[An animal model of non-hereditary Alzheimer's disease and its behavioral and pathologic changes].
An animal model of non-hereditary AD was built by lesioning nucleus basalis of Meynert (nbM) and to investigate the behavioral alteration by Morris water maze, the pathological changes by special staining for senile plaques(SPs), enzymatic cytochemical staining for AChE, and immunocytochemical staining for beta amyloid protein (beta AP) and tau protein. Transmission electron microscopic observation has also been made. Results showed: (1) loss of learning and memory ability; (2) occurrence of necrotic granules in cytoplasm and inclusion in axon hillock; accumulation of necrotic cell, and formation of SPs under light microscope; (3) accumulation of microtubules and formation of inclusion, increase of lysosome and edema and vacuolation of neurons and neuroterminals under electron microscopy; (4) decrease of synaptic density; (5) sharp decrease of AChE (acetylcholinesterase) positive fibers and neurons shown by immunocytochemical staining; (6) overexpression of beta AP and tau protein.
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Laboratory of Neurobiology Shanxi Medical University, Taiyuan.
D000110:Acetylcholinesterase / Q000378:metabolism; D000544:Alzheimer Disease / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D020532:Basal Nucleus of Meynert / Q000473:pathology; D004195:Disease Models, Animal; D007608:Kainic Acid; D017397:Prefrontal Cortex / Q000378:metabolism / Q000473:pathology; D051381:Rats
D016229:Amyloid beta-Peptides; D000110:Acetylcholinesterase; D007608:Kainic Acid