PMID- 25288155
OWN - NLM
STAT- MEDLINE
DCOM- 20160808
LR  - 20220408
IS  - 1559-1182 (Electronic)
IS  - 0893-7648 (Linking)
VI  - 52
IP  - 3
DP  - 2015 Dec
TI  - Moderate Treadmill Exercise Protects Synaptic Plasticity of the Dentate Gyrus and 
      Related Signaling Cascade in a Rat Model of Alzheimer's Disease.
PG  - 1067-1076
LID - 10.1007/s12035-014-8916-1 [doi]
AB  - The dentate gyrus (DG) of the hippocampus is known to be more resistant to the 
      effects of various external factors than other hippocampal areas. This study 
      investigated the neuroprotective effects of moderate treadmill exercise on 
      early-phase long-term potentiation (E-LTP) and its molecular signaling pathways 
      in the DG of amyloid beta rat model of sporadic Alzheimer's disease (AD). Animals 
      were preconditioned to run on treadmill for 4 weeks and concurrently received ICV 
      infusion of Abeta(1)(-)(4)(2) peptides (250 pmol/day) during the third and fourth weeks of 
      exercise training. We utilized in vivo electrophysiological recordings to assess 
      the effect of exercise and/or AD pathology on basal synaptic transmission and 
      E-LTP magnitude of the perforant pathway synapses in urethane-anesthetized rats. 
      Immunoblotting analysis was used to quantify changes in the levels of learning 
      and memory-related key signaling molecules. The AD-impaired basal synaptic 
      transmission and suppression of E-LTP in the DG were prevented by prior moderate 
      treadmill exercise. In addition, exercise normalized the basal levels of memory 
      and E-LTP-related signaling molecules including Ca(2+)/calmodulin-dependent 
      protein kinase II (CaMKII), calcineurin (PP2B), and brain-derived neurotrophic 
      factor (BDNF). Exercise also prevented the reduction of phosphorylated CaMKII and 
      aberrant increase of PP2B seen after E-LTP induction in amyloid-infused rats. Our 
      data suggests that by restoring the balance of kinase-phosphatase, 4 weeks of 
      moderate treadmill exercise prevents DG synaptic deficits and deleterious 
      alterations in signaling pathways associated with AD.
FAU - Dao, An T
AU  - Dao AT
AD  - Department of PPS, College of Pharmacy, University of Houston, Houston, TX, 
      77204-5037, USA.
FAU - Zagaar, Munder A
AU  - Zagaar MA
AD  - Department of PPS, College of Pharmacy, University of Houston, Houston, TX, 
      77204-5037, USA.
FAU - Alkadhi, Karim A
AU  - Alkadhi KA
AD  - Department of PPS, College of Pharmacy, University of Houston, Houston, TX, 
      77204-5037, USA. kalkadhi@uh.edu.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141008
PL  - United States
TA  - Mol Neurobiol
JT  - Molecular neurobiology
JID - 8900963
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Peptide Fragments)
RN  - 0 (amyloid beta-protein (1-42))
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
RN  - EC 3.1.3.16 (Calcineurin)
SB  - IM
EIN - Mol Neurobiol. 2018 Jan;55(1):901. PMID: 28983833
MH  - Alzheimer Disease/physiopathology/*therapy
MH  - Amyloid beta-Peptides/toxicity
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/biosynthesis
MH  - Calcineurin/metabolism
MH  - Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism
MH  - Dentate Gyrus/*physiopathology
MH  - Excitatory Postsynaptic Potentials/physiology
MH  - *Exercise Therapy
MH  - Humans
MH  - Long-Term Potentiation
MH  - Male
MH  - Nerve Tissue Proteins/metabolism
MH  - *Neuronal Plasticity
MH  - Peptide Fragments/toxicity
MH  - Perforant Pathway/physiology
MH  - Phosphorylation
MH  - Physical Conditioning, Animal/*physiology
MH  - Protein Processing, Post-Translational
MH  - Rats
MH  - Rats, Wistar
MH  - Running/physiology
MH  - Signal Transduction/physiology
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - BDNF
OT  - Basal synaptic transmission
OT  - Early LTP
OT  - Memory
OT  - Treadmill exercise
EDAT- 2014/10/08 06:00
MHDA- 2016/08/09 06:00
CRDT- 2014/10/08 06:00
PHST- 2014/08/12 00:00 [received]
PHST- 2014/09/28 00:00 [accepted]
PHST- 2014/10/08 06:00 [entrez]
PHST- 2014/10/08 06:00 [pubmed]
PHST- 2016/08/09 06:00 [medline]
AID - 10.1007/s12035-014-8916-1 [pii]
AID - 10.1007/s12035-014-8916-1 [doi]
PST - ppublish
SO  - Mol Neurobiol. 2015 Dec;52(3):1067-1076. doi: 10.1007/s12035-014-8916-1. Epub 
      2014 Oct 8.