroke and that methylcobalamin or hydroxycobalamin should be used instead of cyanocobalamin.

Study on the Association of Homocysteine and C-Reactive Protein with Neurofunctional Changes in Patients with Acute Ischemic Stroke After Endovascular Stent Treatment

 If there is anything here on stroke recovery I have no clue.

Study on the Association of Homocysteine and C-Reactive Protein with Neurofunctional Changes in Patients with Acute Ischemic Stroke After Endovascular Stent Treatment

This article was originally published here

Neuropsychiatr Dis Treat. 2022 Apr 13;18:881-889. doi: 10.2147/NDT.S356331. eCollection 2022.

ABSTRACT

OBJECTIVE: 

To examine the association of homocysteine (HCY) and C-reactive protein (CRP) with neurofunctional changes in patients with acute ischemic stroke (AIS) after stent treatment.

METHODS: 

A total of 110 patients with AIS treated with stents were divided into a high HCY group (n = 59) and a normal HCY group (n = 51) based on the HCY level. Pearson correlation analysis and logistic linear regression analysis were used to analyze the related factors that affect the National Institutes of Health Stroke Scale (NIHSS) score changes after stent treatment.

RESULTS: 

(1) The area under the receiver operating characteristic (ROC) curve for HCY was 0.995 (95% confidence interval [CI]: 0.984-1.005, P = 0.000), and the best predictive value was 12.75 µmol/L (sensitivity 89.9%, specificity 98.0%). The area under the ROC curve for CRP was 0.665 (95% CI: 0.564-0.767, P = 0.003), and the best predictive value was 9.7 mg/L; (2) comparison between the high HCY group and the normal HCY group showed statistical differences (P < 0.05) in HCY, CRP, and the NIHSS score at admission, the NIHSS score after treatment, gender, history of diabetes, and history of atrial fibrillation; (3) both HCY and CRP were proven to be correlated with the NIHSS score after treatment (0.188, P = 0.050) and (0.194, P = 0.042), respectively, using Pearson correlation analysis; (4) HCY, low-density lipoprotein, CRP, cystatin C, glucose, history of atrial fibrillation, history of diabetes, and the NIHSS score at admission as the risk factors.

CONCLUSION: 

High HCY and CRP levels are related to the neurofunctional changes in patients with AIS treated with stents and can be used as indicators to assess the risk of treating AIS with stents and as serum markers to predict prognoses.

PMID:35444419 | PMC:PMC9014111 | DOI:10.2147/NDT.S356331

 

The Brain Benefits of Onions (Yes, Onions)

 How many decades will it take before your doctor informs the hospital dietician to get these on the menu? In time for your children's and grandchildren's strokes? Or maybe YOU should run the stroke hospital, you can't do any worse.

The Brain Benefits of Onions (Yes, Onions)

Fri, July 23, 2021, 9:42 AM

Who doesn’t love the fragrance of onions cooking on the stove? It warms the heart and whets the appetite for a good, hearty meal. Now we’re learning that those onions not only smell good, they may also help protect our brains from the effects of aging.

Onions, a staple in many cultures and diets around the world, are a nutrition powerhouse. They’re loaded with vitamin C, flavonoids, potassium and B vitamins. And it’s those B vitamins that may be beneficial for your brain.

To learn more, check out this article on Staying Sharp: Avocado-Palooza

A Harvard study showed that vitamin B (folate) seems to sweep away the debris that can clog the brain and lead to cognitive decline as people age. Folate breaks down a compound called homocysteine, which can build up in the blood and increase the risk of stroke and dementia.

You could pop a vitamin B tablet, but experts say it’s better to go straight to the source — and one of the best sources is the humble onion. So to help keep your brain healthy, get chopping and get your folates the tasty way.

Want to find out about the upsides of onions? Read Brain Benefits of Onions May Leave You Crying for More

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This content is provided for informational purposes only and is not intended to provide any expert, professional or specialty advice or recommendations. Readers are urged to consult with their medical providers for all questions.

