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Author Notes:

Corresponding author at: Department of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta University, 1120 15th Street, CA 3050, Augusta, GA 30912, USA. Tel.: (706) 721-7025; fax: (706) 721-8685. Email: minruiwang@gmail.com (R. Wang)

The authors have no conflicts of interest to disclose.

Subjects:

Research Funding:

This study was supported by research grant NS086929 from the National Institute of Neurological Disorders and Stroke, National Institutes of Health USA; an American Heart Association grant-in-aid 15GRNT25240004, and National Natural Science Foundation grants of China: 61575065 (to CYL), and 31171354 (to RMW).

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Geriatrics & Gerontology
  • Neurosciences
  • Neurosciences & Neurology
  • Alzheimer's disease
  • Low-level laser therapy
  • Mitochondrial dysfunction
  • Inflammation
  • Cognition
  • CYTOCHROME-C-OXIDASE
  • GLOBAL CEREBRAL-ISCHEMIA
  • ALZHEIMERS-DISEASE BRAIN
  • NF-KAPPA-B
  • OXIDATIVE STRESS
  • MITOCHONDRIAL DYSFUNCTION
  • NEURODEGENERATIVE DISEASES
  • NEURONAL DEATH
  • NADPH OXIDASE
  • ATP-SYNTHASE

Low-level laser therapy for beta amyloid toxicity in rat hippocampus

Tools:

Journal Title:

Neurobiology of Aging

Volume:

Volume 49

Publisher:

, Pages 165-182

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Beta amyloid (Aβ) is well accepted to play a central role in the pathogenesis of Alzheimer's disease (AD). The present work evaluated the therapeutic effects of low-level laser irradiation (LLI) on Aβ-induced neurotoxicity in rat hippocampus. Aβ 1–42 was injected bilaterally to the hippocampus CA1 region of adult male rats, and 2-minute daily LLI treatment was applied transcranially after Aβ injection for 5 consecutive days. LLI treatment suppressed Aβ-induced hippocampal neurodegeneration and long-term spatial and recognition memory impairments. Molecular studies revealed that LLI treatment: (1) restored mitochondrial dynamics, by altering fission and fusion protein levels thereby suppressing Aβ-induced extensive fragmentation; (2) suppressed Aβ-induced collapse of mitochondrial membrane potential; (3) reduced oxidized mitochondrial DNA and excessive mitophagy; (4) facilitated mitochondrial homeostasis via modulation of the Bcl-2-associated X protein/B-cell lymphoma 2 ratio and of mitochondrial antioxidant expression; (5) promoted cytochrome c oxidase activity and adenosine triphosphate synthesis; (6) suppressed Aβ-induced glucose-6-phosphate dehydrogenase and nicotinamide adenine dinucleotide phosphate oxidase activity; (7) enhanced the total antioxidant capacity of hippocampal CA1 neurons, whereas reduced the oxidative damage; and (8) suppressed Aβ-induced reactive gliosis, inflammation, and tau hyperphosphorylation. Although development of AD treatments has focused on reducing cerebral Aβ levels, by the time the clinical diagnosis of AD or mild cognitive impairment is made, the brain is likely to have already been exposed to years of elevated Aβ levels with dire consequences for multiple cellular pathways. By alleviating a broad spectrum of Aβ-induced pathology that includes mitochondrial dysfunction, oxidative stress, neuroinflammation, neuronal apoptosis, and tau pathology, LLI could represent a new promising therapeutic strategy for AD.

Copyright information:

© 2016 Elsevier Inc.

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