PMID- 25590048
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 2376-0478 (Print)
IS  - 2376-0478 (Electronic)
IS  - 2376-0478 (Linking)
VI  - 1
IP  - 1
DP  - 2014
TI  - Astrocyte mediated MMP-9 activation in the synapse dysfunction: An implication in 
      Alzheimer disease.
LID - e243 [pii]
AB  - Alzheimer's disease (AD) is a progressive neurodegenerative disorder that occurs 
      due to spasms of the neurons, resulting in loss of memory and behavioral changes. 
      In particular, synaptic loss has been described as an early event in the 
      pathogenesis of AD. The increasing evidences have suggested the role of many 
      matrix metalloproteinase (MMPs) in central nervous system (CNS) pathology. Many 
      studies showed that MMPs enzymes are important for the pathophysiological process 
      during Alzheimer's disease (AD). It is usually believed that the synaptic 
      dysfunction and synapse loss contribute to the cognitive deficits of patients 
      with AD. Cerebrovascular events such as blood-brain barrier (BBB) disruption lead 
      to neuronal damage as well as neuroinflammation. BBB dysfunctions are observed at 
      an early post injury time point, and are associated with activation of proteases, 
      such as MMPs especially MMP-9 which is actively engage in a neuronal injury in 
      the most of the neurodegenerative disorders. BBB opening is accompanied by 
      astrocytic activation, BBB injury and dysregulation of cerebral blood flow. 
      Activated MMPs disrupt neurovascular unit (NVU) which may starve the neurons and 
      affect the synapse function by altering synaptic plasticity and ultimately lead 
      to cognitive decline. However, how MMPs implicated in synaptic dysfunction what 
      are the mechanism associated with this disparity needs to discuss for better 
      understanding the role of MMP-9 in pathogenesis of AD. In this review, we focused 
      on the role of astrocytes and MMP-9 in synaptic dysfunction. We also, underlined 
      possible pharmacological strategies for drug development that might offer more 
      insight into the pathogenesis of cerebrovascular disease such as stroke and 
      Vascular dementia.
FAU - Kamat, Pradip K
AU  - Kamat PK
AD  - Division of Physiology and Biophysics, University of Louisville, School of 
      Medicine, (KY) 40202, USA.
FAU - Swarnkar, Supriya
AU  - Swarnkar S
AD  - Scripp Institute, Jupiter, Florida, 33458, USA.
FAU - Rai, Shivika
AU  - Rai S
AD  - Division of Pharmacology, Central Drug Research Institute (CDRI), P.O. Box 173, 
      Lucknow (U.P.) 226001, India.
FAU - Kumar, Vijay
AU  - Kumar V
AD  - Department of Zoology, RN. College Hajipur, Vaishali, Bihar, 844101, India.
FAU - Tyagi, Neetu
AU  - Tyagi N
AD  - Division of Physiology and Biophysics, University of Louisville, School of 
      Medicine, (KY) 40202, USA.
LA  - eng
GR  - R01 HL107640/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Ther Targets Neurol Dis
JT  - Therapeutic targets for neurological diseases
JID - 101645414
PMC - PMC4290019
MID - NIHMS630721
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - Astrocyte
OT  - MMPs
OT  - Neurovascular unit
OT  - synapse remodeling
COIS- Conflicting interests: None
EDAT- 2015/01/16 06:00
MHDA- 2015/01/16 06:01
PMCR- 2015/01/12
CRDT- 2015/01/16 06:00
PHST- 2015/01/16 06:00 [entrez]
PHST- 2015/01/16 06:00 [pubmed]
PHST- 2015/01/16 06:01 [medline]
PHST- 2015/01/12 00:00 [pmc-release]
AID - e243 [pii]
AID - 10.14800/ttnd.243 [doi]
PST - ppublish
SO  - Ther Targets Neurol Dis. 2014;1(1):e243. doi: 10.14800/ttnd.243.