 

Role of Homocysteine in the Ischemic Stroke and Development of Ischemic Tolerance

Someplace in all these big words is some useful information to be acted upon, which will never occur.  You put an RFP out to researchers, pay for it with foundation grants and write the results up in a stroke protocol available in a public database. 

Role of Homocysteine in the Ischemic Stroke and Development of Ischemic Tolerance   

Ján Lehotský^1*, Barbara Tothová¹, Maria Kovalská^1,2, Dušan Dobrota¹, Anna Beňová¹, Dagmar Kalenská¹ and Peter Kaplán¹

• ¹Institute of Medical Biochemistry and BioMed, Jessenius Faculty of Medicine, Comenius University in Bratislava, Martin, Slovakia
• ²Institute of Histology and Embryology, Jessenius Faculty of Medicine, Comenius University in Bratislava, Martin, Slovakia

Homocysteine (Hcy) is a toxic, sulfur-containing intermediate of methionine metabolism. Hyperhomocysteinemia (hHcy), as a consequence of impaired Hcy metabolism or defects in crucial co-factors that participate in its recycling, is assumed as an independent human stroke risk factor. Neural cells are sensitive to prolonged hHcy treatment, because Hcy cannot be metabolized either by the transsulfuration pathway or by the folate/vitamin B12 independent remethylation pathway. Its detrimental effect after ischemia-induced damage includes accumulation of reactive oxygen species (ROS) and posttranslational modifications of proteins via homocysteinylation and thiolation. Ischemic preconditioning (IPC) is an adaptive response of the CNS to sub-lethal ischemia, which elevates tissues tolerance to subsequent ischemia. The main focus of this review is on the recent data on homocysteine metabolism and mechanisms of its neurotoxicity. In this context, the review documents an increased oxidative stress and functional modification of enzymes involved in redox balance in experimentally induced hyperhomocysteinemia. It also gives an interpretation whether hyperhomocysteinemia alone or in combination with IPC affects the ischemia-induced neurodegenerative changes as well as intracellular signaling. Studies document that hHcy alone significantly increased Fluoro-Jade C- and TUNEL-positive cell neurodegeneration in the rat hippocampus as well as in the cortex. IPC, even if combined with hHcy, could still preserve the neuronal tissue from the lethal ischemic effects. This review also describes the changes in the mitogen-activated protein kinase (MAPK) protein pathways following ischemic injury and IPC. These studies provide evidence for the interplay and tight integration between ERK and p38 MAPK signaling mechanisms in response to the hHcy and also in association of hHcy with ischemia/IPC challenge in the rat brain. Further investigations of the protective factors leading to ischemic tolerance and recognition of the co-morbid risk factors would result in development of new avenues for exploration of novel therapeutics against ischemia and stroke.

Introduction

Many experimental and clinical studies provide evidence that co-morbid disorders are potential risk factors for development of vascular disorders in humans including stroke (Lehotský et al., 2009a; Kwon et al., 2014). At present, there are several known factors elevating the risk of ischemic stroke which include transient ischemic attack (TIA), arterial diseases, atrial fibrillation, improper diet and/or obesity and physical inactivity (Dirnagl et al., 2009). As it has been verified by many studies, even mild hyperhomocysteinemia (hHcy) may increase the risk for clinical manifestations of stroke, probably due to the pleiotropic biochemical properties of homocysteine (Hcy) and its impact on venous and arterial atherosclerotic modifications (Refsum et al., 1998; Steele et al., 2013; Kwon et al., 2014; Petras et al., 2014; Williams et al., 2014). In fact, Hcy suppresses NO production by endothelial cells and platelets and increases generation of reactive oxygen species (ROS) by the release of arachidonic acid from the platelets. It also inhibits glutathione peroxidase and thus stimulates proliferation of endothelial cells (see Petras et al., 2014, for review). In addition, Hcy has been shown to inhibit methyltransferases, to suppress DNA repair and to facilitate apoptosis when accumulated inside the cells. Autooxidation of Hcy metabolites results in H₂0₂ accumulation (Boldyrev et al., 2013) and challlenging neurons to Hcy metabolites for longer period leads to necrotic cell death (Ziemińska et al., 2003). Clinical studies suggest that elevated homocysteine level frequently parallels progressive aging as well as neurodegenerative and acute disorders of the CNS, e.g., Alzheimer's disease or Parkinson's disease (Dionisio et al., 2010). Designing appropriate animal models relevant to the clinical conditions of human stroke is an important step for studying the disease ethiology. Until now, only sparse studies have been developed to explore the mutual effect of HCy and ischemic preconditioning (IPC) in animal models of ischemic stroke.

