Paper
17 February 2011 Transcranial laser therapy alters amyloid precursor protein processing and improves mitochondrial function in a mouse model of Alzheimer's disease
Thomas McCarthy, Jin Yu, Salim El-Amouri, Sebastiano Gattoni-Celli, Steve Richieri, Luis De Taboada, Jackson Streeter, Mark S. Kindy
Author Affiliations +
Proceedings Volume 7887, Mechanisms for Low-Light Therapy VI; 78870K (2011) https://doi.org/10.1117/12.877028
Event: SPIE BiOS, 2011, San Francisco, California, United States
Abstract
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, Aβ peptides (Aβ1-40 and Aβ1-42 ), APP cleavage products (sAPPα, CTFβ) and mitochondrial activity. Administration of TLT was associated with a significant, dose-dependent reduction in amyloid load as indicated by the numbers of Aβ plaques. Levels of Aβ1-40 and Aβ1-42 levels were likewise reduced in a dose-dependent fashion. All TLT doses produced an increase in brain sAPPα and a decrease in CTFβ levels consistent with an increase in α-secretase activity and a decrease in β-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.
© (2011) COPYRIGHT Society of Photo-Optical Instrumentation Engineers (SPIE). Downloading of the abstract is permitted for personal use only.
Thomas McCarthy, Jin Yu, Salim El-Amouri, Sebastiano Gattoni-Celli, Steve Richieri, Luis De Taboada, Jackson Streeter, and Mark S. Kindy "Transcranial laser therapy alters amyloid precursor protein processing and improves mitochondrial function in a mouse model of Alzheimer's disease", Proc. SPIE 7887, Mechanisms for Low-Light Therapy VI, 78870K (17 February 2011); https://doi.org/10.1117/12.877028
Lens.org Logo
CITATIONS
Cited by 8 scholarly publications.
Advertisement
Advertisement
RIGHTS & PERMISSIONS
Get copyright permission  Get copyright permission on Copyright Marketplace
KEYWORDS
Brain

Acquisition tracking and pointing

Laser therapeutics

Proteins

Alzheimer's disease

Tissues

Mouse models

RELATED CONTENT

Mechanisms of low level light therapy
Proceedings of SPIE (February 10 2006)
Photobiomodulation on senescence
Proceedings of SPIE (October 27 2006)
Role of reactive oxygen species in low level light therapy
Proceedings of SPIE (February 18 2009)
Raman spectroscopy of Alzheimer's diseased tissue
Proceedings of SPIE (July 01 2004)

Back to Top