Lipids modulates Tau and amyloid-β proteins in Alzheimer's disease.

Alzheimer's disease (AD) is a multifaceted neurodegenerative condition, marked by memory loss and a steady deterioration in cognitive function. Lipid metabolism, which encompasses different lipid types such sphingolipids, cholesterol, fat-soluble vitamins, and fatty acids, is one of the key components of AD pathogenesis. These lipids are essential for many cellular functions, and the onset and course of AD are greatly influenced by their dysregulation. Sphingolipids, which include gangliosides, sulfatides, ceramides, and sphingomyelins, are essential for signal transduction, myelin sheath development, and the integrity of cell membranes. Sphingolipid metabolism is altered in AD, as seen by changes in ceramide levels and a reduction in sulfatides. These changes are associated with inflammation and neuronal death. Additionally, sphingomyelins and gangliosides are implicated; specific alterations in their concentrations have been reported in brains affected by AD, suggesting their participation in amyloid-β (Aβ) pathology and neurodegeneration.