Microglial activation and tau propagate jointly across Braak stages

 

With the extra risk created by your stroke you need your  doctor and stroke hospital to initiate research that can prevent dementia.

Your risk of dementia, has your doctor told you of this?

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

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

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

4. Dementia Risk Doubled in Patients Following Stroke September 2018

The latest here:

Microglial activation and tau propagate jointly across Braak stages

• Tharick A. Pascoal,
• Andrea L. Benedet,
• Nicholas J. Ashton,
• Min Su Kang,
• Joseph Therriault,
• Mira Chamoun,
• Melissa Savard,
• Firoza Z. Lussier,
• Cécile Tissot,
• Thomas K. Karikari,
• Julie Ottoy,
• Sulantha Mathotaarachchi,
• Jenna Stevenson,
• Gassan Massarweh,
• Michael Schöll,
• Mony J. de Leon,
• Jean-Paul Soucy,
• Paul Edison,
• Kaj Blennow,
• Henrik Zetterberg,
• Serge Gauthier &
• Pedro Rosa-Neto 

Nature Medicine (2021)Cite this article

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Abstract

Compelling experimental evidence suggests that microglial activation is involved in the spread of tau tangles over the neocortex in Alzheimer’s disease (AD). We tested the hypothesis that the spatial propagation of microglial activation and tau accumulation colocalize in a Braak-like pattern in the living human brain. We studied 130 individuals across the aging and AD clinical spectrum with positron emission tomography brain imaging for microglial activation ([¹¹C]PBR28), amyloid-β (Aβ) ([¹⁸F]AZD4694) and tau ([¹⁸F]MK-6240) pathologies. We further assessed microglial triggering receptor expressed on myeloid cells 2 (TREM2) cerebrospinal fluid (CSF) concentrations and brain gene expression patterns. We found that [¹¹C]PBR28 correlated with CSF soluble TREM2 and showed regional distribution resembling TREM2 gene expression. Network analysis revealed that microglial activation and tau correlated hierarchically with each other following Braak-like stages. Regression analysis revealed that the longitudinal tau propagation pathways depended on the baseline microglia network rather than the tau network circuits. The co-occurrence of Aβ, tau and microglia abnormalities was the strongest predictor of cognitive impairment in our study population. Our findings support a model where an interaction between Aβ and activated microglia sets the pace for tau spread across Braak stages.

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