In this paper we summarize current overview on homocysteine conversion steps in the organism and present the genetic and metabolic causes of hyperhomocysteinemia-related neurotoxicity. Based on the results from our laboratory, we also document, in this context, that mutual effect of experimental hyperhomocysteinemia (hHCy) and ischemic insult with or without pre-ischemic challenge can have different outcomes on the extent of neuronal degeneration as well as on the intracellular signaling pathways leading to the preconditioning phenomenon.

More at link.

Elevated Total Homocysteine Levels in Acute Ischemic Stroke Are Associated With Long-Term Mortality

You'll have to see what your doctor does with this information to reduce your risk of dying.
An updated stroke protocol on not dying would be the best.
http://stroke.ahajournals.org/content/46/9/2419.abstract

1. Zhihong Shi, MD, PhD;
2. Yalin Guan, MD, MS;
3. Ya Ruth Huo, BA, MD;
4. Shuling Liu, RN, MS;
5. Meilin Zhang, PhD;
6. Hui Lu, MD, MS;
7. Wei Yue, MD, MS;
8. Jinhuan Wang, MD, PhD;
9. Yong Ji, MD, PhD

+ Author Affiliations

1. From the Tianjin Key Laboratory of Cerebrovascular and Neurodegenerative Diseases (Z.S., Y.G., S.L., H.L., W.Y., J.W., Y.J.), Department of Neurology (Z.S., Y.G., S.L., H.L., W.Y., Y.J.), and Department of Neurosurgery (J.W.), Tianjin Huanhu Hospital, Tianjin, China; School of Medicine, University of New South Wales, Kensington, NSW, Australia (Y.R.H.); and Department of Nutrition and Food Science, School of Public Health, Tianjin Medical University, Tianjin, China (M.Z.).

1. Correspondence to Yong Ji, MD, PhD, Department of Neurology, Tianjin Huanhu Hospital, Qixiangtai Rd 122, Hexi, Tianjin 300060, China. E-mail jiyongusa@126.com

Abstract

Background and Purpose—Total homocysteine (tHcy) levels are associated with secondary vascular events and mortality after stroke. The aim of this study was to investigate whether tHcy levels in the acute phase of a stroke contribute to the recurrence of cerebro-cardiovascular events and mortality.

Methods—A total of 3799 patients were recruited after hospital admission for acute ischemic stroke. Levels of tHcy were measured within 24 hours after primary admission. Patients were followed for a median of 48 months.

Results—During the follow-up period, 233 (6.1%) patients died. After adjustment for age, smoking status, diabetes mellitus, and other cardiovascular risk factors, patients in the highest tHcy quartile (>18.6 μmol/L) had a 1.61-fold increased risk of death (adjusted hazard ratio [HR], 1.61; 95% confidence interval [CI], 1.03–2.53) compared with patients in the lowest quartile (≤10 μmol/L). Further subgroup analysis showed that this correlation was only significant in the large-artery atherosclerosis stroke subtype (adjusted HR, 1.80; 95% CI, 1.05–3.07); this correlation was not significant in the small-vessel occlusion subtype (adjusted HR, 0.80; 95% CI, 0.30–2.12). The risk of stroke-related mortality was 2.27-fold higher for patients in the third tHcy quartile (adjusted HR, 2.27; 95% CI, 1.06–4.86) and 2.15-fold more likely for patients in the fourth quartile (adjusted HR, 2.15; 95% CI, 1.01–4.63) than for patients in the lowest tHcy quartile. The risk of cardiovascular-related mortality and the risk of recurrent ischemic stroke were not associated with tHcy levels.

