Topic: beta-amyloid peptide (Aβ)

One of the primary pathological factors implicated in Alzheimer's disease (AD) is the beta-amyloid peptide (Aβ), known for its various toxic effects including decreased cytosolic ATP levels and elevated intracellular calcium. Our laboratory's research has revealed that Aβ treatments induce alterations in mitochondrial morphology and dynamics in animal models of AD, leading to increased ROS generation and potential leakage of mitochondrial elements like mitochondrial DNA (mtDNA) into the cytoplasm. MtDNA can activate the inflammatory response via cyclic GMP-AMP synthase (cGAS), triggering proin