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NEUROLOGY 1987;37:161
© 1987 American Academy of Neurology

Alzheimer's disease

Low cerebral somatostatin levels correlate with impaired cognitive function and cortical metabolism

C. A. Tamminga, N. L. Foster, P. Fedio, E. D. Bird and T. N. Chase

Experimental Therapeutics Branch (Drs. Tamminga. Foster, Fedio, and Chase), National Institute of Neurological and Communicative Disorders and Stroke, Bethesda, MD; the Maryland Psychiatric Research Center, Department of Psychiatry (Dr. Tamminga), University of Maryland, Baltimore, MD; and the Ralph Lowell Laboratory (Dr. Bird), McLean Hospital, Harvard Medical School, Belmont, MA.

Somatostatin-like immunoreactivity in Alzheimer CSF was significantly lower than in that from age-matched controls. The degree of reduction correlated with indices of intellectual impairment and decline in cortical glucose utilization as determined by PET. There was a close association between reduction in CSF somatostatin and glucose hypometabolism in the parietal lobe. In postmortem cortical tissue from Alzheimer patients, somatostatin levels were lower in posterior parietal but not in anterior frontal cortex. Loss of somatostatin-containing neurons, especially in the parietal association cortex, may be a critical determinant for Alzheimer dementia.

Address correspondence and reprint requests to Dr. Tamminga, Room 5C215, NINCDS, Bethesda, MD 20892.

The Brain Tissue Resource Center is supported by PHS grant NM/NS 31862.

Received December 23, 1985. Accepted for publication April 24, 1986.






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