PMID- 25888325
OWN - NLM
STAT- MEDLINE
DCOM- 20150925
LR  - 20220408
IS  - 1750-1326 (Electronic)
IS  - 1750-1326 (Linking)
VI  - 10
DP  - 2015 Apr 3
TI  - Synaptic dysfunction and septin protein family members in neurodegenerative 
      diseases.
PG  - 16
LID - 10.1186/s13024-015-0013-z [doi]
LID - 16
AB  - Cognitive decline and disease progression in different neurodegenerative diseases 
      typically involves synaptic dysfunction preceding the neuronal loss. The synaptic 
      dysfunction is suggested to be caused by imbalanced synaptic plasticity i.e. 
      enhanced induction of long-term depression and concomitantly decreased long-term 
      potentiation accompanied with excess stimulation of extrasynaptic 
      N-Methyl-D-aspartate (NMDA) receptors due to various disturbances in pre- and 
      postsynaptic sites. Recent research has identified neurodegenerative 
      disease-related changes in protein accumulation and aggregation, gene expression, 
      and protein functions, which may contribute to imbalanced synaptic function. 
      Nevertheless, a comprehensive understanding of the mechanisms regulating synaptic 
      plasticity in health and disease is still lacking and therefore characterization 
      of new candidates involved in these mechanisms is needed. Septins, a highly 
      conserved group of guanosine-5'-triphosphate (GTP)-binding proteins, show high 
      neuronal expression and are implicated in the regulation of synaptic vesicle 
      trafficking and neurotransmitter release. In this review, we first summarize the 
      evidence how synaptic dysfunction is related to the pathogenesis of Alzheimer's, 
      Parkinson's and Huntington's disease and frontotemporal lobar degeneration. Then, 
      we discuss different aspects of the potential involvement of the septin family 
      members in the regulation of synaptic function in relation to the pathogenesis of 
      neurodegenerative diseases.
FAU - Marttinen, Mikael
AU  - Marttinen M
AD  - Institute of Biomedicine, University of Eastern Finland, P.O. Box 1627, 70211, 
      Kuopio, Finland. mikael.marttinen@uef.fi.
AD  - Institute of Clinical Medicine - Neurology, University of Eastern Finland, 
      Kuopio, Finland. mikael.marttinen@uef.fi.
AD  - Department of Neurology, Kuopio University Hospital, Kuopio, Finland. 
      mikael.marttinen@uef.fi.
FAU - Kurkinen, Kaisa Ma
AU  - Kurkinen KM
AD  - Institute of Biomedicine, University of Eastern Finland, P.O. Box 1627, 70211, 
      Kuopio, Finland. kaisa.kurkinen@uef.fi.
AD  - Institute of Clinical Medicine - Neurology, University of Eastern Finland, 
      Kuopio, Finland. kaisa.kurkinen@uef.fi.
AD  - Department of Neurology, Kuopio University Hospital, Kuopio, Finland. 
      kaisa.kurkinen@uef.fi.
FAU - Soininen, Hilkka
AU  - Soininen H
AD  - Institute of Clinical Medicine - Neurology, University of Eastern Finland, 
      Kuopio, Finland. Hilkka.Soininen@kuh.fi.
AD  - Department of Neurology, Kuopio University Hospital, Kuopio, Finland. 
      Hilkka.Soininen@kuh.fi.
FAU - Haapasalo, Annakaisa
AU  - Haapasalo A
AD  - Institute of Clinical Medicine - Neurology, University of Eastern Finland, 
      Kuopio, Finland. annakaisa.haapasalo@uef.fi.
AD  - Department of Neurology, Kuopio University Hospital, Kuopio, Finland. 
      annakaisa.haapasalo@uef.fi.
FAU - Hiltunen, Mikko
AU  - Hiltunen M
AD  - Institute of Biomedicine, University of Eastern Finland, P.O. Box 1627, 70211, 
      Kuopio, Finland. mikko.hiltunen@uef.fi.
AD  - Institute of Clinical Medicine - Neurology, University of Eastern Finland, 
      Kuopio, Finland. mikko.hiltunen@uef.fi.
AD  - Department of Neurology, Kuopio University Hospital, Kuopio, Finland. 
      mikko.hiltunen@uef.fi.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20150403
PL  - England
TA  - Mol Neurodegener
JT  - Molecular neurodegeneration
JID - 101266600
RN  - EC 3.6.1.- (Septins)
SB  - IM
MH  - Animals
MH  - Humans
MH  - *Long-Term Potentiation
MH  - Neurodegenerative Diseases/*metabolism/pathology
MH  - Neuronal Plasticity/*physiology
MH  - Septins/*metabolism
MH  - Synapses/metabolism
MH  - Synaptic Transmission/*physiology
PMC - PMC4391194
EDAT- 2015/04/19 06:00
MHDA- 2015/09/26 06:00
PMCR- 2015/04/03
CRDT- 2015/04/19 06:00
PHST- 2014/12/15 00:00 [received]
PHST- 2015/03/23 00:00 [accepted]
PHST- 2015/04/19 06:00 [entrez]
PHST- 2015/04/19 06:00 [pubmed]
PHST- 2015/09/26 06:00 [medline]
PHST- 2015/04/03 00:00 [pmc-release]
AID - 10.1186/s13024-015-0013-z [pii]
AID - 13 [pii]
AID - 10.1186/s13024-015-0013-z [doi]
PST - epublish
SO  - Mol Neurodegener. 2015 Apr 3;10:16. doi: 10.1186/s13024-015-0013-z.