Reduced Numbers of Somatostatin Receptors in the Cerebral Cortex in Alzheimer's Disease

• Published in: Science (American Association for the Advancement of Science) 1985-07, Vol.229 (4710), p.289-291
• Main Authors: Beal, M. Flint, Mazurek, Michael F., Tran, Vinh T., Chattha, Geetinder, Bird, Edward D., Martin, Joseph B.
• Format: Article
• Language: English
• Subjects: Adult; Aged; Alzheimer Disease - metabolism; Alzheimer's disease; Alzheimers disease; Biological and medical sciences; Brain; Brain research; Cerebral cortex; Cerebral Cortex - analysis; Cholinergics; Chromatography, High Pressure Liquid; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Female; Frontal Lobe - analysis; Hippocampus; Humans; Male; Medical sciences; Middle Aged; Nervous system diseases; Neurology; Neurons; Neurons - metabolism; Neurons - physiology; Neuroscience; Radioimmunoassay; Receptors; Receptors, Cell Surface - analysis; Receptors, Somatostatin; Somatostatin - metabolism; Somatostatin - physiology; Somatostatin receptors; Temporal Lobe - analysis
• ISSN: 0036-8075; 1095-9203
• DOI: 10.1126/science.2861661

Somatostatin receptor concentrations were measured in patients with Alzheimer's disease and controls. In the frontal cortex (Brodmann areas 6, 9, and 10) and temporal cortex (Brodmann area 21), the concentrations of somatostatin in receptors in the patients were reduced to approximately 50 percent of control values. A 40 percent reduction was seen in the hippocampus, while no significant changes were found in the cingulate cortex, postcentral gyrus, temporal pole, and superior temporal gyrus. Scatchard analysis showed a reduction in receptor number rather than a change in affinity. Somatostatin-like immunoreactivity was significantly reduced in both the frontal and temporal cortex. Somatostatin-like immunoreactivity was linearly related to somatostatin-receptor binding in the cortices of Alzheimer's patients. These findings may reflect degeneration of postsynaptic neurons or cortical afferents in the patients' cerebral cortices. Alternatively, decreased somatostatinlike immunoreactivity in Alzheimer's disease might indicate increased release of somatostatin and down regulation of postsynaptic receptors.