Topic: vascular scars

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

Microglia cover the whole brain parenchyma, where each microglia cell occupies a fixed position and, through its projections, surveils its own territory (Kierdorf and Prinz, 2017). Genetic (Bruttger et al., 2015) or pharmacologic (Elmore et al., 2014) partial ablation of adult microglia is followed by a recovery of their number and coverage of the brain parenchyma, supporting a fundamental role of microglial spatial organization in local surveillance (Nimmerjahn et al., 2005). Neurological disorders, particularly Alzheimer’s Disease (AD), associate with dysfunctional microglia, which cluster a

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