Topic: extracellular ATP

Alzheimer's Disease (AD) is the primary cause of dementia, characterized by irreversible neurodegeneration resulting in memory loss and cognitive decline. Growing evidence suggests that neuroinflammation plays a pivotal role in AD, with extracellular ATP (eATP) as one of the key players in this process. Our project aims at investigating whether eATP influences microglia activation, AD-associated neuroinflammation and neuronal Ca2+ excitability in an AD mouse model (B6.152H) expressing human PS2-N141I and APP Swedish mutations. We conducted experiments at various disease stages: pre- and post-A

Acute brain slices represent a “workhorse” model for studying the central nervous system (CNS) from nanoscale events to complex circuits. While slice preparation inherently involves tissue damage, it is unclear how microglia, the main immune cells and damage sensors of the CNS react to this injury and shape neuronal activity ex vivo. To this end, we investigated microglial phenotypes and contribution to network organisation and functioning in acute brain slices. The comprehensive assesment of microglial states in acute brain slices demonstrated time-dependent microglial phenotype changes that