Insulin resistance and Cholesterol dyshomeostasis involve α-Synuclein and Amyloid beta interactions in Neurodegenerative diseases

Epidemiological studies indicate that diabetes Parkinson’s disease (PD) and Alzheimer’s disease (AD) are closely linked with dysregulated cholesterol pathways that involve molecular genetics, cell biology and insulin resistance in the pathogenesis of these diseases. In Parkinson’s disease the α-synculein protein is an amyloidogenic protein shown to bind to cholesterol. The binding of AD amyloid beta (A) has been associated with cholesterol in membranes with the regulation of liver A metabolism regulated by plasma cholesterol levels. The peripheral sink abeta hypothesis is closely associated with cholesterol regulation and possibly connected to the metabolism of A and α-synuclein protein in diabetes, AD, PD and Huntington’s disease. Interests in proteins and their interactions with membrane lipids in neurodegenerative diseases have accelerated with the existence A and α-synuclein pathologies in individuals with neurodegeneration. The role of molecular genetics with relevance to neurological diseases has gained major interest in anti-aging genes that determine circadian rhythm, insulin resistance and protein aggregation. Diets that activate these genes have become important to control cellular cholesterol, alpha synuclein and amyloid beta levels that may slow down the progression of PD. These genes may regulate immune responses that are connected to mitochondrial dysfunction in neurodegenerative diseases. Drug therapy in Parkinson’s disease has become of importance to clinical drug research with activation of genes essential to maintain cholesterol metabolism and the pharmacy of drugs.