Green tea consumption and cerebral white matter lesions in community-dwelling older adults without dementia

 Not changing my mind on this; coffee is the way to go! Much more research on coffee. 

How coffee protects against Parkinson’s Aug. 2014  

Coffee May Lower Your Risk of Dementia Feb. 2013

Coffee drinkers rejoice! Drinking coffee could lower the risk of Alzheimer’s disease 

And this: Coffee's Phenylindanes Fight Alzheimer's Plaque December 2018

Coffee Drinking Tied to Better Survival, but Timing Matters

Longer overall and cardiovascular mortality only observed among morning drinkers. 

The latest here:

Green tea consumption and cerebral white matter lesions in community-dwelling older adults without dementia

• Shutaro Shibata,
• Moeko Noguchi-Shinohara,
• Ayano Shima,
• Taro Ozaki,
• Yuta Usui,
• Yasuyuki Taki,
• Kazuhiro Uchida,
• Takanori Honda,
• Jun Hata,
• Tomoyuki Ohara,
• Tatsuya Mikami,
• Tetsuya Maeda,
• Masaru Mimura,
• Kenji Nakashima,
• Jun-ichi Iga,
• Minoru Takebayashi,
• Toshiharu Ninomiya &
• Kenjiro Ono
• On behalf of the Japan Prospective Studies Collaboration for Aging and Dementia (JPSC-AD) study group

npj Science of Food volume 9, Article number: 2 (2025) Cite this article

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Abstract

This study investigated the association between green tea or coffee consumption with cerebral white matter lesions and hippocampal and total brain volumes among 8766 community-dwelling participants recruited from the Japan Prospective Studies Collaboration for Aging and Dementia between 2016 and 2018. A Food Frequency Questionnaire was used to assess green tea and coffee consumption, whereas brain magnetic resonance imaging was performed to assess cerebral white matter lesions, hippocampal volume, and total brain volume. Multivariable-adjusted analysis revealed significant correlations between fewer cerebral white matter lesions and higher green tea consumption, whereas no significant differences were found between green tea consumption and hippocampal or total brain volume. Regarding coffee consumption, no significant differences were observed in cerebral white matter lesions or hippocampal or total brain volumes. Hence, higher green tea consumption was associated with fewer cerebral white matter lesions, suggesting that it may be useful in preventing dementia.

Association between fibrinogen and white matter lesions and cerebral atrophy in patients with acute ischemic stroke

 ABSOLUTELY FUCKING USELESS RESEARCH! Associations DO NOTHING to get survivors recovered!

My doctor told me I had a bunch of white matter hyperintensities but never showed me them on any scan, so I don't know the size, location or any intervention needed, because my doctor knew nothing and did nothing.

This told me nothing useful. Like how to reverse white matter hyperintensities.

Association between fibrinogen and white matter lesions and cerebral atrophy in patients with acute ischemic stroke

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https://doi.org/10.1016/j.jstrokecerebrovasdis.2024.108008

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Highlights

• •

  In patients with acute ischemic stroke (AIS), increased fibrinogen levels were independently associated with white matter hyperintensity.

• •

  Moreover, higher levels of fibrinogen were also independently associated with increased risk of cerebral atrophy in AIS.

• •

  Fibrinogen has the potential to serve as a biomarker for identifying cerebral small vessel disease (CSVD).

Abstract

Background

Inflammation is a potential mechanism underlying the development of white matter lesions (WMLs) and cerebral atrophy. We aimed to investigate the relationship of fibrinogen levels with WMLs and cerebral atrophy in patients with acute ischemic stroke (AIS).

Methods

A total of 701 AIS patients were enrolled. Participants were divided into four groups according to the quartiles of fibrinogen levels: Q1 < 2.58 g/L, Q2: 2.58-3.12 g/L, Q3: 3.12-3.67 g/L, Q4: ≥ 3.67 g/L. White matter hyperintensity (WMH), periventricular hyperintensity (PVH) and deep white matter hyperintensity (DWMH) were defined according to the Fazekas scale. Cerebral atrophy was defined according to global cortical atrophy scores. Univariate and multivariate logistic regression were used to explore the relationship of fibrinogen levels and WMHs, PVH, DWMH and cerebral atrophy.

