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Galanin immunoreactivity is increased in the nucleus basalis of meynert in Alzheimer's disease
Author(s) -
Beal M. Flint,
MacGarvey Usha,
Swartz Kenton J.
Publication year - 1990
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410280207
Subject(s) - nucleus basalis , galanin , medicine , endocrinology , neuropeptide , cholinergic , neurotransmitter , acetylcholine , neurochemical , choline acetyltransferase , somatostatin , cholinergic neuron , neuroscience , biology , chemistry , central nervous system , receptor
A depletion of large cholinergic neurons in the nucleus basalis of Meynert is a consistent finding in Alzheimer's disease (AD). The nucleus basalis of Meynert also contains interneurons and afferents that may modulate its functioning. In the present study we examined neurochemical markers for neuropeptides, amino acid neurotransmitters, and monoaminergic neurotransmitters in postmortem samples of the nucleus basalis in 16 control subjects and 30 patients with AD. There were no significant changes in glutamate, aspartate, taurine, gamma‐aminobutyric acid (GABA), and catecholamines; however, concentrations of serotonin, 5‐hydroxyindoleacetic acid, and 5‐hydroxytryptophol were significantly reduced. Choline acetyltransferase activity was significantly reduced, consistent with previous reports. Galanin immunoreactivity was significantly increased twofold in the patients with AD, but there were no significant changes in substance P, somatostatin, or neuropeptide Y immunoreactivity. Since galanin inhibits acetylcholine release, and produces cognitive deficits in animals, increased galanin immunoreactivity in the nucleus basalis of Meynert in AD may contribute to the cognitive deficits that characterize the illness.