PMID- 17889623
OWN - NLM
STAT- MEDLINE
DCOM- 20080325
LR  - 20131121
IS  - 1568-1637 (Print)
IS  - 1568-1637 (Linking)
VI  - 7
IP  - 1
DP  - 2008 Jan
TI  - Hormesis: a promising strategy to sustain endogenous neuronal survival pathways 
      against neurodegenerative disorders.
PG  - 21-33
AB  - The brain developed adaptive mechanisms in the face of changing environments and 
      stresses imposed on the nervous system. The addition of glutamate as the major 
      excitatory amino acid neurotransmitter to the brain's complement of amino acids 
      and peptides dictated a coordinated transcriptional and translational program to 
      meet the demands of excitatory neurotransmission. One such program is the ability 
      of neurons to sustain and maintain their survival given the nature of 
      glutamate-mediated receptor activation. The unique development of endogenous 
      neuronal pathways activated by glutamate receptors transformed neurons and 
      allowed them to survive under conditions of high energy demands. These same 
      endogenous survival pathways also mediate plastic responses to meet another 
      demand of the brain, adaptation. An endogenous protein that plays a central role 
      in glutamate receptor-mediated survival pathways is brain-derived neurotrophic 
      factor (BDNF). Intermittent but frequent synaptic ionotropic glutamate receptor 
      activation ensures neuronal survival through a BDNF autocrine loop. In sharp 
      contrast, overactivation of ionotropic glutamate receptors leads to neuronal cell 
      death. Thus, innovative strategies that induce endogenous neuronal survival 
      pathways through low-level activation of ionotropic glutamate receptors or those 
      that bypass receptor activation but upregulate endogenous survival pathways may 
      not only prevent neurodegenerative disorders that involve glutamate as a final 
      common pathway that kills neurons, but may also provide treatment alternatives 
      critical for neurons to survive stressful conditions such as stroke, status 
      epilepticus and hypoglycemic-induced neuronal cell death.
FAU - Marini, Ann M
AU  - Marini AM
AD  - Department of Neurology, Uniformed Services University of the Health Sciences, 
      Bethesda, MD 20814, USA. amarini@usuhs.mil
FAU - Jiang, Hong
AU  - Jiang H
FAU - Pan, Hongna
AU  - Pan H
FAU - Wu, Xuan
AU  - Wu X
FAU - Lipsky, Robert H
AU  - Lipsky RH
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20070824
PL  - England
TA  - Ageing Res Rev
JT  - Ageing research reviews
JID - 101128963
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (NF-kappa B)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/physiology
MH  - Cyclic AMP Response Element-Binding Protein/physiology
MH  - Extracellular Signal-Regulated MAP Kinases/genetics/physiology
MH  - Glutamic Acid/physiology
MH  - Humans
MH  - NF-kappa B/physiology
MH  - Neurodegenerative Diseases/*drug therapy
MH  - Phosphatidylinositol 3-Kinases/physiology
MH  - Receptors, N-Methyl-D-Aspartate/drug effects/physiology
MH  - Signal Transduction/drug effects/*physiology
RF  - 158
EDAT- 2007/09/25 09:00
MHDA- 2008/03/26 09:00
CRDT- 2007/09/25 09:00
PHST- 2007/03/01 00:00 [received]
PHST- 2007/07/31 00:00 [revised]
PHST- 2007/07/31 00:00 [accepted]
PHST- 2007/09/25 09:00 [pubmed]
PHST- 2008/03/26 09:00 [medline]
PHST- 2007/09/25 09:00 [entrez]
AID - S1568-1637(07)00041-4 [pii]
AID - 10.1016/j.arr.2007.07.003 [doi]
PST - ppublish
SO  - Ageing Res Rev. 2008 Jan;7(1):21-33. doi: 10.1016/j.arr.2007.07.003. Epub 2007 
      Aug 24.