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BDNF and cognitive function in Alzheimer’s disease

Published online by Cambridge University Press:  01 September 2022

A. Sidenkova*
Affiliation:
Ural State Medical University, Psychiatry, Yekaterinburg, Russian Federation

Abstract

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Introduction

Alzheimer’s disease (AD) is a neurodegenerative pathology that develops mainly in elderly and senile people. Disruption of BDNF transport or suppression of its production appears to be typical for people of old age. Objective: To investigate the influence of Alzheimer’s disease on the secretion of brain factors and correlate with neuropsychological profiles.

Objectives

12 men (2) and women (10) with Alzheimer’s disease were examined. The average age of the subjects was 76.25 + 4.89. Methods: MMSE, ADAS-COG, laboratory - BDNF was performed using the G7611 BDNF Emax (R) ImmunoAssaySystem 5 x 96 wells, BDNF Emax® Immunological test.

Methods

2 patients have mild dementia, 8 patients have moderate dementia, 2 patients have severe dementia. The average age of patients with mild dementia was 72.0 + 1.0. The average MMSE score is 16.7 + 3.4.

Results

Correlation analysis showed a close relationship between a pronounced decrease in memory in memory tests (ADAS-COG) and a pronounced decrease in blood BDNF content (r = 0.676). A close statistically significant relationship was found between a low result of the recognition test and a low blood BDNF content (r = 0.598).

Conclusions

We assume that blood BDNF is a marker of pathologically accelerated aging of the central nervous system, since low test results for mnestic function are an indicator of severe degeneration in Alzheimer’s disease.

Disclosure

No significant relationships.

Type
Abstract
Creative Commons
Creative Common License - CCCreative Common License - BY
This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.
Copyright
© The Author(s), 2022. Published by Cambridge University Press on behalf of the European Psychiatric Association
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