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Research Article| Volume 78, ISSUE 1, P1-16, March 1987

Somatostatin content and release measured in cerebral biopsies from demented patients

DOI:https://doi.org/10.1016/0022-510X(87)90073-6
Somatostatin content and release measured in cerebral biopsies from demented patients
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      Abstract

      Somatostatin-like immunoreactivity (SLIR) has been assayed in frontal and temporal cortex obtained at diagnostic craniotomy and post-mortem from patients with histologically verified Alzheimer's disease. SLIR content was not significantly different from controls in the frontal and temporal lobes, except in the temporal cortex post-mortem. The K+ -stimulated release of endogenous SLIR from tissue prisms (‘mini-slices’) prepared from neocortex obtained at diagnostic craniotomy from Alzheimer patients was not below the control values. Indices of cholinergic varicosities in similar samples from the frontal and temporal lobes are reduced; accordingly, somatostatin does not seem to be as prominently involved in these regions. Patients with Alzheimer's disease underwent neuropsychological assessment shortly before sampling the temporal lobe. Scores for WAIS full scale and the verbal subscale and the Token Test (measure of language comprehension) significantly correlated with the SLIR content; mean values (fmole/mg protein) were 817, 1468 and 1363 for aphasic and non-aphasic Alzheimer patients and controls, respectively. Ventricular fluid obtained from Alzheimer patients during surgery, did not have a significantly different SLIR content compared to controls. SLIR contents of ventricular fluid and neocortex from demented patients, without any specific histological changes in the sample obtained at diagnostic craniotomy, were also not significantly different from controls. Previously, we have shown that these demented patients, as well as those with histologically verified Alzheimer's disease, have a reduced SLIR content of lumbar fluid so it seems that somatostatin neurones located outside the frontal and temporal lobes are affected relatively early in the disease process.

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      Article info

      Publication history

      Accepted: September 1, 1986
      Received in revised form: September 1, 1986
      Received: June 28, 1986

      Footnotes

      ☆This was supported by the Brain Research Trust, the Medical Research Council and the Miriam Marks Charitable Trust.

      Identification

      DOI: https://doi.org/10.1016/0022-510X(87)90073-6

      Copyright

      © 1987 Published by Elsevier Inc.

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