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Protective effects of low-intensity pulsed ultrasound on aluminum-induced cerebral damage in Alzheimer's disease rat model.

Abstract
The protein expressions of neurotrophic factors can be enhanced by low-intensity pulsed ultrasound (LIPUS) stimulation in the brain. The purpose of this study was to demonstrate the protective effect of LIPUS stimulation against aluminum-induced cerebral damage in Alzheimer's disease rat model. LIPUS was administered 7 days before each aluminum chloride (AlCl3) administration, and concomitantly given with AlCl3 daily for a period of 6 weeks. Neurotrophic factors in hippocampus were measured by western blot analysis. Behavioral changes in the Morris water maze and elevated plus maze were examined in rats after administration of AlCl3. Various biochemical analyses were performed to evaluate the extent of brain damages. LIPUS is capable of prompting levels of brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF), and vascular endothelial growth factor (VEGF) in rat brain. AlCl3 administration resulted in a significant increase in the aluminum concentration, acetylcholinesterase activity and beta-amyloid (Aβ) deposition in AlCl3 treated rats. LIPUS stimulation significantly attenuated aluminum concentration, acetylcholinesterase activity, Aβ deposition and karyopyknosis in AlCl3 treated rats. Furthermore, LIPUS significantly improved memory retention in AlCl3-induced memory impairment. These experimental results indicate that LIPUS has neuroprotective effects against AlCl3-induced cerebral damages and cognitive dysfunction.
AuthorsWei-Ting Lin, Ran-Chou Chen, Wen-Wei Lu, Shing-Hwa Liu, Feng-Yi Yang
JournalScientific reports (Sci Rep) Vol. 5 Pg. 9671 (Apr 15 2015) ISSN: 2045-2322 [Electronic] England
PMID25873429 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Amyloid beta-Peptides
  • Nerve Growth Factors
  • Aluminum
  • Acetylcholinesterase
Topics
  • Acetylcholinesterase (metabolism)
  • Aluminum (adverse effects)
  • Alzheimer Disease (genetics, metabolism, pathology, therapy)
  • Amyloid beta-Peptides (metabolism)
  • Animals
  • Blood-Brain Barrier (metabolism)
  • Brain (drug effects, metabolism, pathology, radiation effects)
  • Cerebral Cortex (drug effects, pathology, radiation effects)
  • Disease Models, Animal
  • Enzyme Activation
  • Gene Expression
  • Male
  • Memory
  • Nerve Growth Factors (genetics, metabolism)
  • Permeability
  • Rats
  • Ultrasonic Waves

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