title: Hesperidin ameliorates behavioral impairments and neuropathology of transgenic APP/PS1 mice.
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.
authors.affiliation: Division of Immunopathology of the Nervous System, Institute of Pathology and Neuropathology, University of Tuebingen, Calwer Street 3, D-72076 Tuebingen, Germany.
authors.forename: Chaoyun
authors.initials: C
authors.lastname: Li
authors.affiliation: Division of Immunopathology of the Nervous System, Institute of Pathology and Neuropathology, University of Tuebingen, Calwer Street 3, D-72076 Tuebingen, Germany.
authors.forename: Caroline
authors.initials: C
authors.lastname: Zug
authors.affiliation: College of Automation, Chongqing University of Posts and Telecommunications, Chongqing 400065, China.
authors.forename: Hongchun
authors.initials: H
authors.lastname: Qu
authors.affiliation: Division of Immunopathology of the Nervous System, Institute of Pathology and Neuropathology, University of Tuebingen, Calwer Street 3, D-72076 Tuebingen, Germany.
authors.forename: Hermann
authors.initials: H
authors.lastname: Schluesener
authors.affiliation: 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.
authors.forename: Zhiyuan
authors.initials: Z
authors.lastname: Zhang
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy* / Q000473:pathology / Q000523:psychology; D016564:Amyloid beta-Protein Precursor / Q000172:deficiency / Q000235:genetics; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000473:pathology*; D004195:Disease Models, Animal; D006569:Hesperidin / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D017628:Microglia / Q000187:drug effects / Q000276:immunology; D058225:Plaque, Amyloid / Q000188:drug therapy; D053764:Presenilin-1 / Q000172:deficiency / Q000235:genetics; D011597:Psychomotor Performance / Q000187:drug effects*; D012919:Social Behavior; D016212:Transforming Growth Factor beta / Q000276:immunology; D016896:Treatment Outcome
chemical_list: D016564:Amyloid beta-Protein Precursor; D053764:Presenilin-1; D016212:Transforming Growth Factor beta; D006569:Hesperidin
keywords: Alzheimer's disease; Behavioral deficit; Cerebral amyloidosis; Hesperidin; Neuro-inflammation; Transgenic mouse model