title: Electroacupuncture attenuates reference memory impairment associated with astrocytic NDRG2 suppression in APP/PS1 transgenic mice.
abstract: Electroacupuncture (EA) has demonstrated therapeutic potential for the treatment of Alzheimer's disease (AD). A previous study reported that N-myc downstream-regulated gene 2 (NDRG2) was upregulated in the brain of patients with AD. In the present study, we investigated the effects of repeated EA administration on reference memory impairment and the role of NDRG2 in an amyloid precursor protein (APP)/presenilin-1 (PS1) double transgenic mouse model. Age-matched wild-type and transgenic mice were treated with EA (once per day for 30 min) for 4 weeks (four courses of 5 days EA administration and 2 days rest) beginning at 10 months of age. At seven and ten postnatal months of age and following a 4-week EA treatment regime, mice received training in the Morris water maze (MWM) and a probe test. Brain tissue was analyzed via Western blot and double-label immunofluorescence. Beginning at 7 months of age, APP/PS1 mice began to exhibit deficits in reference memory in the MWM test, an impairment associated with upregulation of glial fibrillary acidic protein (GFAP) and NDRG2. Four weeks of EA administration significantly ameliorated cognitive impairments and suppressed GFAP and NDRG2 upregulation. In conclusion, our findings demonstrated that EA administration can alleviate reference memory deficits and suppress NDRG2 upregulation in an AD transgenic mouse model. This study provides supportive evidence for EA as an effective therapeutic intervention for AD, as well as NDRG2 as a novel target for AD treatment.
authors.affiliation: Department of Anesthesiology, Xijing Hospital, The Fourth Military Medical University, Xi'an, 710032, Shaanxi Province, China.
authors.forename: Feng
authors.initials: F
authors.lastname: Wang
authors.forename: Haixing
authors.initials: H
authors.lastname: Zhong
authors.forename: Xuying
authors.initials: X
authors.lastname: Li
authors.forename: Ye
authors.initials: Y
authors.lastname: Peng
authors.forename: Renee
authors.initials: R
authors.lastname: Kinden
authors.forename: Wei
authors.initials: W
authors.lastname: Liang
authors.forename: Xin
authors.initials: X
authors.lastname: Li
authors.forename: Ming
authors.initials: M
authors.lastname: Shi
authors.forename: Lixin
authors.initials: L
authors.lastname: Liu
authors.forename: Qiang
authors.initials: Q
authors.lastname: Wang
authors.forename: Lize
authors.initials: L
authors.lastname: Xiong
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism / Q000628:therapy*; D016229:Amyloid beta-Peptides / Q000235:genetics; D016564:Amyloid beta-Protein Precursor / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D001253:Astrocytes / Q000378:metabolism*; D001522:Behavior, Animal / Q000502:physiology; D004195:Disease Models, Animal; D015671:Electroacupuncture; D008568:Memory / Q000502:physiology; D008569:Memory Disorders / Q000628:therapy*; D051379:Mice; D008822:Mice, Transgenic; D053764:Presenilin-1 / Q000378:metabolism*
chemical_list: D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D053764:Presenilin-1; C580804:presenilin 1, mouse