Literature DB >> 3789664

Widespread reduction of somatostatin-like immunoreactivity in the cerebral cortex in Alzheimer's disease.

M F Beal, M F Mazurek, C N Svendsen, E D Bird, J B Martin.   

Abstract

Although several studies have documented reduced concentrations of somatostatin-like immunoreactivity (SLI) in the cerebral cortex in Alzheimer's disease, there is controversy concerning the extent and importance of these changes. We measured SLI in brains obtained post mortem from 12 patients with pathologically confirmed Alzheimer's disease and from 13 neurologically normal controls. All major cortical and subcortical regions were examined. Widespread reductions of SLI in Alzheimer's disease cerebral cortex were found, with the most profound changes seen in temporal lobe; but there also were major reductions in both the frontal and occipital cortex. There were no significant reductions in subcortical regions. Characterization of SLI by high-pressure liquid chromatography showed no significant difference in profiles between Alzheimer's disease and control frontal cortex. These results suggest that the reduction in somatostatin immunoreactivity in Alzheimer's disease may be caused by degeneration of intrinsic somatostatin cortical neurons.

Entities:  

Mesh:

Substances:

Year:  1986        PMID: 3789664     DOI: 10.1002/ana.410200408

Source DB:  PubMed          Journal:  Ann Neurol        ISSN: 0364-5134            Impact factor:   10.422


  10 in total

1.  NADPH-diaphorase-positive cell populations in the human amygdala and temporal cortex: neuroanatomy, peptidergic characteristics and aspects of aging and Alzheimer's disease.

Authors:  J W Unger; W Lange
Journal:  Acta Neuropathol       Date:  1992       Impact factor: 17.088

2.  Age-associated changes in hippocampal-dependent cognition in Diversity Outbred mice.

Authors:  Ming Teng Koh; Amy M Spiegel; Michela Gallagher
Journal:  Hippocampus       Date:  2014-06-11       Impact factor: 3.899

Review 3.  Molecular pharmacology of somatostatin receptors.

Authors:  D Hoyer; H Lübbert; C Bruns
Journal:  Naunyn Schmiedebergs Arch Pharmacol       Date:  1994-11       Impact factor: 3.000

Review 4.  Alterations of sleep oscillations in Alzheimer's disease: A potential role for GABAergic neurons in the cortex, hippocampus, and thalamus.

Authors:  Fumi Katsuki; Dmitry Gerashchenko; Ritchie E Brown
Journal:  Brain Res Bull       Date:  2022-07-15       Impact factor: 3.715

5.  Brain-wide reconstruction of inhibitory circuits after traumatic brain injury.

Authors:  Jan C Frankowski; Alexa Tierno; Shreya Pavani; Quincy Cao; David C Lyon; Robert F Hunt
Journal:  Nat Commun       Date:  2022-06-14       Impact factor: 17.694

6.  Reduced cerebral cortical but elevated striatal concentration of somatostatin-like immunoreactivity in dominantly inherited olivopontocerebellar atrophy.

Authors:  S J Kish; Y Robitaille; M el-Awar; L Schut; L DiStefano; M J Ball; M F Mazurek
Journal:  J Neurol Neurosurg Psychiatry       Date:  1993-09       Impact factor: 10.154

7.  Diffuse Lewy body disease. Neuropathological and biochemical studies of six patients.

Authors:  D W Dickson; P Davies; R Mayeux; H Crystal; D S Horoupian; A Thompson; J E Goldman
Journal:  Acta Neuropathol       Date:  1987       Impact factor: 17.088

Review 8.  GABAergic Inhibitory Interneuron Deficits in Alzheimer's Disease: Implications for Treatment.

Authors:  Yilan Xu; Manna Zhao; Yuying Han; Heng Zhang
Journal:  Front Neurosci       Date:  2020-06-30       Impact factor: 4.677

9.  Somatostatin Ameliorates β-Amyloid-Induced Cytotoxicity via the Regulation of CRMP2 Phosphorylation and Calcium Homeostasis in SH-SY5Y Cells.

Authors:  Seungil Paik; Rishi K Somvanshi; Helen A Oliveira; Shenglong Zou; Ujendra Kumar
Journal:  Biomedicines       Date:  2021-01-02

Review 10.  Somatostatin and Somatostatin-Containing Interneurons-From Plasticity to Pathology.

Authors:  Monika Liguz-Lecznar; Grzegorz Dobrzanski; Malgorzata Kossut
Journal:  Biomolecules       Date:  2022-02-15
  10 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.