PMID- 24878979
OWN - NLM
STAT- MEDLINE
DCOM- 20140925
LR  - 20220408
IS  - 0172-780X (Print)
IS  - 0172-780X (Linking)
VI  - 35
IP  - 2
DP  - 2014
TI  - Systematic hypothesis for post-stroke depression caused inflammation and 
      neurotransmission and resultant on possible treatments.
PG  - 104-9
AB  - Post-stroke depression (PSD) is a prevalent complex psychiatric disorder that 
      causes delay to functional recovery from rehabilitation and also increases 
      cognitive impairment. The etiology of PSD remains controversial and appears to be 
      physical and psycho-social in origin, alone or in combination. The causes of PSD 
      as well as the mechanisms conferring beneficial antidepressant effects in the 
      context of ischemic brain injury are still unknown. In addition, appropriate 
      treatment strategies for therapy to prevent stroke-induced depression-like 
      behavior remain to be developed. This paper, therefore, proposes two hypotheses 
      for post-stroke depression: The inflammatory hypothesis, which is the increased 
      production of proinflammatory cytokines resulting from brain ischemia in cerebral 
      areas causing the pathogenesis of post-stroke depression and the glutamate 
      hypothesis, where the excess glucocorticoids released from stress-induced 
      over-activation of hypothalamus-pituitary-adrenal (HPA) lead to dysfunction of 
      glutamatergic transmission. Neurotrophins, especially brain-derived neurotrophic 
      factor (BDNF) and vascular endothelial growth factor (VEGF) both play various 
      roles in the central nervous system (CNS), attenuate apoptosis in cultured 
      neurons, stimulate neurogenesis and increase survival and protect neuronal 
      tissues from cell death induced by ischemia or depression. We also touch upon 
      recent treatment strategies including inhibition of pro-inflammatory cytokines, 
      SSRI, neurotrophins and cell-based therapies. In the present review, we provide 
      an overview of recent evidence concerning the mechanisms of post-stroke 
      depression and propose four prospective treatment strategies so as to provide 
      references for clinical evidence-based medications.
FAU - Li, Weiyun
AU  - Li W
AD  - Institute of Neuroscience, Zhejiang University School of Medicine, Hangzhou, 
      China.
FAU - Ling, Shucai
AU  - Ling S
AD  - Institute of Neuroscience, Zhejiang University School of Medicine, Hangzhou, 
      China.
FAU - Yang, Yang
AU  - Yang Y
AD  - Institute of Neuroscience, Zhejiang University School of Medicine, Hangzhou, 
      China.
FAU - Hu, Zhiying
AU  - Hu Z
AD  - Department of Obstetrics and Gynecology, Hangzhou Red Cross Hospital, Hangzhou, 
      China.
FAU - Davies, Henry
AU  - Davies H
AD  - Institute of Neuroscience, Zhejiang University School of Medicine, Hangzhou, 
      China.
FAU - Fang, Marong
AU  - Fang M
AD  - Institute of Neuroscience, Zhejiang University School of Medicine, Hangzhou, 
      China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Sweden
TA  - Neuro Endocrinol Lett
JT  - Neuro endocrinology letters
JID - 8008373
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Antidepressive Agents)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Nerve Growth Factors)
RN  - 3KX376GY7L (Glutamic Acid)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/therapeutic use
MH  - Antidepressive Agents/therapeutic use
MH  - Depressive Disorder/*complications/physiopathology/*therapy
MH  - Encephalitis/*etiology/physiopathology/*therapy
MH  - Glutamic Acid/physiology
MH  - Humans
MH  - Inflammation Mediators/antagonists & inhibitors/physiology
MH  - Nerve Growth Factors/physiology
MH  - Neural Stem Cells/transplantation
MH  - Stroke/*complications/physiopathology/therapy
MH  - Synaptic Transmission/*physiology
EDAT- 2014/06/01 06:00
MHDA- 2014/09/26 06:00
CRDT- 2014/06/01 06:00
PHST- 2014/02/22 00:00 [received]
PHST- 2014/04/12 00:00 [accepted]
PHST- 2014/06/01 06:00 [entrez]
PHST- 2014/06/01 06:00 [pubmed]
PHST- 2014/09/26 06:00 [medline]
AID - NEL350214A03 [pii]
PST - ppublish
SO  - Neuro Endocrinol Lett. 2014;35(2):104-9.