Regulation of lipid dysmetabolism and neuroinflammation linked with Alzheimer's disease through modulation of Dgat2.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β (Aβ) plaque accumulation, cognitive decline, lipid dysregulation, and neuroinflammation. Mutations in the Amyloid Precursor Protein (APP), and accumulation of A contribute to AD, however, underlying mechanisms linking beta amyloid to lipid metabolism and neuroinflammation remain unclear. Using models, we demonstrate that and lead to progressive locomotor impairments, disrupted sleep activity, memory deficits, lipid dysregulation, loss of synaptic integrity, and neuroinflammation.