Conclusions—Our findings suggest that elevated tHcy levels in the acute phase of an ischemic stroke can predict mortality, especially in stroke patients with the large-vessel atherosclerosis subtype.

Effects of differences in serum total homocysteine, folate, and vitamin B 12 on cognitive impairment in stroke patients.

Your doctor should have a readily available stroke protocol to address this problem if you have this.
DEMAND IT!!!

Effects of differences in serum total homocysteine, folate, and vitamin B 12 on cognitive impairment in stroke patients.

Jiang B, Chen Y, Yao G, Yao C, Zhao H, Jia X, Zhang Y, Ge J, Qiu E, Ding C.

Abstract

BackgroundVascular cognitive impairment-no dementia (VCIND) refers to the early or mild cognitive impairment induced by cerebral vascular injury. Research shows that serum total homocysteine (tHcy) level is an independent risk factor for cerebral vascular disease and may be closely related to cognitive function.Current studies on the tHcy level in VCIND patients are limited, and the relationship of tHcy with cognitive function remains unclear. This study aims to investigate the tHcy levels in patients with VCIND and to determine their correlation with cognitive function, as well as to provide useful clues for preventing and treating VCIND.
Methods
The tHcy, folate, and vitamin B12 levels in 82 patients with VCIND were reviewed retrospectively and compared with those of 80 stroke patients without cognitive impairment and 69 healthy controls by using the Montreal Cognitive Assessment (MoCA) scale and the event-related potential P300 to evaluate cognitive function.
Results
The tHcy levels in the VCIND group were higher than those in the other two groups, whereas the folate and Vitamin B12 levels in the VCIND group were lower than those of the other two groups. The tHcy levels in the stroke group were higher than those in the control group, and the folate and vitamin B12 levels in the stroke group were lower than those in the control group. The patients in the VCIND group with high tHcy exhibited lower MoCA scores and prolonged P300 latency than those in with normal tHcy. Correlation analysis showed that tHcy level is positively correlated with P300 latency period and negatively correlated with MoCA score.
Conclusion
The tHcy levels were significantly higher and the vitamin B12 and folate levels were significantly lower in the patients with VCIND than those in the other groups. The high tHcy levels in the VCIND patients may be correlated with impaired cognitive function.

Effect of Folate and Mecobalamin on Hip Fractures in Patients With Stroke

Only 8 years old. How incompetent is your stroke hospital if they haven't put this into place yet? Seems like a fireable offense for the hospital board of directors to enforce. Why would you even go to a hospital if they can't even read and apply research  to their areas of expertise? The following of Joint Commission standards is even more of a reason to never set foot in such a hospital. No innovation. But then I'm a stupid non-medical stroke survivor, they would have to be stupider than me to not see  where they can apply research to stroke protocols.
http://jama.jamanetwork.com/article.aspx?articleid=200453

