Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Monday, May 4, 2026

Midlife Vitamin D Levels Linked to Later Tau-PET Deposition

 I just exited midlife at age 70, so my stuff is already baked in. But then I have way more than 16 years to go, so maybe still time.

Midlife Vitamin D Levels Linked to Later Tau-PET Deposition


 Higher circulating vitamin D levels in early midlife are associated with lower tau deposition on brain positron emission tomography (PET) imaging in later midlife among adults without dementia, according to a study published in Neurology Open Access. In a prospective cohort study of adults without dementia from the Framingham Heart Study Generation 3 cohort, researchers evaluated whether serum 25-hydroxyvitamin D measured in early midlife is associated with later tau and amyloid burden on brain PET imaging.Serum 25-hydroxyvitamin D levels were assessed at examination cycle 1 between 2002 and 2005. Participants subsequently underwent amyloid PET and/or tau PET imaging between 2016 and 2019. [H]igher vitamin D levels in midlife may offer protection against pathologic tau deposition in the brain, while low vitamin D may represent a potentially modifiable risk factor for healthy middle-aged individuals seeking to reduce dementia risk. A total of 793 participants were included, of whom 53% were women, and the mean [SD] age was 39 [8] years. Of the participants, 424 underwent amyloid PET imaging, and 369 underwent tau PET. The mean (SD) interval between vitamin D measurement and PET imaging was 16.2 (2.4) years. Outcomes included global and composite tau-PET burden and amyloid-PET burden. In fully adjusted models, higher serum 25-hydroxyvitamin D levels were associated with lower global tau-PET burden (β=−0.022; 95% CI, −0.040 to −0.004;P=.010) and lower composite tau-PET burden (β=−0.023; 95% CI, −0.043 to −0.003;P=.016). In contrast, serum 25-hydroxyvitamin D levels were not associated with amyloid-PET burden (β=0.001; 95% CI, −0.024 to 0.024;P=.987). When analyzed using a clinical cutoff (<30 vs ≥30 ng/mL), serum 25-hydroxyvitamin D levels were not significantly associated with tau or amyloid PET outcomes in fully adjusted models. Baseline mean (SD) serum 25-hydroxyvitamin D level was 38 (15) ng/mL, with 34% of participants below 30 ng/mL. Sensitivity analyses excluding individuals taking vitamin D supplements yielded similar findings, with persistent associations between higher serum 25-hydroxyvitamin D and lower tau burden. Study limitations include a lack of repeated vitamin D measurements over time, and the long interval between vitamin D assessment and PET imaging, which may introduce exposure misclassification. This study suggests that higher vitamin D levels in midlife may offer protection against pathologic tau deposition in the brain, while low vitamin D may represent a potentially modifiable risk factor for healthy middle-aged individuals seeking to reduce dementia risk,” concluded the authors.

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