作者: Alexander P. Auchus , Robert C. Green , Charles B. Nemeroff
DOI: 10.1016/0197-4580(94)90102-3
关键词: Hippocampal formation 、 Nucleus basalis 、 Endocrinology 、 Cerebral cortex 、 Galanin 、 Neuropeptide 、 Neuroscience 、 Cortex (anatomy) 、 Central nervous system 、 Medicine 、 Internal medicine 、 Alzheimer's disease
摘要: Given the clinical features of AD, severe atrophy cerebral cortex that accompanies disease, and predominant cortical location plaques tangles, it is not surprising to find most consistent changes in neuropeptides this disease occurring cortex. The neuropeptide have been reproducibly demonstrated AD are reduced hippocampal neocortical SS CRF concentrations a CSF level SS. In cortex, found GABAergic local circuit neurons layers II, III, VI. function these well established, although cells may act integrate flow incoming outgoing information If true, then dysfunction integration could produce widespread failure cerebrocortical function, resulting various neurobehavioral deficits seen AD. interpretation subcortical brain regions, either those project or efferent targets projections, also uncertain. observed abnormalities regions less than Perhaps intriguing result increases galanin-immunoreactive terminals nucleus basalis brains. Galanin has shown inhibit acetylcholine release impair memory rats (46,113).(ABSTRACT TRUNCATED AT 250 WORDS)