Neuroplasticity and the progression of Alzheimer's disease.
A neurobiological hypothesis is proposed to explain the relation between the percentage cell loss in the cholinergic basal forebrain and the density of neuritic plaques in cortex, as found by Arendt et al. (1985) in Alzheimer's disease: When cells in the cholinergic basal forebrain die, their cortical synaptic target sites can be reoccupied by axonal sprouting of other neurons from the basal forebrain. This neuroplasticity hypothesis leads to equations that are consistent with the quantitative data of Arendt et al. (1985), and it makes specific predictions that can be tested experimentally. Moreover, this hypothesis suggests that the more rapid course of the presenile form of Alzheimer's disease and its more extensive pathology can be understood as a consequence of the decline in neuroplasticity with age.
D000375:Aging / Q000502:physiology; D000544:Alzheimer Disease / Q000473:pathology / Q000503:physiopathology*; D000818:Animals; D005544:Forecasting; D006801:Humans; D008959:Models, Neurological; D009473:Neuronal Plasticity