Low-Level Laser Therapy to the Bone Marrow Ameliorates Neurodegenerative Disease Progression in a Mouse Model of Alzheimer's Disease: A Minireview

被引:35
作者
Oron, Amir [1 ]
Oron, Uri [2 ,3 ]
机构
[1] Kaplan Med Ctr, Dept Orthoped Surg, Rehovot, Israel
[2] Tel Aviv Univ, George S Wise Fac Life Sci, Dept Zool, Tel Aviv, Israel
[3] Tel Aviv Univ, Sagol Sch Neurosci, Tel Aviv, Israel
关键词
amyloid beta (A beta); bone marrow (BM); mesenchymal stem cells (MSC); Alzheimer's disease (AD); low-level laser therapy (LLLT); exosomes; MESENCHYMAL STEM-CELLS; POWER DENSITIES; DIFFERENTIATION; NEUROGENESIS; IRRADIATION; INDUCTION; MICROGLIA; STROKE; SAFETY;
D O I
10.1089/pho.2015.4072
中图分类号
R61 [外科手术学];
学科分类号
摘要
Objective: This communication reviews the ability of low-level laser therapy (LLLT) to stimulate mesenchymal stem cells (MSCs) in autologous bone marrow (BM) to enhance the capacity of MSCs to infiltrate the brain, clear beta-amyloid, and improve cognition. Background: We recently reported that LLLT applied to the BM enhanced the proliferation of MSCs and their mobilization toward the ischemic heart region, suggesting a possible application of this approach in regenerative medicine and neurodegenerative diseases. It was also shown that circulating monocytes can infiltrate the brain and reduce brain amyloid load in an Alzheimer's disease (AD) mouse model. Methods and Results: MSCs from wild-type mice stimulated with LLLT demonstrated an increased ability to maturate toward a monocyte lineage and to increase phagocytosis of soluble A beta in vitro. Furthermore, weekly LLLT for 2 months to the BM, starting at 4 months of age (progressive stage of the disease in these 5XFAD transgenic male mice), improved memory and spatial learning, compared to a sham-treated AD mouse model. Histology revealed a significant reduction in A beta brain burden in the laser-treated mice compared to the nonlaser-treated ones. Conclusions: The application of LLLT to the BM is suggested as a therapeutic approach in progressive stages of AD, and its potential role in mediating MSC therapy in brain amyloidogenic disease is implied.
引用
收藏
页码:627 / 630
页数:4
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