Alzheimer's disease (AD) is the most common neurodegenerative disease. One of the main pathology markers of AD is the beta-amyloid plaques (βA1-42) created from residues of the badly processed amyloid precursor protein. The accumulation of these plaques can induce neuroinflammation and oxidative stress and impair antioxidant mechanisms, culminating in cognitive and memory deficits. New therapies are necessary to treat AD as the approved drugs do not treat the progress of the disease. Transcranial low-intensity pulsed ultrasound (LIPUS) affects brain metabolism and could be tested as a treatment for AD. This study was aimed at evaluating the LIPUS treatment in a model of AD induced by βA1-42 intracerebroventricularly (ICV) and its effects on learning memory, neurotrophins, neuroinflammation and oxidative status. βA1-42 was administered ICV 24 h before the start of a 5-wk LIPUS treatment. The treatment with LIPUS improved recognition memory, as well as increasing nerve growth factor β and brain-derived neurotrophic factor levels in the hippocampus and cortex. There was a decrease in protein damage in the hippocampus treated with LIPUS. Neuroinflammation and oxidative stress were not present in the AD model used. The results indicated that LIPUS is a novel and promising adjuvant strategy for treatment of the late stage of AD.
Keywords: Learning and memory; Neuroinflammation; Neurotrophins; Oxidative stress.
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