PMID- 23946409
OWN - NLM
STAT- MEDLINE
DCOM- 20131023
LR  - 20220410
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 33
IP  - 33
DP  - 2013 Aug 14
TI  - Low-level laser therapy rescues dendrite atrophy via upregulating BDNF 
      expression: implications for Alzheimer's disease.
PG  - 13505-17
LID - 10.1523/JNEUROSCI.0918-13.2013 [doi]
AB  - Downregulation of brain-derived neurotrophic factor (BDNF) in the hippocampus 
      occurs early in the progression of Alzheimer's disease (AD). Since BDNF plays a 
      critical role in neuronal survival and dendrite growth, BDNF upregulation may 
      contribute to rescue dendrite atrophy and cell loss in AD. Low-level laser 
      therapy (LLLT) has been demonstrated to regulate neuronal function both in vitro 
      and in vivo. In the present study, we found that LLLT rescued neurons loss and 
      dendritic atrophy via upregulation of BDNF in both Abeta-treated hippocampal neurons 
      and cultured APP/PS1 mouse hippocampal neurons. Photoactivation of transcription 
      factor CRE-binding protein (CREB) increased both BDNF mRNA and protein 
      expression, since knockdown CREB blocked the effects of LLLT. Furthermore, 
      CREB-regulated transcription was in an ERK-dependent manner. Inhibition of ERK 
      attenuated the DNA-binding efficiency of CREB to BDNF promoter. In addition, 
      dendrite growth was improved after LLLT, characterized by upregulation of Rac1 
      activity and PSD-95 expression, and the increase in length, branching, and spine 
      density of dendrites in hippocampal neurons. Together, these studies suggest that 
      upregulation of BDNF with LLLT by activation of ERK/CREB pathway can ameliorate 
      Abeta-induced neurons loss and dendritic atrophy, thus identifying a novel pathway 
      by which LLLT protects against Abeta-induced neurotoxicity. Our research may provide 
      a feasible therapeutic approach to control the progression of AD.
FAU - Meng, Chengbo
AU  - Meng C
AD  - MOE Key Laboratory of Laser Life Science and Institute of Laser Life Science, 
      College of Biophotonics, South China Normal University, Guangzhou 510631, China.
FAU - He, Zhiyong
AU  - He Z
FAU - Xing, Da
AU  - Xing D
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Brain-Derived Neurotrophic Factor)
SB  - IM
MH  - Alzheimer Disease/*metabolism
MH  - Animals
MH  - Apoptosis/radiation effects
MH  - Atrophy/pathology
MH  - Blotting, Western
MH  - Brain-Derived Neurotrophic Factor/*biosynthesis
MH  - Cell Line, Tumor
MH  - Cell Survival/radiation effects
MH  - Chromatin Immunoprecipitation
MH  - Dendrites/metabolism/pathology/*radiation effects
MH  - Disease Models, Animal
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Humans
MH  - Immunohistochemistry
MH  - Low-Level Light Therapy/*methods
MH  - MAP Kinase Signaling System/physiology/radiation effects
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Up-Regulation
PMC - PMC6705158
EDAT- 2013/08/16 06:00
MHDA- 2013/10/24 06:00
PMCR- 2014/02/14
CRDT- 2013/08/16 06:00
PHST- 2013/08/16 06:00 [entrez]
PHST- 2013/08/16 06:00 [pubmed]
PHST- 2013/10/24 06:00 [medline]
PHST- 2014/02/14 00:00 [pmc-release]
AID - 33/33/13505 [pii]
AID - 0918-13 [pii]
AID - 10.1523/JNEUROSCI.0918-13.2013 [doi]
PST - ppublish
SO  - J Neurosci. 2013 Aug 14;33(33):13505-17. doi: 10.1523/JNEUROSCI.0918-13.2013.