ABSTRACT

ABSTRACT | METHODS | RESULTS | COMMENT | ARTICLE INFORMATION | REFERENCES

Context  Stroke increases the risk of subsequent hip fracture by 2 to 4 times. Hyperhomocysteinemia is a risk factor for both ischemic stroke and osteoporotic fractures in elderly men and women. Treatment with folate and mecobalamin (vitamin B₁₂) may improve hyperhomocysteinemia.
Objective  To investigate whether treatment with folate and vitamin B₁₂ reduces the incidence of hip fractures in patients with hemiplegia following stroke.
Design, Setting, and Patients  A double-blind, randomized controlled study of 628 consecutive patients aged 65 years or older with residual hemiplegia at least 1 year following first ischemic stroke, who were recruited from a single Japanese hospital from April 1, 2000, to May 31, 2001. Patients were assigned to daily oral treatment with 5 mg of folate and 1500 μg of mecobalamin, or double placebo; 559 completed the 2-year follow-up.
Main Outcome Measure  Incidence of hip fractures in the 2 patient groups during the 2-year follow-up.
Results  At baseline, patients in both groups had high levels of plasma homocysteine and low levels of serum cobalamin and serum folate. After 2 years, plasma homocysteine levels decreased by 38% in the treatment group and increased by 31% in the placebo group (P<.001). The number of hip fractures per 1000 patient-years was 10 and 43 for the treatment and placebo groups, respectively (P<.001). The adjusted relative risk, absolute risk reduction, and the number needed to treat for hip fractures in the treatment vs placebo groups were 0.20 (95% confidence interval [CI], 0.08-0.50), 7.1% (95% CI, 3.6%-10.8%), and 14 (95% CI, 9-28), respectively. No significant adverse effects were reported.
Conclusion  In this Japanese population with a high baseline fracture risk, combined treatment with folate and vitamin B₁₂ is safe and effective in reducing the risk of a hip fracture in elderly patients following stroke.

The risk of a hip fracture in patients after stroke is 2 to 4 times higher than that in age-matched healthy control patients.¹ These fractures usually occur relatively late after stroke onset and affect the paretic side of the body.^2- 5 Hip fractures are associated with more deaths, disabilities, and medical costs than all other osteoporosis-related fractures combined.⁶ We previously measured the bone mineral density (BMD) in patients with stroke in the second metacarpal bone and demonstrated a decrease in the bone mass in the hemiplegic limb that corresponded to the degree of palsy and vitamin D deficiency,⁷ which may explain why hip fractures in patients poststroke occur almost exclusively on the hemiplegic side of the body.

A close association between plasma homocysteine and risk of ischemic stroke has been reported,^8- 11 and plasma homocysteine levels are higher in patients with ischemic stroke in both acute^12- 13 and convalescent phases.^14- 17 In patients with homocysteinuria, a rare autosomal recessive biochemical abnormality, there is an increased prevalence of skeletal abnormalities,^18- 20 including osteoporosis, a primary risk factor for hip fracture. Thus, elevated plasma homocysteine concentrations may be associated with osteoporosis and increase the risk of a hip fracture. An increased homocysteine level appears to be a strong and independent risk factor for an osteoporotic fracture of the bones, including the hip, in older men and women.^21- 22

In the remethylation cycle, homocysteine is salvaged for methionine synthesis by the addition of a methyl group by methionine synthase.²³ Vitamin B₁₂ (cobalamin) is an essential cofactor for methionine synthase and N⁵-methyl-tetrahydrofolate serves as the methyl donor. Therefore, there are close relationships between plasma homocysteine and cobalamin and folate.^{8- 9,24- 26}

We previously demonstrated a reduction in plasma homocysteine levels by combination therapy with folate and vitamin B₁₂ in patients with ischemic stroke.²⁶ Our goal for this study was to investigate the efficacy of the combined therapy for decreasing the risk of fractures, particularly in the hip, in a 2-year trial in elderly patients with hemiplegia following ischemic stroke.

Preventing Alzheimer’s disease-related gray matter atrophy by B-vitamin treatment

Since we have a higher chance of dementia and alzheimers due to our stroke, ask your doctor what s/he is doing for you to prevent that. You do expect an answer? Don't you?
http://www.pnas.org/content/110/23/9523.abstract 

