Somatostatin replacement therapy for alzheimer dementia

M Maral Mouradian, Jerome Blin, Marianne Giuffra, Isabella J.E. Heuser, Fabio Baronti, John Ownby, Thomas N. Chase

Research output: Contribution to journalArticle

24 Scopus citations

Abstract

Somatostatin is consistently diminished in brains of patients with Alzheimer's disease. To evaluate whether pharmacological restoration of this transmitter deficit has therapeutic value, the synthetic analogue octreotide was administered intravenously to 14 Alzheimer patients under double‐blind, placebo‐controlled conditions. At the highest dose administered, spinal fluid concentrations approximated those found in brains of experimental animals receiving behaviorally effective amounts of the drug. Neuropsychological testing, however, showed no clinically significant improvement. Coadministration of octreotide and physostigmine to 1 patient also failed to improve cognition. Positron emission tomographic studies in 6 patients revealed a generalized decrease in glucose metabolism as a result of octreotide infusion. These findings suggest that stimulation of the somatostatin system has no value in the symptomatic treatment of Alzheimer dementia.

Original languageEnglish (US)
Pages (from-to)610-613
Number of pages4
JournalAnnals of Neurology
Volume30
Issue number4
DOIs
StatePublished - Jan 1 1991

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology

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    Mouradian, M. M., Blin, J., Giuffra, M., Heuser, I. J. E., Baronti, F., Ownby, J., & Chase, T. N. (1991). Somatostatin replacement therapy for alzheimer dementia. Annals of Neurology, 30(4), 610-613. https://doi.org/10.1002/ana.410300415