Results

Among 701 AIS patients, 498 (71.0 %), 425 (60.6 %), 442 (63.1 %), and 560 (79.9 %) had WMHs, PVH, DWMH and cerebral atrophy, respectively. After adjustment for potential covariates, the highest fibrinogen quartiles were significantly associated with increased risk of WMHs (odds ratio [OR] 1.97, 95 % confidence intervals [CI] 1.10-3.50), PVH (OR 1.85, 95 % CI 1.08-3.16) and cerebral atrophy (OR 2.53, 95 % CI 1.19-5.40) but not DWMH (OR 1.37 95 % CI 0.81-2.31) compared with the lowest fibrinogen quartile. Moreover, the association between elevated fibrinogen levels and the risk of WMLs and cerebral atrophy remained significant as continuous variables.

Conclusions

Increased baseline fibrinogen levels were independently associated with WMHs, PVH and cerebral atrophy in patients with ischemic stroke. Fibrinogen could be the potential blood biomarker of WMLs and cerebral atrophy.

No association between migraine frequency, white matter lesions and silent brain infarctions: A study in a series of women with chronic migraine

They seem to have totally missed testing migraine with aura, that data point should have been included by the senior researcher.

Migraine with aura – but not without – increases risk of stroke  Sept. 2017

The latest here:

No association between migraine frequency, white matter lesions and silent brain infarctions: A study in a series of women with chronic migraine

Meilán A, Larrosa D, Ramón C

European Journal of Neurology|May 21, 2020

Since silent infarctions (SIs) and hyperintense white matter lesions (WMLs) are related to the frequency of migraine, researchers analyzed their prevalence and anatomical distribution in chronic migraine (CM) patients. In total, 96 women with CM [mean age 43 (range 16–65) years] and 29 women with episodic migraine (EM) [mean age 36 (range 16–58) years] had 1.5‐T MRI following the CAMERA protocol. In 59 (61.5%) women with CM and 17 (58.6%) women with EM, white matter lesions were found. Compared with the anticipated prevalence at this age, this investigation demonstrates that the prevalence of WMLs in CM and EM has been increased, in most cases small, deep and frontal. The results, however, do not support a combination of WMLs or SIs with a higher frequency of attacks but with the presence of vascular risk factors and mainly age > 45 years.

Read the full article on European Journal of Neurology.

Association of intensive vs standard blood pressure control with cerebral white matter lesions

My doctor told me I had a bunch of white matter lesions right after my stroke. He never showed me any scans so he might have just been pulling crap out of his ass. In today's world this should be a protocol to intensively treat blood pressure. But I'm sure your doctor and stroke hospital are incompetent and won't have this in place in the next month. It is YOUR RESPONSIBILITY to train your doctor in this. Otherwise it will never get done.  And you will bear the burden of this problem while your doctor doesn't face any consequences for incompetency. 

Oops, my bad. Suggesting I know more than your doctor. Don't listen to me I'm not medically trained, but I do keep up with research.

Association of intensive vs standard blood pressure control with cerebral white matter lesions

JAMA | August 15, 2019

The SPRINT MIND Investigators for the SPRINT Research Group - Via performing a sub-study of a randomized clinical trial that included 449 hypertensive individuals with longitudinal brain MRI, researchers assessed the correlation of intensive blood pressure treatment with cerebral white matter lesion and brain volumes. Mean white matter lesion volume progressed from 4.57 to 5.49 cm³ vs a rise from 4.40 to 5.85 cm³ in the standard treatment group. Mean total brain volume reduced from 1,134.5 to 1,104.0 cm³ in the intensive treatment group vs a drop from 1,134.0 to 1,107.1 cm³ in the standard treatment group. Hence, among hypertensive adults, targeting a systolic blood pressure of < 120 mmHg vs < 140 mm Hg was significantly related to a smaller increase in cerebral white matter lesion volume and a higher reduction in total brain volume; however, the variations were small.

Read the full article on JAMA

Abnormal functional connectivity density in patients with ischemic white matter lesions: An observational study

So what if they cause cognitive problems?  Fucking useless research with no solutions provided to fix those problems. I supposedly have a bunch of these although my doctor never showed me any scans.
http://www.mdlinx.com/internal-medicine/medical-news-article/2016/09/28/white-matter-lesions/6865315/?news_id=881&newsdt=100116&subspec_id=488&

Medicine, 09/28/2016Ding JR, et al.

In this observational study, authors produced new insights into how white matter lesions cause cognitive and motor decline from cortical functional connectivity perspective.

