Senile Dementia of the Alzheimer type is accompanied by a loss of cholinergic neurons, a hypertrophy of galanin-immunoreactive axonal plexuses ending on the remaining cholinergic neurons, and a doubling of the amount of galanin peptide detectable by radioimmunoassay in the nucleus basalis of Meynert. This is accompanied by the preservation of receptors labeled by 125I-galanin over rest islands of Meynert neurons detected by quantitative autoradiography. The present study shows that there is tissue-specific expression of the galanin gene demonstrated by in situ hybridization using an oligonucleotide probe complementary to porcine galanin mRNA in the Alzheimer nucleus of Meynert. These combined studies indicate a significant plastic response of galanin in the Alzheimer brain as compared to age-matched controls which may be important in the progress of the disease as well as in the development of pharmacological therapies for the disease.

Keywords:
Basal forebrain, Acetylcholine, Degeneration, Hyperinnervation, Hybridization, in situ
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© 1990 S. Karger AG, Basel
1991
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