Farfara Dorit, Tuby Hana, Trudler Dorit, Doron-Mandel Ella, Maltz Lidya, Vassar Robert J, Frenkel Dan, Oron Uri
Department of Neurobiology, George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel.
J Mol Neurosci. 2015 Feb;55(2):430-6. doi: 10.1007/s12031-014-0354-z. Epub 2014 Jul 4.
Low-level laser therapy (LLLT) has been used to treat inflammation, tissue healing, and repair processes. We recently reported that LLLT to the bone marrow (BM) led to proliferation of mesenchymal stem cells (MSCs) and their homing in the ischemic heart suggesting its role in regenerative medicine. The aim of the present study was to investigate the ability of LLLT to stimulate MSCs of autologous BM in order to affect neurological behavior and β-amyloid burden in progressive stages of Alzheimer's disease (AD) mouse model. MSCs from wild-type mice stimulated with LLLT showed to increase their ability to maturate towards a monocyte lineage and to increase phagocytosis activity towards soluble amyloid beta (Aβ). Furthermore, weekly LLLT to BM of AD mice for 2 months, starting at 4 months of age (progressive stage of AD), improved cognitive capacity and spatial learning, as compared to sham-treated AD mice. Histology revealed a significant reduction in Aβ brain burden. Our results suggest the use of LLLT as a therapeutic application in progressive stages of AD and imply its role in mediating MSC therapy in brain amyloidogenic diseases.
低强度激光疗法(LLLT)已被用于治疗炎症、组织愈合和修复过程。我们最近报道,对骨髓(BM)进行LLLT可导致间充质干细胞(MSCs)增殖并归巢至缺血心脏,提示其在再生医学中的作用。本研究的目的是探讨LLLT刺激自体BM来源的MSCs的能力,以影响阿尔茨海默病(AD)小鼠模型进展期的神经行为和β-淀粉样蛋白负荷。用LLLT刺激的野生型小鼠的MSCs显示出向单核细胞系成熟的能力增强,以及对可溶性淀粉样β蛋白(Aβ)的吞噬活性增加。此外,从4月龄(AD进展期)开始,对AD小鼠的BM每周进行2个月的LLLT,与假手术治疗的AD小鼠相比,改善了认知能力和空间学习能力。组织学检查显示脑内Aβ负荷显著降低。我们的结果表明LLLT可作为AD进展期的一种治疗方法,并暗示其在介导脑淀粉样变性疾病的MSC治疗中的作用。