Abstract
Alzheimer’s disease pathology is a multifactorial, long-lasting, irreversible process within the CNS resulting in neuronal death. This process starts years prior to the appearance of the first clinical symptoms, such as cognitive decline and loss of short-term memory. Pathological processes mainly include accumulation of neurotoxic amyloid-b in plaques and neurofibrillary tangles containing hyperphosphorylated tau protein. Disorders in endogenous lipid metabolism have been associated with the development and progress of Alzheimer’s disease pathology. Here, we present the recent advances in our understanding of the coherency between the proteinaceous initiators, amyloid-b and tau, and phospholipids, sphingolipids, cholesterol and oxysterols as representatives of membrane lipids within the CNS. Furthermore, new strategies for the overall interruption of these harmful interactions are discussed.