Topic: Aβ accumulation

Aims: α-synuclein is a protein that is highly expressed in brain neurons. Its normal function is still unknown, but it is thought to be crucial to the onset of dementia with Lewy bodies (DLB). As of now, DLB cannot be sufficiently explained by mutations in the α-synuclein protein because there are so few α-synuclein mutations found in DLB. Nevertheless, several studies have revealed that individuals with DLB also co-exhibit Aβ accumulation in the brain, suggesting that Aβ could be involved in α-synuclein neurotoxicity. However, the exact molecular mechanism behind Aβ-induced α-synuclein toxici

Aging is the main risk factor for Alzheimer’s disease (AD), a prevalent and devastating neurodegenerative pathology with no effective cure. Research efforts aimed at understanding the link between pathological aging (senescence) and AD are crucial for developing pharmacological therapeutic strategies. Mitochondrial dysfunction and mitophagy defects are observed during senescence and AD, and studies suggest that they might lead to Aβ accumulation. Our goal in this project was to explore if a reduced removal of dysfunctional mitochondria during aging is a key contributor to amyloid pathology and