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Published on: December 26, 2016
Microglia modulation with 1070-nm light attenuates Aβ burden and cognitive impairment in Alzheimer's disease mouse
Lechan Tao1, Qi Liu1, Fuli Zhang1
1State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Med-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, 200030, China.
Abstract:
Photobiomodulation, by utilizing low-power light in the visible and near-infrared spectra to trigger biological responses in cells and tissues, has been considered as a possible therapeutic strategy for Alzheimer's disease (AD), while its specific mechanisms have remained elusive. Here, we demonstrate that cognitive and memory impairment in an AD mouse model can be ameliorated by 1070-nm light via reducing cerebral β-amyloid (Aβ) burden, the hallmark of AD. The glial cells, including microglia and astrocytes, play important roles in Aβ clearance. Our results show that 1070-nm light pulsed at 10 Hz triggers microglia rather than astrocyte responses in AD mice. The 1070-nm light-induced microglia responses with alteration in morphology and increased colocalization with Aβ are sufficient to reduce Aβ load in AD mice. Moreover, 1070-nm light pulsed at 10 Hz can reduce perivascular microglia and promote angiogenesis to further enhance Aβ clearance. Our study confirms the important roles of microglia and cerebral vessels in the use of 1070-nm light for the treatment of AD mice and provides a framework for developing a novel therapeutic approach for AD.
Insights
Photobiomodulation using 1070-nm light improves cognition in an Alzheimer's disease (AD) mouse model by reducing amyloid plaques. This therapy activates microglia, enhancing amyloid clearance and promoting brain repair.
Area of Science:
- Neuroscience
- Biomedical Engineering
- Cell Biology
Background:
- Photobiomodulation (PBM) uses low-power light to stimulate cellular responses, showing potential for Alzheimer's disease (AD) therapy.
- The precise mechanisms of PBM in AD remain unclear, necessitating further investigation into its cellular and molecular effects.
Purpose of the Study:
- To investigate the therapeutic effects and underlying mechanisms of 1070-nm light photobiomodulation in an Alzheimer's disease mouse model.
- To determine if 1070-nm light can ameliorate cognitive and memory deficits associated with AD pathology.
Main Methods:
- Utilized an established Alzheimer's disease mouse model.
- Administered 1070-nm light pulsed at 10 Hz to AD mice.
- Assessed cognitive and memory functions.
- Analyzed cerebral beta-amyloid (Aβ) burden, glial cell responses (microglia and astrocytes), perivascular microglia, and angiogenesis.
Main Results:
- 1070-nm light treatment significantly ameliorated cognitive and memory impairments in AD mice.
- The light therapy reduced cerebral Aβ burden by activating microglia, not astrocytes.
- Microglial activation involved morphological changes and increased colocalization with Aβ, leading to reduced Aβ load.
- 1070-nm light also reduced perivascular microglia and promoted angiogenesis, further supporting Aβ clearance.
Conclusions:
- 1070-nm light photobiomodulation is a viable therapeutic strategy for Alzheimer's disease, effectively reducing Aβ burden and improving cognitive function in a mouse model.
- The therapeutic effects are mediated by the activation of microglia and enhancement of cerebral vascularization, highlighting the role of glial cells and angiogenesis in AD treatment.
- This study provides a mechanistic framework for developing novel photobiomodulation-based therapies for Alzheimer's disease.
