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Int J Neuropsychopharmacol. 2015 Jan 7;18(7):pyu116. doi: 10.1093/ijnp/pyu116.

Isolation Housing Exacerbates Alzheimer's Disease-Like Pathophysiology in Aged APP/PS1 Mice.

Author information

1
Jiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, Nanjing, Jiangsu, China (Drs Huang MD, Wang MD, Cao Ms, Gao Ms, N. Xiao Ms, Hu MD, PhD, and M. Xiao MD, PhD); Department of Rehabilitation Sciences, University of Kentucky Center for Excellence in Rural Health, Hazard, KY (Dr Marshall PhD).
2
Jiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, Nanjing, Jiangsu, China (Drs Huang MD, Wang MD, Cao Ms, Gao Ms, N. Xiao Ms, Hu MD, PhD, and M. Xiao MD, PhD); Department of Rehabilitation Sciences, University of Kentucky Center for Excellence in Rural Health, Hazard, KY (Dr Marshall PhD). mingx@njmu.edu.cn.

Abstract

BACKGROUND:

Alzheimer's disease is a neurodegenerative disease characterized by gradual declines in social, cognitive, and emotional functions, leading to a loss of expected social behavior. Social isolation has been shown to have adverse effects on individual development and growth as well as health and aging. Previous experiments have shown that social isolation causes an early onset of Alzheimer's disease-like phenotypes in young APP695/PS1-dE9 transgenic mice. However, the interactions between social isolation and Alzheimer's disease still remain unknown.

METHODS:

Seventeen-month-old male APP695/PS1-dE9 transgenic mice were either singly housed or continued group housing for 3 months. Then, Alzheimer's disease-like pathophysiological changes were evaluated by using behavioral, biochemical, and pathological analyses.

RESULTS:

Isolation housing further promoted cognitive dysfunction and Aβ plaque accumulation in the hippocampus of aged APP695/PS1-dE9 transgenic mice, associated with increased γ-secretase and decreased neprilysin expression. Furthermore, exacerbated hippocampal atrophy, synapse and myelin associated protein loss, and glial neuroinflammatory reactions were observed in the hippocampus of isolated aged APP695/PS1-dE9 transgenic mice.

CONCLUSIONS:

The results demonstrate that social isolation exacerbates Alzheimer's disease-like pathophysiology in aged APP695/PS1-dE9 transgenic mice, highlighting the potential role of group life for delaying or counteracting the Alzheimer's disease process.

KEYWORDS:

APP/PS1 mice; Alzheimer’s disease; hippocampus; memory deficiency; social isolation; β-amyloid

PMID:
25568286
PMCID:
PMC4540096
DOI:
10.1093/ijnp/pyu116
[Indexed for MEDLINE]
Free PMC Article

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