The Reversal of Memory Deficits in an Alzheimer's Disease Model Using Physical and Cognitive Exercise

被引：22

作者：

Dare, Leticia R. ^{[1
]}

Garcia, Alexandre ^{[1
]}

Soares, Caroline B. ^{[1
]}

Lopes, Luiza ^{[1
]}

Neves, Ben-Hur S. ^{[1
]}

Dias, Daniel V. ^{[2
]}

Mello-Carpes, Pamela B. ^{[1
]}

机构：

[1] Fed Univ Pampa, Physiol Res Grp, Uruguaiana, Brazil

[2] Univ Fed Triangulo Mineiro, Dept Struct Biol, Uberaba, MG, Brazil

来源：

FRONTIERS IN BEHAVIORAL NEUROSCIENCE | 2020年 / 14卷

关键词：

Alzheimer's disease; physical exercise; cognitive exercise; oxidative damage; A beta neurotoxicity; OXIDATIVE STRESS; PEPTIDES; EXTRACT; BRAIN; RATS;

D O I：

10.3389/fnbeh.2020.00152

中图分类号：

B84 [心理学]; C [社会科学总论]; Q98 [人类学];

学科分类号：

03 ; 0303 ; 030303 ; 04 ; 0402 ;

摘要：

Alzheimer's disease (AD) is the leading cause of dementia in the world, accounting for 50-75% of cases. Currently, there is limited treatment for AD. The current pharmacological therapy minimizes symptom progression but does not reverse brain damage. Studies focused on nonpharmacological treatment for AD have been developed to act on brain plasticity and minimize the neurotoxicity caused by the amyloid-beta (A beta) peptide. Using a neurotoxicity model induced by A beta in rats, the present study shows that physical (PE) and cognitive exercise (CE) reverse recognition memory deficits (with a prominent effect of long-term object recognition memory), decrease hippocampal lipid peroxidation, restore the acetylcholinesterase activity altered by A beta neurotoxicity, and seems to reverse, at least partially, hippocampal tissue disorganization.

引用

页数：10

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