Morgan Barkley

Abstract Obesity including genetic obesity accelerates age-related cognitive decline and disrupts circadian regulation, increasing the risk of neurodegenerative disorders. These effects are mediated in part by metabolic dysregulation, neuroinflammation, and altered sleep–circadian cycles, yet the molecular and lifestyle factors that modify obesity-associated brain dysfunction remain poorly defined.

ABCA1 ATP-binding cassette transporter A1 ACC acetyl-CoA carboxylase AD Alzheimer's disease ApoE apolipoprotein E APP amyloid precursor protein Aβ amyloid-β BMP bis-phosphates Dgat2 diacylglycerol O-acyltransferase 2 Dgat2 KD diacylglycerol O-acyltransferase 2 knockdown FAS fatty acid synthase GWAS genome-wide association studies PSEN1 presenilin1 PSEN2 presenilin2 Srebp sterol regulatory element binding protein TREM2 triggering receptor expressed on myeloid cells 2 TRF time-restricted...

Abstract Alzheimers disease (AD) is a progressive neurodegenerative disorder marked by amyloid-beta; (ab-42) plaque accumulation, cognitive decline, lipid dysregulation, and neuroinflammation. While mutations in the Amyloid Precursor Protein (APP) and Ab-42 accumulation contribute to AD, the mechanisms linking Ab-42; to lipid metabolism and neuroinflammation remain unclear.