Methods

• Researchers manipulated functional connectivity density mapping (FCDM) to analyze changes in brain functional connectivity in 16 patients with ischemic WMLs and 13 controls.
• Both short– and long–range FCD maps were quantified, and group comparisons were conducted between the 2 groups.
• They conducted a correlation analysis between regions with altered FCD and cognitive test scores (Mini–Mental State Examination [MMSE] and Montreal Cognitive Assessment [MoCA]) in the patient group.

Results

• They observed that patients with ischemic WMLs exhibited reduced short–range FCD in the temporal cortex, primary motor cortex, and subcortical region, which could account for inadequate top–down attention, impaired motor, memory, and executive function associated with WMLs.
• The positive correlation between primary motor cortex and MoCA scores yielded evidence for the influences of cognitive function on behavioral performance.
• The inferior parietal cortex exhibited increased short–range FCD, reflecting a hyper bottom–up attention to compensate for the inadequate top–down attention for language comprehension and information retrieval in patients with WMLs.
• Moreover, the prefrontal and primary motor cortex showed increased long–range FCD and the former positively correlated with MoCA scores, which recommended a strategy of cortical functional reorganization to compensate for motor and executive deficits.

Go to PubMed Go to Abstract Print Article Summary Cat 2 CME Report

Calcium supplementation and risk of dementia in women with cerebrovascular disease

Be careful out there.
http://www.mdlinx.com/internal-medicine/medical-news-article/2016/08/22/cerebrovascular-disease-calcium-supplementation-dementia/6824758/?

Neurology®, 08/22/2016 Kern J, et al.

This longitudinal population–based study coordinated to describe the association between calcium supplementation with the development of dementia in women with cerebrovascular disease after a 5–year follow–up. The study found that calcium supplementation may increase the risk of developing dementia in elderly women. These findings need to be confirmed, because this sample was relatively small and the study was observational.

Methods

• The authors derived this sample from the Prospective Population Study of Women and H70 Birth Cohort Study in Gothenburg, Sweden.
• They included 700 dementia–free women aged 70–92 years.
• The women underwent comprehensive neuropsychiatric and somatic examinations, at baseline in 2000–2001, and at follow–up in 2005–2006.
• They performed a CT scan in 447 participants at baseline.
• They collected information on the use and dosage of calcium supplements, and diagnosed dementia according to DSM–III–R criteria.

Results

• As compare to women not given supplementation (n = 602), the women who treated with calcium supplements (n = 98) were at a higher risk of developing dementia (odds ratio [OR] 2.10, 95% confidence interval [CI] 1.01–4.37, p = 0.046) and the subtype stroke–related dementia (vascular dementia and mixed dementia) (OR 4.40, 95% CI 1.54–12.61, p = 0.006).
• As per this stratified analyses, calcium supplementation was connected with the development of dementia in groups with a history of stroke (OR 6.77, 95% CI 1.36–33.75, p = 0.020) or presence of white matter lesions (OR 2.99, 95% CI 1.28–6.96, p = 0.011), but not in groups without these conditions.

Go to PubMed Go to Abstract Print Article Summary Cat 2 CME Report

Resistance Training and White Matter Lesion Progression in Older Women: Exploratory Analysis of a 12-Month Randomized Controlled Trial

You'll have to send your doctor after the exact weight lifting protocol used in this study. Because our fucking failures of stroke associations do not have publicly available research findings.
http://www.ncbi.nlm.nih.gov/pubmed/26456233

Bolandzadeh N^1,2,3,4,5, Tam R⁶, Handy TC⁷, Nagamatsu LS⁸, Hsu CL^1,3,4,5, Davis JC^1,5,9,10, Dao E^1,3,4,5, Beattie BL^5,11, Liu-Ambrose T^1,2,3,4,5.

Author information

Abstract

OBJECTIVES:

To assess whether resistance training (RT) slows the progression of white matter lesions (WMLs) in older women.

DESIGN:

Secondary analysis of a 52-week randomized controlled trial of RT, the Brain Power Study.

SETTING:

Community center and research center.

PARTICIPANTS:

Of 155 community-dwelling women aged 65 to 75 enrolled in the Brain Power Study, 54 who had evidence of WMLs on magnetic resonance imaging (MRI) at baseline were included in this secondary analysis.

INTERVENTION:

Participants were randomized to once-weekly RT (1× RT), twice-weekly RT (2× RT), or twice-weekly balance and tone (BAT). Assessors were blinded to participant assignments.

