The key points of the hypothesis. The developing human brain (12-15 weeks' gestation) exhibit 30-35% of aneuploid cells [28], which are formed during neurogenesis (prenatal brain development). This process becomes exhausted soon after birth. At later developmental stage, adult neurogenesis starts, being, however, significantly less productive in terms of the amount of cells formed. Abnormal clearance of aneuploid cells leads to postnatal brain diseases, which are featured by GIN and CIN confined to the brain. Some of these diseases are associated with accelerated aging (i.e. Alzheimer's disease and ataxia-telangiectasia). Normal brain development leads to decrease of aneuploidy rates, which achieves averagely 10% [9,10,14]. The presence of aneuploid cells in the brain from the early prenatal development to the late ontogeny is hypothesized to give rise to GIN and CIN in the brain of elderly individuals. This is partially confirmed by analyzing controls in molecular neurocytogenetic studies of the diseased brain [5,7,12-14,16-20]. Mitotic errors during adult neurogenesis can also produce aneuploid cells throughout aging.