PMID- 28824455
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220408
IS  - 1664-042X (Print)
IS  - 1664-042X (Electronic)
IS  - 1664-042X (Linking)
VI  - 8
DP  - 2017
TI  - Repetitive Transcranial Magnetic Stimulation Ameliorates Cognitive Impairment by 
      Enhancing Neurogenesis and Suppressing Apoptosis in the Hippocampus in Rats with 
      Ischemic Stroke.
PG  - 559
LID - 10.3389/fphys.2017.00559 [doi]
LID - 559
AB  - Cognitive impairment is a serious mental deficit caused by stroke that can 
      severely affect the quality of a survivor's life. Repetitive transcranial 
      magnetic stimulation (rTMS) is a well-known rehabilitation modality that has been 
      reported to exert neuroprotective effects after cerebral ischemic injury. In the 
      present study, we evaluated the therapeutic efficacy of rTMS against post-stroke 
      cognitive impairment (PSCI) and investigated the mechanisms underlying its 
      effects in a middle cerebral artery occlusion (MCAO) rat model. The results 
      showed that rTMS ameliorated cognitive deficits and tended to reduce the sizes of 
      cerebral lesions. In addition, rTMS significantly improved cognitive function via 
      a mechanism involving increased neurogenesis and decreased apoptosis in the 
      ipsilateral hippocampus. Moreover, brain-derived neurotrophic factor (BDNF) and 
      its receptor, tropomyosin-related kinase B (TrkB), were clearly upregulated in 
      ischemic hippocampi after treatment with rTMS. Additionally, further studies 
      demonstrated that rTMS markedly enhanced the expression of the apoptosis-related 
      B cell lymphoma/leukemia gene 2 (Bcl-2) and decreased the expression of the 
      Bcl-2-associated protein X (Bax) and the number of TUNEL-positive cells in the 
      ischemic hippocampus. Both protein levels and mRNA levels were investigated. Our 
      findings suggest that after ischemic stroke, treatment with rTMS promoted the 
      functional recovery of cognitive impairments by inhibiting apoptosis and 
      enhancing neurogenesis in the hippocampus and that this mechanism might be 
      mediated by the BDNF signaling pathway.
FAU - Guo, Feng
AU  - Guo F
AD  - Department of Rehabilitation Medicine, Tongji Hospital, Tongji Medical College, 
      Huazhong University of Science and TechnologyWuhan, China.
FAU - Lou, Jicheng
AU  - Lou J
AD  - Department of Obstetrics and Gynecology, The Central Hospital of WuhanWuhan, 
      China.
FAU - Han, Xiaohua
AU  - Han X
AD  - Department of Rehabilitation Medicine, Tongji Hospital, Tongji Medical College, 
      Huazhong University of Science and TechnologyWuhan, China.
FAU - Deng, Yuguo
AU  - Deng Y
AD  - Department of Rehabilitation Medicine, Tongji Hospital, Tongji Medical College, 
      Huazhong University of Science and TechnologyWuhan, China.
FAU - Huang, Xiaolin
AU  - Huang X
AD  - Department of Rehabilitation Medicine, Tongji Hospital, Tongji Medical College, 
      Huazhong University of Science and TechnologyWuhan, China.
LA  - eng
PT  - Journal Article
DEP - 20170802
PL  - Switzerland
TA  - Front Physiol
JT  - Frontiers in physiology
JID - 101549006
PMC - PMC5539749
OTO - NOTNLM
OT  - BDNF signaling pathway
OT  - cognitive impairment
OT  - focal cerebral ischemia
OT  - hippocampal neurogenesis
OT  - rTMS
EDAT- 2017/08/22 06:00
MHDA- 2017/08/22 06:01
PMCR- 2017/08/02
CRDT- 2017/08/22 06:00
PHST- 2017/03/07 00:00 [received]
PHST- 2017/07/17 00:00 [accepted]
PHST- 2017/08/22 06:00 [entrez]
PHST- 2017/08/22 06:00 [pubmed]
PHST- 2017/08/22 06:01 [medline]
PHST- 2017/08/02 00:00 [pmc-release]
AID - 10.3389/fphys.2017.00559 [doi]
PST - epublish
SO  - Front Physiol. 2017 Aug 2;8:559. doi: 10.3389/fphys.2017.00559. eCollection 2017.