Modulation of Amyloid‐beta Metabolism by TIMP2 and MMP2 Through Extracellular Matrix Interactions in Mouse Models of Alzheimer's Pathology

TIMP2 deficiency exacerbates amyloid pathology by affecting MMP2-associated astrocyte modulation of ECM. Restoring TIMP2 improves cognitive and pathological outcomes, highlighting its therapeutic potential in AD. These findings suggest that TIMP2-targeted strategies may represent a novel approach for addressing amyloid accumulation and downstream effects in AD. Funded by: NHI/NIA 1RF1AG072300, R01AG061382, Alzheimer's Association 24AARF-1201458.

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Publication Details

Journal
Alzheimer s & Dementia
Published
2025-12-01
DOI
https://doi.org/10.1002/alz70855_101110
Primary Topic
Protease and Inhibitor Mechanisms
Type
article
Field-Weighted Citation Impact
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article

Modulation of Amyloid‐beta Metabolism by TIMP2 and MMP2 Through Extracellular Matrix Interactions in Mouse Models of Alzheimer's Pathology

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Protease and Inhibitor Mechanisms
article

Modulation of Amyloid‐beta Metabolism by TIMP2 and MMP2 Through Extracellular Matrix Interactions in Mouse Models of Alzheimer's Pathology

Ana Catarina Ferreira, Sarah M. Philippi, John F. Crary, Claudia De Sanctis, Joseph M. Castellano, Jacob L. Rosenstadt, Alejandro B. Grau‐Perales, Suhani Yerapathi, Brittany M. Hemmer
article en

Abstract

TIMP2 deficiency exacerbates amyloid pathology by affecting MMP2-associated astrocyte modulation of ECM. Restoring TIMP2 improves cognitive and pathological outcomes, highlighting its therapeutic potential in AD. These findings suggest that TIMP2-targeted strategies may represent a novel approach for addressing amyloid accumulation and downstream effects in AD. Funded by: NHI/NIA 1RF1AG072300, R01AG061382, Alzheimer's Association 24AARF-1201458.

Alzheimer s & DementiaVol. 21(S1)
Allen Institute for Brain Science (US), Icahn School of Medicine at Mount Sinai (US)
Openalex Percentile: Top 34%
Protease and Inhibitor Mechanisms
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