Topic: non-productive angiogenesis

In previous studies, we identified low-perfused vascular abnormalities, termed “vascular scars”, surrounding A-beta plaques in Alzheimer's disease mouse models. We hypothesized that these vascular scars result from non-productive angiogenesis, a process in which total or partial reduction of the DLL4/NOTCH pathway leads to erratic angiogenesis and disassembly of vessels into non-conducting structures1. In this study, our objective was to investigate whether restoring the NOTCH pathway in brain endothelial cells could enhance vessel stability around A-beta plaques. To this aim, we injected the

Dementia is a term for several diseases that affect memory, thinking, and daily activity performance. The most prevalent form of dementia is Alzheimer’s disease (AD), which explains 60-70% of dementia cases (World Health Organization [WHO], 2023). AD is a neurodegenerative disorder characterized by brain atrophy, gliosis, Abeta and tau proteinopathies, and vascular dysfunction. Previously, our group has described that a non-productive angiogenesis (NPA) phenomenon occurs around Abeta plaques, giving rise to disassembled, low-perfused vascular structures, which we have called vascular scars (Va