Cell cycle activation and aneuploid neurons in Alzheimer's disease.

摘要: Alzheimer's disease (AD) is a chronic neurodegenerative disorder, characterized by synaptic degeneration associated with fibrillar aggregates of the amyloid-s peptide and microtubule-associated protein tau. The progression neurofibrillary throughout brain during AD follows predictive pattern which provides basis for neuropathological staging disease. This selective neuronal vulnerability against matches regional degree plasticity inversely recapitulates ontogenetic phylogenetic development links cell death to neuroplasticity development. Here, we summarize recent evidence loss differentiation control as critical pathogenetic event in AD, reactivation cycle partial or full replication DNA giving rise neurons content above diploid level. Neurons an aneuploid set chromosomes are also present at low frequency normal where they appear be well tolerated. In however, number highly increased, rather this chromosomal aberrancy occurs. finding add aneuploidy list molecular events that shared between neurodegeneration oncogenesis. It defines signature directs our attention failure potential therapeutic target AD.