Beta Amyloid, Tau Protein, and Neuroinflammation: An Attempt to Integrate Different Hypotheses of Alzheimer’s Disease Pathogenesis

Abstract Alzheimer’s disease (AD) is a neurodegenerative that inevitably results in dementia and death. Currently, there are no pathogenetically grounded methods for the prevention treatment of AD, all current regimens symptomatic unable to significantly delay development dementia. The accumulation β-amyloid peptide (Aβ), which spontaneous, aggregation-prone, neurotoxic product processing signaling protein APP (Amyloid Precursor Protein), brain tissues, primarily hippocampus frontal cortex, was long time considered main cause changes AD. However, attempts treat AD based on decreasing Aβ production aggregation did not bring significant clinical results. More more arguments arising favor fact overproduction most cases initial cause, but concomitant event pathological processes course sporadic concept neuroinflammation has come fore, suggesting inflammatory responses play leading role initiation both tissue periphery. hypothesis about key pathogenesis opens up new opportunities search ways prevent this socially disease.