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Behav Brain Res. 2015 Mar 15;281:32-42. doi: 10.1016/j.bbr.2014.12.012. Epub 2014 Dec 12.

Hesperidin ameliorates behavioral impairments and neuropathology of transgenic APP/PS1 mice.

Author information

1
Division of Immunopathology of the Nervous System, Institute of Pathology and Neuropathology, University of Tuebingen, Calwer Street 3, D-72076 Tuebingen, Germany.
2
College of Automation, Chongqing University of Posts and Telecommunications, Chongqing 400065, China.
3
Division of Immunopathology of the Nervous System, Institute of Pathology and Neuropathology, University of Tuebingen, Calwer Street 3, D-72076 Tuebingen, Germany. Electronic address: zhiyuan.zhang@medizin.uni-tuebingen.de.

Abstract

In addition to cognitive impairments, deficits in non-cognitive behaviors are also common neurological sequelae in Alzheimer's disease and its animal models. Hesperidin, a flavanone glycoside found abundantly in citrus fruits, was orally given (100 mg/kg body weight) to 5-month-old transgenic APP/PS1 mice, a mouse model of cerebral amyloidosis for Alzheimer's disease. After a relatively short-term treatment of 10 days, hesperidin significantly restored deficits in non-cognitive nesting ability and social interaction. Further immunohistochemical analysis showed significantly attenuated β-amyloid deposition, plaque associated APP expression, microglial activation and TGF-β immunoreactivity in brains of APP/PS1 mice, which suggests that ameliorated behavioral impairments might be attributable to reduced Aβ deposition and attenuated neuro-inflammatory reaction. Additionally, efficient anti-inflammatory effects of hesperidin were confirmed in vitro. Our findings suggest that hesperidin might be a potential candidate for the treatment of AD or even other neurodegenerative diseases.

KEYWORDS:

Alzheimer's disease; Behavioral deficit; Cerebral amyloidosis; Hesperidin; Neuro-inflammation; Transgenic mouse model

PMID:
25510196
DOI:
10.1016/j.bbr.2014.12.012
[Indexed for MEDLINE]

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