Hippocampal and Parahippocampal Somatostatin 28 and Neuropeptide Y Containing Neurons in Alzheimer's Disease (Part 2 of 2)

Abstract

The somatostatinergic innervation, and by comparison that of neuropeptide Y, was examined by immunocytochemistry, in the hippocampal formation of 6 patients with clinically and neuropathologically confirmed diagnosis of Alzheimer's disease (AD) and 4 matched controls. The quantitative assessment of the somatostatin and neuropeptide Y immunoreactive cell perikarya was conducted on regularly spaced sections covering the span of the whole hippocampus and parahippocampal cortex. The estimated total number of somatostatin or neuropeptide Y containing neurons was similar in the hippocampal formation of patients with AD and controls. By contrast, the density of the somatostatinergic fibers and terminals as estimated by the optical density of the somatostatin neuropil, significantly decreased by 30-45% in all the hippocampal subregions and the parahippocampal cortex, whereas the density of the neuropeptide Y immunoreactive neuropil significantly decreased (45%) only in the parahippocampal cortex. Numerous enlarged fibers containing somatostatin or neuropeptide Y, some of which were observed within senile plaques, were detected in the brain of patients with AD. These data suggest that in AD, somatostatin and neuropeptide Y containing cell bodies in the hippocampus and parahippocampal gyrus are anatomically preserved, in spite of an altered terminal field.

Neuropathobiology of Senile Dementia and Mechanism of Action of Nootropic Drugs

“…Most consistent changes have been reported in corticotrophin releasing factor (DeSouza et al 1986;Whitehouse et al 1987), and somatostatin (somatotropin release-inhibiting factor, SRIF) [reviewed by Bissette & Myers 1992;Cervera-Pierot et al 1992). …”

Neurochemical Differences in the CSF between Binswanger's and Alzheimer's Disease

“…Pathological changes in the white matter could interfere with the connections among somatostatinergic cortical intemeurons affecting somatostatinergic fibers. Another possible explanation is that direct damage to the white matter of the hippocampal cortex, one of the major foci of somatostatinergic activity, leads to decreased levels of SLI [50][51][52][53], Some SDAT studies reported a specific cell loss of somatostatin-immunoreactive perikarya and axons whereas in others somatostatin-immunoreactive peri karya number was preserved and only the density of somatostatin-immunoreactive fibers was altered. These discrepancies suggest that modifications of somatostatin CSF o f SLI, HVA and 5-HIAA in Binswanger's and A lzheim er's Disease levels might result from altered mechanisms occurring at the transcriptional and/or posttranscriptional level [52].…”

Characterization and distribution of Hxt1, a Na + /Cl − ‐dependent orphan transporter, in the human brain

“…Immunohistochemical staining of mounted sections (12 µm) was carried out with purified anti-Rxt1 antibodies (1:1,000 dilution; overnight incubation at room temperature) as already described (Cervera-Pierrot et al, 1992).…”