Activation of PKA/SIRT1 signaling pathway by photobiomodulation therapy reduces Aβ levels in Alzheimer's disease models
Zhang Z, Shen Q, Wu X, Zhang D, Xing D
Aging cell · 114 citations
How it was studied
- Design
- Animal study (classified by our AI screen)
- Studied in
- People, plus animal or lab work
- Main outcome
- Health markers and function
Who paid for it
- Funding
- Independent funding
- Government
- National Natural Science Foundation of China
- Government
- Natural Science Foundation of Guangdong Province
- Grants
- National Natural Science Foundation of China (61361160414); National Natural Science Foundation of China (2014A030313419); National Natural Science Foundation of China (31470072); Natural Science Foundation of Guangdong Province (2014A030313419)
Based on 2 listed funder(s) and full-text disclosure statement.
Publication
- Published
- 2019-10-30 · Aging Cell · vol. 19 · issue 1 · p. e13054
- Publisher
- Wiley
- Cited
- 139 citations · more than 98% of similar papers · 9.0× the field average
- Impact
- Top 10% most cited in its field
- References
- 40 works
- Access
- Open access (journal) · CC-BY
- Research areas
- Laser Applications in Dentistry and Medicine · Biochemical effects in animals · Sirtuins and Resveratrol in Medicine
- Keywords
- Neuroprotection, Amyloid precursor protein, Neuroscience, Biology, Amyloid precursor protein secretase, Alzheimer's disease, Disease, ADAM10, Amyloid (mycology), Cell biology, Medicine, Internal medicine, Biochemistry, Enzyme
- MeSH
- animals, mice, transgenic, humans, mice, alzheimer disease, disease models, animal, sirtuin 1, amyloid beta-peptides, low-level light therapy
5 authors
From CN
- Zhan ZhangSouth China Normal University
- Qi ShenSouth China Normal University
- Xiaolei WuSouth China Normal University
- Di ZhangSouth China Normal University
- Da Xing · correspondingSouth China Normal University
Abstract
A hallmark of Alzheimer's disease (AD) is the accumulation of amyloid-β (Aβ), which correlates significantly with progressive cognitive deficits. Although photobiomodulation therapy (PBMT), as a novel noninvasive physiotherapy strategy, has been proposed to improve neuronal survival, decrease neuron loss, ameliorate dendritic atrophy, and provide overall AD improvement, it remains unknown whether and how this neuroprotective process affects Aβ levels. Here, we report that PBMT reduced Aβ production and plaque formation by shifting amyloid precursor protein (APP) processing toward the nonamyloidogenic pathway, thereby improving memory and cognitive ability in a mouse model of AD. More importantly, a pivotal protein, SIRT1, was involved in this process by specifically up-regulating ADAM10 and down-regulating BACE1, which is dependent on the cAMP/PKA pathway in APP/PS1 primary neurons and SH-SY5Y cells stably expressing human APP Swedish mutation (APPswe). We further found that the activity of the mitochondrial photoacceptor cytochrome c oxidase (CcO) was responsible for PBMT-induced activation of PKA and SIRT1. Together, our research suggests that PBMT as a viable therapeutic strategy has great potential value in improving cognitive ability and combatting AD.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).
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