Neighborhood disadvantage, systemic inflammation, and tau pathology: a link between social determinants of health and Alzheimer's disease risk

These preliminary findings suggest that neighborhood disadvantage may contribute to AD risk through systemic inflammation and vascular dysfunction, leading to increased tau pathology. However, the observed racial differences in p-tau217, with Black participants showing lower levels despite higher ADI scores and AD risk, align with prior studies. This raises questions about differences in tau processing, clearance, or non-tau pathways of neurodegeneration. Future research should examine whether inflammation-driven vascular dysfunction contributes disproportionately to cognitive decline in Black populations. Longitudinal studies are needed to assess whether interventions targeting inflammation and vascular health could mitigate AD risk and whether tau biomarkers accurately capture AD pathology across diverse populations. Understanding these mechanisms is crucial for ensuring equity in AD diagnosis and treatment.

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Publication Details

Journal
Alzheimer s & Dementia
Published
2025-12-01
DOI
https://doi.org/10.1002/alz70856_105926
Primary Topic
Dementia and Cognitive Impairment Research
Type
article
Field-Weighted Citation Impact
0.00
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article

Neighborhood disadvantage, systemic inflammation, and tau pathology: a link between social determinants of health and Alzheimer's disease risk

Danielle D. Verble, Brittany Butts, Kelly D. S. Likos, Jordan Watson et al.
Alzheimer s & Dementia
Dementia and Cognitive Impairment Research
article

Neighborhood disadvantage, systemic inflammation, and tau pathology: a link between social determinants of health and Alzheimer's disease risk

Danielle D. Verble, Brittany Butts, Kelly D. S. Likos, Jordan Watson, Christopher Herring, Enid Swatson, Arin Watson, Sofie Ragins, Julia Kamara, Whitney Wharton, Chloe Park
article en

Abstract

These preliminary findings suggest that neighborhood disadvantage may contribute to AD risk through systemic inflammation and vascular dysfunction, leading to increased tau pathology. However, the observed racial differences in p-tau217, with Black participants showing lower levels despite higher ADI scores and AD risk, align with prior studies. This raises questions about differences in tau processing, clearance, or non-tau pathways of neurodegeneration. Future research should examine whether inflammation-driven vascular dysfunction contributes disproportionately to cognitive decline in Black populations. Longitudinal studies are needed to assess whether interventions targeting inflammation and vascular health could mitigate AD risk and whether tau biomarkers accurately capture AD pathology across diverse populations. Understanding these mechanisms is crucial for ensuring equity in AD diagnosis and treatment.

Alzheimer s & DementiaVol. 21(S2)
Emory University (US)
Openalex Percentile: Top 28%
Dementia and Cognitive Impairment Research
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