Brain evolution and Alzheimer's disease.
It is argued that rapid evolution of the hominid brain was accomplished by the molecular mechanisms of "regulatory evolution" and "gene duplication". These genomic processes may have made newly elaborated brain regions--including the association neocortices and parts of the hippocampal formation, nucleus basalis of Meynert and amygdaloid body--vulnerable to Alzheimer's disease, by increasing the value of a disease-specific genomic character function. Trisomy 21, it is proposed, further increases this value.
D000544:Alzheimer Disease / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D005075:Biological Evolution; D001921:Brain / Q000378:metabolism / Q000503:physiopathology; D003704:Dementia / Q000473:pathology / Q000503:physiopathology; D004314:Down Syndrome / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D005786:Gene Expression Regulation; D006801:Humans; D008954:Models, Biological; D005810:Multigene Family; D018377:Neurotransmitter Agents / Q000378:metabolism
D018377:Neurotransmitter Agents