Loss of cortical GABA uptake sites in Alzheimer's disease

M.D. Simpson, A. J. Cross, P Slater, J F Deakin

Research output: Contribution to journalArticlepeer-review


[3H]Nipecotic acid bound to membranes of human brain in a saturable, reversible manner which was totally dependent on the presence of sodium ions. The potencies of compounds in inhibiting the specific binding of [3H]nipecotic acid were closely correlated with their potencies in inhibiting the neuronal uptake of [3H]GABA. Compounds selective for GABA receptors were inactive. [3H]Nipecotic acid appears to label neuronal high affinity GABA uptake sites. The binding of [3H]nipecotic acid was substantially reduced in the temporal cortex of brains from subjects with Alzheimer-type dementia, but not in other brain regions. It is concluded that some loss of GABA terminals occurs in this disease.

Original languageEnglish
Pages (from-to)219-226
Number of pages8
JournalJournal of Neural transmission
Issue number3
Publication statusPublished - Oct 1988


  • Aged
  • Aged, 80 and over
  • Alzheimer Disease
  • Binding, Competitive
  • Cerebral Cortex
  • Humans
  • Nipecotic Acids
  • Proline
  • Receptors, GABA-A
  • gamma-Aminobutyric Acid
  • Journal Article
  • Research Support, Non-U.S. Gov't


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