Bart De Strooper
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As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.Articles
Human microglial transitions at the Aβ–tau inflection point associate with divergent pathways to dementia and resilience
Abstract Alzheimer’s disease (AD) is not an inevitable outcome of pathology but a dynamic process shaped by how brain cells respond to amyloid-β (Aβ) and tau. To disentangle these responses, we combined spatial transcriptomics and single-nucleus RNA sequencing of the superior frontal cortex from octogenarians living with or without dementia and from cognitively intact centenarians with comparable Aβ accumulation.
Aβ plaques induce local pre-synaptic toxicity in human iPSC-derived neuron xenografts
ArticleVolume 21, Issue 1102754Open access 1VIB KU Leuven Center for Brain & Disease Research, Leuven, Belgium 2KU Leuven, Department of Neurosciences, Leuven Brain Institute, 3000 Leuven, Belgium 3VIB BioImaging Core, 3000 Leuven, Belgium 4UK Dementia Research Institute, University College London, London, UK Publication History: Received May 16, 2025; Revised November 30, 2025; Accepted December 1, 2025; Published online January 2, 2026 DOI: 10.1016/j.stemcr.2025.102754 External LinkAlso...
The APOE isoforms differentially shape the transcriptomic and epigenomic landscapes of human microglia xenografted into a mouse model of Alzheimer’s disease | Nature Communications
Abstract Microglia play a key role in the response to amyloid beta in Alzheimer’s disease (AD). In this context, the major transcriptional response of microglia is the upregulation of APOE, the strongest late-onset AD risk gene. Of its three isoforms, APOE2 is thought to be protective, while APOE4 increases AD risk. We hypothesised that the isoforms change gene regulatory patterns that link back to biological function by shaping microglial transcriptomic and chromatin landscapes.
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