Microglial reactivity attenuates ptau <sub>231</sub> ‐related amyloid accumulation in preclinical Alzheimer’s disease

These findings suggest that soluble tau phosphorylation at early disease stages may enhance TREM2-mediated microglial reactivity, which may in turn be a protective mechanism against Aβ aggregation. This may suggest that elevated p-tau<sub>231</sub> in the preclinical phase may initiate a microglial response that slows fibrillar Aβ accumulation (e.g., via phagocytosis). This may later transition to detrimental inflammation as the disease progresses. Enhancing microglial function in preclinical AD might therefore be a promising therapeutic strategy to delay or prevent Aβ buildup.

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Publication Details

Journal
Alzheimer s & Dementia
Published
2025-12-01
DOI
https://doi.org/10.1002/alz70862_110128
Primary Topic
Neuroinflammation and Neurodegeneration Mechanisms
Type
article
Field-Weighted Citation Impact
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article

Microglial reactivity attenuates ptau 231 ‐related amyloid accumulation in preclinical Alzheimer’s disease

Henrik Zetterberg, Wiesje Pelkmans, Armand González Escalante, Gemma Salvadó et al.
Alzheimer s & Dementia
Neuroinflammation and Neurodegeneration Mechanisms
article

Microglial reactivity attenuates ptau 231 ‐related amyloid accumulation in preclinical Alzheimer’s disease

Henrik Zetterberg, Wiesje Pelkmans, Armand González Escalante, Gemma Salvadó, Juan Domingo Gispert, Gwendlyn Kollmorgen, Kaj Blennow, Clara Quijano‐Rubio, Marc Suárez‐Calvet, Mahnaz Shekari
article en

Abstract

These findings suggest that soluble tau phosphorylation at early disease stages may enhance TREM2-mediated microglial reactivity, which may in turn be a protective mechanism against Aβ aggregation. This may suggest that elevated p-tau<sub>231</sub> in the preclinical phase may initiate a microglial response that slows fibrillar Aβ accumulation (e.g., via phagocytosis). This may later transition to detrimental inflammation as the disease progresses. Enhancing microglial function in preclinical AD might therefore be a promising therapeutic strategy to delay or prevent Aβ buildup.

Alzheimer s & DementiaVol. 21(S8)
Roche (Switzerland) (CH), University of Science and Technology of China (CN), University of Wisconsin–Madison (US), Universitat Pompeu Fabra (ES), Lund University (SE), Sahlgrenska University Hospital (SE), Spanish National Centre for Cardiovascular Research (ES), Sorbonne Université (FR), Roche Pharma AG (Germany) (DE), Biomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine (ES), Pasqual Maragall Foundation (ES), Pitié-Salpêtrière Hospital (FR), Barcelonaβeta Brain Research Center (ES), Hospital Del Mar (ES), Centro de Investigación Biomédica en Red de Fragilidad y Envejecimiento Saludable (ES), Institut du Cerveau (FR), Hospital del Mar Research Institute (ES), University College London (GB), University of Gothenburg (SE)
Openalex Percentile: Top 39%
Neuroinflammation and Neurodegeneration Mechanisms
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