Abstract

Is it possible to prevent atrophy of key brain regions related to cognitive decline and Alzheimer’s disease (AD)? One approach is to modify nongenetic risk factors, for instance by lowering elevated plasma homocysteine using B vitamins. In an initial, randomized controlled study on elderly subjects with increased dementia risk (mild cognitive impairment according to 2004 Petersen criteria), we showed that high-dose B-vitamin treatment (folic acid 0.8 mg, vitamin B6 20 mg, vitamin B12 0.5 mg) slowed shrinkage of the whole brain volume over 2 y. Here, we go further by demonstrating that B-vitamin treatment reduces, by as much as seven fold, the cerebral atrophy in those gray matter (GM) regions specifically vulnerable to the AD process, including the medial temporal lobe. In the placebo group, higher homocysteine levels at baseline are associated with faster GM atrophy, but this deleterious effect is largely prevented by B-vitamin treatment. We additionally show that the beneficial effect of B vitamins is confined to participants with high homocysteine (above the median, 11 µmol/L) and that, in these participants, a causal Bayesian network analysis indicates the following chain of events: B vitamins lower homocysteine, which directly leads to a decrease in GM atrophy, thereby slowing cognitive decline. Our results show that B-vitamin supplementation can slow the atrophy of specific brain regions that are a key component of the AD process and that are associated with cognitive decline. Further B-vitamin supplementation trials focusing on elderly subjets with high homocysteine levels are warranted to see if progression to dementia can be prevented. 

Do not self-prescribe. I told this to a nurse, she said overdosing on B vitamins is not good.

Unmasking the benefits of B vitamins in stroke prevention

Not much to go on here, can't tell if this is dietary or supplements. Your doctor should be subscribing to The Lancet. You can check out other commentary here:
http://oc1dean.blogspot.com/2011/12/jama-commentary-contends-vitamin.html
The Lancet here:
 http://www.thelancet.com/journals/laneur/article/PIIS1474-4422%2812%2970094-7/fulltext
 Vitamin B12 and folate are key mediators of homocysteine metabolism. Low plasma vitamin B12 and folate concentrations are associated with hyperhomocysteinaemia, with consequent premature atherosclerosis and increased risk of cardiovascular and cerebrovascular disease.1,2 In a meta-analysis of observational studies, a 25% reduction in homocysteine concentrations (roughly 3 μmol/L [0·41 mg/L]) corresponded with an 11% lower risk of ischaemic heart disease and a 19% lower risk of stroke.3 The Heart Outcomes Prevention Evaluation 2 (HOPE 2) trial4 and re-analysis of data from the Vitamin Intervention for Stroke Prevention (VISP) study5 (both trials in which patients received high doses of B vitamins) have confirmed these findings for stroke.

JAMA Commentary Contends Vitamin Therapy Can Still Reduce Stroke

Ok, lets quit arguing and come to a consensus, lives are at stake.
http://www.medicalnewstoday.com/releases/239580.php
A commentary by Dr. David Spence of The University of Western Ontario and Dr. Meir Stampfer of the Harvard School of Public Health in today's Journal of the American Medical Association (JAMA) argues that vitamin therapy still has a role to play in reducing stroke.

Vitamin B therapy was once widely used to lower homocysteine levels. Too much of this amino acid in the bloodstream was linked to increased risk of stroke and heart attack. But several randomized trials found lowering homocysteine levels with B vitamins did not result in a cardiovascular benefit. And a study by Dr. Spence, a scientist with the Robarts Research Institute at Western's Schulich School of Medicine & Dentistry, found Vitamin B therapy actually increased cardiovascular risk in patients with diabetic nephropathy.

Dr. Spence says this commentary provides insights that overturn the widespread belief that "homocysteine is dead." He says two key issues have been overlooked in the interpretation of the clinical trials: the key role of vitamin B12, and the newly recognized role of renal failure.

"It is now clear that the large trials showing no benefit of vitamin therapy obscured the benefit of vitamin therapy because they lumped together patients with renal failure and those with good renal function. The vitamins are harmful in renal failure, and beneficial in patients with good renal function, and they cancel each other out," says Dr. Spence, the author of "How to Prevent Your Stroke." The authors also contend most of the trials did not use a high enough dose of vitamin B12.