Saratov State University, Saratov, Russia.
Lovelace Biomedical Research Institute, Albuquerque, NM, USA.
Adv Exp Med Biol. 2021;1269:57-61. doi: 10.1007/978-3-030-48238-1_9.
Here, we demonstrate the therapeutic effects of transcranial photobiomodulation (tPBM, 1267 nm, 32 J/cm, a 9-day course) in mice with the injected model of Alzheimer's disease (AD) associated with accumulation of beta-amyloid (Aβ) in the brain resulting in neurocognitive deficit vs. the control group (CG) (the neurological severity score (NNS), AD 3.67 ± 0.58 vs. CG 1.00 ± 0.26%, p < 0.05) and mild cerebral hypoxia (AD 72 ± 6% vs. CG 97 ± 2%, p < 0.001). The course of tPBM improved neurocognitive status of mice with AD (NNS, AD 2.03 ± 0.14 vs. CG 1.00 ± 0.26, vs. 2.03 ± 0.14, p < 0.05) due to stimulation of clearance of Aβ from the brain via the meningeal lymphatic vessels (the immunohistochemical and confocal data) and an increase in blood oxygen saturation of the brain tissues (the pulse oximetry data) till 85 ± 2%, p < 0.05. These results open breakthrough strategies for non-pharmacological therapy of AD and clearly demonstrate that tPBM might be a promising therapeutic target for preventing or delaying AD based on stimulation of oxygenation of the brain tissues and activation of clearance of toxic molecules via the cerebral lymphatics.
在这里,我们展示了经颅光生物调节(tPBM,1267nm,32J/cm,9 天疗程)在注射阿尔茨海默病(AD)相关β-淀粉样蛋白(Aβ)在大脑中积累导致神经认知缺陷的小鼠模型中的治疗效果,与对照组(CG)相比(神经严重程度评分(NNS),AD 为 3.67±0.58,CG 为 1.00±0.26%,p<0.05)和轻度脑缺氧(AD 为 72±6%,CG 为 97±2%,p<0.001)。tPBM 疗程改善了 AD 小鼠的神经认知状态(NNS,AD 为 2.03±0.14,CG 为 1.00±0.26,与 2.03±0.14 相比,p<0.05),这是由于通过脑膜淋巴管清除大脑中的 Aβ(免疫组织化学和共聚焦数据)以及脑组织血氧饱和度增加(脉搏血氧数据)至 85±2%,p<0.05。这些结果为 AD 的非药物治疗开辟了突破性策略,并清楚地表明,tPBM 可能是通过刺激脑组织的氧合和通过脑淋巴清除有毒分子来预防或延迟 AD 的有前途的治疗靶点。