PMID- 24748365
OWN - NLM
STAT- MEDLINE
DCOM- 20160301
LR  - 20211021
IS  - 1573-7365 (Electronic)
IS  - 0885-7490 (Print)
IS  - 0885-7490 (Linking)
VI  - 30
IP  - 2
DP  - 2015 Apr
TI  - Role of social factors on cell death, cerebral plasticity and recovery after 
      stroke.
PG  - 497-506
LID - 10.1007/s11011-014-9544-1 [doi]
AB  - Stroke is a serious global health care problem. It is now is the fourth leading 
      cause of death and the primary cause of adult disability in the United States. 
      Substantial evidence from both experimental and clinical studies has demonstrated 
      that social isolation (SI) can increase stroke incidence and impair recovery. 
      Epidemiological studies demonstrate that an increasing number of patients are 
      living alone, and as the aging population increases, loneliness will only 
      increase in prevalence. SI is increasingly identified as an independent risk 
      factor for all-cause mortality. In contrast, individuals with high levels of 
      social support exhibit more rapid and extensive functional and cognitive recovery 
      after a wide variety of pathological insults, including stroke. Clinical data 
      suggests that SI is an important risk factor for increased mortality and delayed 
      functional recovery following ischemic stroke. Attesting to the importance of 
      mortality and behavioral factors in stroke outcome is that these same effects can 
      be reproduced in animal models of experimental stroke. This has allowed 
      researchers to identify several mechanistic changes that occur with affiliative 
      interactions. These include decreased systemic inflammation, elaboration of 
      growth factors including brain derived neurotropic factor (BDNF), enhanced 
      neurogenesis, and improved neuroimmune responsiveness in group housed animals. 
      These may mediate the beneficial effects of social interaction on improving 
      stroke recovery and reducing neuronal death. In this review we provide an 
      overview of the effects of SI on ischemic injury and recovery and discuss their 
      clinical and therapeutic implications.
FAU - Venna, Venugopal Reddy
AU  - Venna VR
AD  - Department of Neuroscience, University of Connecticut Health Center, Farmington, 
      CT, 06030, USA.
FAU - McCullough, Louise D
AU  - McCullough LD
LA  - eng
GR  - R01 NS055215/NS/NINDS NIH HHS/United States
GR  - R01 NS077769/NS/NINDS NIH HHS/United States
GR  - R01 NSO77769/PHS HHS/United States
GR  - NS055215/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20140422
PL  - United States
TA  - Metab Brain Dis
JT  - Metabolic brain disease
JID - 8610370
SB  - IM
MH  - *Cell Death
MH  - Humans
MH  - *Neuronal Plasticity
MH  - *Recovery of Function
MH  - *Social Environment
MH  - Social Isolation/*psychology
MH  - *Socioeconomic Factors
MH  - Stroke/psychology/*therapy
MH  - Stroke Rehabilitation
MH  - Treatment Outcome
PMC - PMC4206683
MID - NIHMS588011
EDAT- 2014/04/22 06:00
MHDA- 2016/03/02 06:00
PMCR- 2016/04/01
CRDT- 2014/04/22 06:00
PHST- 2014/03/10 00:00 [received]
PHST- 2014/04/04 00:00 [accepted]
PHST- 2014/04/22 06:00 [entrez]
PHST- 2014/04/22 06:00 [pubmed]
PHST- 2016/03/02 06:00 [medline]
PHST- 2016/04/01 00:00 [pmc-release]
AID - 10.1007/s11011-014-9544-1 [doi]
PST - ppublish
SO  - Metab Brain Dis. 2015 Apr;30(2):497-506. doi: 10.1007/s11011-014-9544-1. Epub 
      2014 Apr 22.