Transcranial laser therapy alters amyloid precursor protein processing and improves mitochondrial function in a mouse model of Alzheimer's Disease

摘要

Transcranial laser therapy (TLT) using a near-infrared energy laser system was tested in the 2x Tg amyloid precursor protein (APP) mouse model of Alzheimer's Disease (AD). TLT was administered 3 times/week at escalating doses, starting at 3 months of age, and was compared to a control group which received no laser treatment. Treatment sessions were continued for a total of six months. The brains were examined for amyloid plaque burden, Ap peptides (APi.40 and AP1.42), APP cleavage products (sAPPa, CTFP) and mitochondrial activity. Administration of TLT was associated with a significant, dose-dependent reduction in amyloid load as indicated by the numbers of Ap plaques. Levels of APi^o and Api^2 levels were likewise reduced in a dose-dependent fashion. All TLT doses produced an increase in brain sAPPa and a decrease in CTFp levels consistent with an increase in a-secretase activity and a decrease in P-secretase activity. In addition, TLT increased ATP levels and oxygen utilization in treated animals suggesting improved mitochondrial function. These studies suggest that TLT is a potential candidate for treatment of AD.