Neuropeptide deficits in schizophrenia vs. Alzheimer's disease cerebral cortex

Steven M. Gabriel*, Michael Davidson, Vahram Haroutunian, Peter Powchik, Linda M. Bierer, Dushyant P. Purohit, Daniel P. Perl, Kenneth L. Davis

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Neuropeptide concentrations were determined in the postmortem cerebral cortex from 19 cognitive-impaired schizophrenics, 4 normal elderly subjects, 4 multi-infarct dementia (MID) cases, and 13 Alzheimer's disease (AD) patients. Only AD patients met criteria for AD. The normal elderly and MID cases were combined into one control group. Somatostatin concentrations were reduced in both schizophrenia and AD. Neuropeptide Y concentrations were reduced only in schizophrenia, and corticotropin-releasing hormone concentrations were primarily reduced in AD. Concentrations of vasoactive intestinal polypeptide and cholecystokinin also were reduced in schizophrenia, although not as profoundly as somatostatin or neuropeptide Y. In AD, cholecystokinin and vasoactive intestinal peptide were unchanged. Neuropeptide deficits in schizophrenics were more pronounced in the temporal and frontal lobes than in the occipital lobe. The mechanisms underlying these deficits in schizophrenia and AD are likely distinct. In schizophrenia, a common neural element, perhaps the cerebral cortical gaba-aminobutyric acid (GABA)-containing neuron, may underlie these deficits.

Original languageEnglish
Pages (from-to)82-91
Number of pages10
JournalBiological Psychiatry
Issue number2
StatePublished - 15 Jan 1996


FundersFunder number
National Institute on AgingP01AG002219


    • Alzheimer's disease
    • Cholecystokinin
    • Corticotropin-releasing hormone
    • Gamma aminobutyric acid
    • Neuropeptide Y
    • Schizophrenia
    • Somatostatin
    • Vasoactive intestinal polypeptide


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