Beatriz Gomez Perez‐Nievas

This study shows that tau aggregates from Alzheimer's disease brains are taken up and processed by human astrocytes, with differences in handling linked to astrocyte responses and gene expression changes.

This study uses proteomics to analyze astrocyte secretome changes in response to soluble Aβ oligomers, identifying dysregulated proteins and potential biomarkers for Alzheimer's disease.

This study shows that astrocytic CXCL1 contributes to Aβ-induced tau mislocalization and synaptotoxicity via CXCR2, suggesting it as a therapeutic target in Alzheimer's disease.

The paper shows that reducing CYFIP2 in mice leads to Alzheimer's disease-like features, suggesting CYFIP2 as a therapeutic target.

This study shows that BIN1 loss in Alzheimer's disease leads to tau mislocalization and altered synaptic structure and tau release.