Low-level laser therapy rescues dendrite atrophy via upregulating BDNF expression: implications for Alzheimer's disease
Meng C, He Z, Xing D
The Journal of neuroscience : the official journal of the Society for Neuroscience · 173 citations
Review labels
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How it was studied
- Design
- In vitro/mechanistic study (classified by our AI screen)
- Studied in
- People, plus animal or lab work
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Independent funding
- Government
- National Natural Science Foundation of China
- Government
- National Key Research and Development Program of China
- Government
- Program for Changjiang Scholars and Innovative Research Team in University
- Grants
- Program for Changjiang Scholars and Innovative Research Team in University (IRT0829); National Key Research and Development Program of China (2011CB910402); National Natural Science Foundation of China (81101741); National Natural Science Foundation of China (31101028); National Key Research and Development Program of China (2011CB910402, 2010CB732602); National Key Research and Development Program of China (2010CB732602)
Based on 3 listed funder(s).
Publication
- Published
- 2013-08-14 · J Neurosci · vol. 33 · issue 33 · pp. 13505–13517
- Publisher
- Society for Neuroscience
- Cited
- 234 citations · more than 99% of similar papers · 10.2× the field average
- Impact
- Top 10% most cited in its field
- References
- 70 works
- Access
- Open access (hybrid journal) · CC-BY-NC-SA
- Research areas
- Laser Applications in Dentistry and Medicine · Photoreceptor and optogenetics research · Transcranial Magnetic Stimulation Studies
- Keywords
- CREB, Downregulation and upregulation, Hippocampal formation, Neurotrophic factors, MAPK/ERK pathway, Brain-derived neurotrophic factor, Gene knockdown, Hippocampus, Neuroscience, Transcription factor, Cell biology, Biology, Internal medicine, Medicine, Signal transduction, Receptor, Cell culture, Biochemistry
- MeSH
- dendrites, cell line, tumor, animals, mice, inbred c57bl, mice, transgenic, humans, mice, alzheimer disease, disease models, animal, atrophy, brain-derived neurotrophic factor, blotting, western, enzyme-linked immunosorbent assay, immunohistochemistry, chromatin immunoprecipitation, reverse transcriptase polymerase chain reaction, apoptosis, cell survival, map kinase signaling system, up-regulation, low-level light therapy
3 authors
From CN
- Chengbo MengSouth China Normal University
- Zhiyong HeSouth China Normal University
- Da XingSouth China Normal University
Abstract
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 Aβ-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 Aβ-induced neurons loss and dendritic atrophy, thus identifying a novel pathway by which LLLT protects against Aβ-induced neurotoxicity. Our research may provide a feasible therapeutic approach to control the progression of AD.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY-NC-SA).
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