[The biochemistry of cerebral aging in man and in experimental models (author's transl)].
The biochemistry of cerebral aging in man is very little known. Two theories form the basis of current studies: the purely genetic theory and the catastrophic error theory (which explains senescence by a series of errors affecting protein synthesis). Whatever the mechanisms envisaged, they result in abnormalities in the biochemical structures of membranes and of cellular metabolism. However, senescence is not a chance phenomenon and certain regions, certain circuits, certain cells and certain metabolisms are more resistant than others. Cholinergic and catecholaminergic pathways are affected more than GABAergic and serotoninergic pathways. The substratum of the morphological lesions seen during senescence is poorly understood. Neurofilaments arranged in spirals characteristic of neurofibrillary degeneration have been isolated and partially analysed. There is no animal model which reproduces all the morphological changes seen in man. However, certain biochemical, structural and metabolic changes are sufficiently well reproduced in rodents in which changes in catecholamine would also seem to exist.
D000109:Acetylcholine / Q000378:metabolism; D000375:Aging; D000682:Amyloid / Q000032:analysis; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002395:Catecholamines / Q000378:metabolism; D004247:DNA / Q000032:analysis; D003704:Dementia / Q000378:metabolism; D004285:Dogs; D004734:Energy Metabolism; D006801:Humans; D008055:Lipids / Q000032:analysis; D009419:Nerve Tissue Proteins / Q000032:analysis; D009454:Neurofibrils; D018377:Neurotransmitter Agents / Q000378:metabolism; D012313:RNA / Q000032:analysis; D011817:Rabbits; D012377:Rodentia
D000682:Amyloid; D002395:Catecholamines; D008055:Lipids; D009419:Nerve Tissue Proteins; D018377:Neurotransmitter Agents; D012313:RNA; D004247:DNA; D000109:Acetylcholine
Biochimie du vieillissement cérébral chez l'homme et dans les modèles expérimentaux.