MEASUREMENTS:

WML volume was measured using MRI at baseline and trial completion.

RESULTS:

At trial completion, the 2× RT group had significantly lower WML volume than the BAT group (P = .03). There was no significant difference between the BAT group and the 1× RT group at trial completion (P = .77). Among participants in the two RT groups, reduced WML progression over 12 months was significantly associated with maintenance of gait speed (correlation coefficient (r) = -0.31, P = .049) but not with executive functions (r = 0.30; P = .06).

CONCLUSION:

Engaging in progressive RT may reduce WML progression.

Major Cause of Dementia Identified Which Could Lead to New Treatments

If silent strokes, aka white matter disease are the probable cause of dementia then the obvious solution is to figure out how exactly to get neurogenesis and neuroplasticity to work. But no, they go down the same failed route of, 'Hey, lets tell people these generic stroke prevention tips', What a goddamn waste of time.
http://www.spring.org.uk/2014/11/major-cause-of-dementia-identified-which-could-lead-to-new-treatments.php?
 These paragraphs show the wrong-headed efforts.

“We don’t yet know whether these small strokes are responsible only some or most of the white matter disease seen in older patients.
But in those where it is the cause, the detection of white matter disease on brain imaging should trigger physicians to treat patients aggressively when managing stroke risk factors such as high blood pressure, diabetes, high cholesterol, cigarette smoking and lack of exercise not only to prevent further strokes, but also to reduce the development of cognitive impairment over time.”

Maybe you want to do this for dementia prevention:
My complete list here:
Dementia prevention 19 ways
Or this for stroke prevention:
Like my 11 Stroke risk reduction ideas. 
 

White Matter Injury in Global Cerebral Ischemia

And maybe finally someone is starting to understand that white matter damage needs research and protocols to recover it.
http://link.springer.com/chapter/10.1007/978-1-4614-9123-1_9

• Shinichi Nakao M.D., Ph.D.,
• Yan Xu Ph.D.

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Abstract

In chronic cerebral hypoperfusion due to aging, global cerebral ischemia after cardiac arrest, acute and chronic hypoxia in asymptomatic stroke, and diffuse axonal injury after traumatic brain injury, white matter lesions occur not only as a result of secondary degeneration caused by neuronal injuries in the gray matter, but also as a direct consequence of the primary ischemic insults. Not enough attention has been directed to the molecular and cellular mechanisms of white matter injuries in humans. Failures in past stroke therapyclinical trials are partly attributed to misrepresentation of the relevance of white matter to human brain pathology in the preclinical data. Most rodent models either ignore white matter's contribution to the injury process and recovery, or inadequately account for this contribution due to a significantly lower proportion of white matter in the rodent brain compared to the human brain. Future development of effective therapies should place an equal emphasis on gray and white matter injuries.

Plasma brain-derived neurotrophic factor and prefrontal white matter integrity in late-onset depression and normal aging

Our researchers should be able to tell us post-stroke what our BDNF and VEGF levels are and how to get them back to normal. Is your depression due to aging or stroke?
http://onlinelibrary.wiley.com/doi/10.1111/acps.12085/abstract;jsessionid=5167ECEF0A5F03D4EF409CB10E60BE55.d01t04?deniedAccessCustomisedMessage=&userIsAuthenticated=false

Objective

To explore the relationship between brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF), cerebral deep white matter lesions (DWMLs), and measures of white matter integrity in patients with late-onset depression, with respect to vascular risk factors.

Method

We examined 22 patients with late-onset depression and 22 matched controls. Quantification of plasma BDNF and VEGF levels were performed with enzyme-linked immunosorbent assay (ELISA) kits. Measures of white matter integrity comprised apparent diffusion coefficient (ADC) and fractional anisotropy (FA), obtained by diffusion tensor imaging (DTI). Effects of DWMLs, FA, ADC, and vascular risk factors on BDNF and VEGF were assessed using multiple linear regression.

Results

The BDNF and VEGF levels did not differ significantly between groups. With pooled data for patients and controls, the BDNF level was positively associated with both number (t = 2.14, P = 0.039) and volume (t = 2.04, P = 0.048) of prefrontal DWMLs and negatively associated with FA in prefrontal normal-appearing white matter (t = −2.40, P = 0.02), adjusted for age and gender. Smoking and hypercholesterolemia was positively associated with the BDNF (t = 2.36, P = 0.023) and VEGF levels (t = 2.28, P = 0.028), respectively.

