670 nm Laser Light and EGCG Complementarily Reduce Amyloid-β Aggregates in Human Neuroblastoma Cells: Basis for Treatment of Alzheimer's Disease?
- 1 January 2012
- journal article
- research article
- Published by Mary Ann Liebert Inc in Photomedicine and Laser Surgery
- Vol. 30 (1), 54-60
- https://doi.org/10.1089/pho.2011.3073
Abstract
Objective: The aim of the present study is to present the results of in vitro experiments with possible relevance in the treatment of Alzheimer's disease (AD). Background Data: Despite intensive research efforts, there is no treatment for AD. One root cause of AD is the extra- and intracellular deposition of amyloid-beta (Aβ) fibrils in the brain. Recently, it was shown that extracellular Aβ can enter brain cells, resulting in neurotoxicity. Methods: After internalization of Aβ42 into human neuroblastoma (SH-EP) cells, they were irradiated with moderately intense 670-nm laser light (1000 Wm−2) and/or treated with epigallocatechin gallate (EGCG). Results: In irradiated cells, Aβ42 aggregate amounts were significantly lower than in nonirradiated cells. Likewise, in EGCG-treated cells, Aβ42 aggregate amounts were significantly lower than in non-EGCG-treated cells. Except for the cells simultaneously laden with Aβ42 and EGCG, there was a significant increase in cell numbers in response to laser irradiation. EGCG alone had no effect on cell proliferation. Laser irradiation significantly increased ATP levels in Aβ42-free cells, when compared to nonirradiated cells. Laser-induced clearance of Aβ42 aggregates occurred at the expense of cellular ATP. Conclusions: Irradiation with moderate levels of 670-nm light and EGCG supplementation complementarily reduces Aβ aggregates in SH-EP cells. Transcranial penetration of moderate levels of red to near-infrared (NIR) light has already been amply exploited in the treatment of patients with acute stroke; the blood–brain barrier (BBB) penetration of EGCG has been demonstrated in animals. We hope that our approach will inspire a practical therapy for AD.Keywords
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