Conclusion

Our results suggest a role for BDNF in the complex pathophysiologic mechanisms underlying DWMLs in both normal aging and late-onset depression.

Large-vessel correlates of cerebral small-vessel disease

Definitely a question for your doctor. How does knowing this prevent your next stroke?
http://www.docguide.com/large-vessel-correlates-cerebral-small-vessel-disease
OBJECTIVE: Our aim was to investigate the relationship of carotid structure and function with MRI markers of cerebral ischemic small-vessel disease. METHODS: The study comprised 1,800 participants (aged 72.5 ± 4.1 years, 59.4% women) from the 3C-Dijon Study, a population-based, prospective cohort study, who had undergone quantitative brain MRI and carotid ultrasound. We used multivariable logistic and linear regression adjusted for age, sex, and vascular risk factors. RESULTS: Presence of carotid plaque and increasing carotid lumen diameter (but not common carotid artery intima-media thickness) were associated with higher prevalence of lacunar infarcts: odds ratio (OR) = 1.60 (95% confidence interval [CI]: 1.09-2.35), p = 0.02 and OR = 1.24 (95% CI: 1.02-1.50), p = 0.03 (by SD increase). Carotid plaque was also associated with large white matter hyperintensity volume (WMHV) (age-specific top quartile of WMHV distribution): OR = 1.32 (95% CI: 1.04-1.67), p = 0.02, independently of vascular risk factors. Increasing Young elastic modulus and higher circumferential wall stress, reflecting augmented carotid stiffness, were associated with increasing WMHV (effect estimate [β]± standard error: 0.0003 ± 0.0001, p = 0.024; β ± standard error: 0.005 ± 0.002, p = 0.008). Large WMHV was also associated with increasing Young elastic modulus (OR = 1.22 [95% CI: 1.04-1.42], p = 0.01) and with decreasing distensibility coefficient (OR = 0.83 [95% CI: 0.69-0.99], p = 0.04), independently of vascular risk factors. Associations of carotid lumen diameter with lacunar infarcts and of carotid stiffness markers with WMHV were independent of carotid plaque. CONCLUSIONS: In addition to and independently of carotid plaque, increasing carotid lumen diameter and markers of carotid stiffness were associated with increasing prevalence of lacunar infarcts and increasing WMHV, respectively.

Assessment of cerebral small vessel disease predicts individual stroke risk

A question for your doctor to answer, I wouldn't presume to get between you and your doctor or therapists. They are the ones with the years of medical education. Assessing risk is pretty much fucking useless, DO THE DAMN RESEARCH THAT PREVENTS STROKE!
Assessment of cerebral small vessel disease predicts individual stroke risk

BACKGROUND 

 Despite several known risk factors it is still difficult to foresee who will develop a stroke and who will not. Vascular brain damage, visualised with MRI, reflects how the brain tolerates the effects of vascular risk factors and may therefore be relevant in predicting individual stroke risk. 

OBJECTIVE 

To examine whether the presence of small vessel disease on brain MRI could improve the prediction of stroke beyond the classic stroke risk factors from the 1991 Framingham Stroke Risk Function. METHODS

 1007 community-dwelling elderly people, free of stroke at baseline were included in the study. Small vessel disease--that is, the presence of silent brain infarcts (SBI) and white matter lesions (WML), was scored on MRI scans obtained in 1995-6. 10-Year stroke risk prediction was assessed by the C statistic and by reclassification adding SBI and WML to a risk model including the classic stroke risk factors. 

RESULTS

 During 10-years of follow-up 99 strokes occurred. Individual stroke risk prediction significantly improved from 0.73 (95% CI 0.67 to 0.78) to 0.75 (0.69 to 0.80) in men and from 0.69 (0.64 to 0.75) to 0.77 (0.71 to 0.82) in women after inclusion of SBI and periventricular WML to the stroke risk factors. Reclassification occurred mainly in the intermediate stroke risk group (men 26%; women 61% reclassified).
 

CONCLUSIONS
 

Assessment of small vessel disease with MRI beyond the classic stroke risk factors improved the prediction of subsequent stroke, especially in women with an intermediate stroke risk. These findings support the use of MRI as a possible tool for better identifying people at high risk of stroke.