Alzheimer's disease (AD) is the leading cause of dementia in the world, accounting for 50-75% of cases. Currently, there is limited treatment for AD. The current pharmacological therapy minimizes symptom progression but does not reverse brain damage. Studies focused on nonpharmacological treatment for AD have been developed to act on brain plasticity and minimize the neurotoxicity caused by the amyloid-beta (Aβ) peptide. Using a neurotoxicity model induced by Aβ in rats, the present study shows that physical (PE) and cognitive exercise (CE) reverse recognition memory deficits (with a prominent effect of long-term object recognition memory), decrease hippocampal lipid peroxidation, restore the acetylcholinesterase activity altered by Aβ neurotoxicity, and seems to reverse, at least partially, hippocampal tissue disorganization.
In 2020 universities had to quickly implement remote education alternatives as a result of the social distancing due to the COVID-19 pandemic. To keep students engaged with the university, we implemented a teaching-learning model that relates physiology contents to the COVID-19 pandemic using online educational platforms. A 1-mo web course was proposed for health sciences students from the Federal University of Pampa. It included synchronous meetings twice a week and asynchronous activities using scientific articles, case studies, and interactive online tools. The students approved the methodology developed, assessing it as dynamic and innovative. They reported that the activity helped to better understand the relations between COVID-19 and physiological systems. The web course also contributed to the identification of reliable sources of news and stimulated the sharing of scientific content with their families. We concluded that the use of online platforms contextualizing the physiology content considering current events helps students in learning human physiology and improves their abilities to apply this information to their daily life, in this specific case, regarding the COVID-19 pandemic.
Background: Alzheimer’s disease (AD) is characterized by the accumulation of the amyloid-β peptide in the brain, leading to early oxidative stress and neurotoxicity. It has been suggested that physical exercise could be beneficial in preventing AD, but studies with multicomponent training are scanty. Objective: Verify the effects of multicomponent exercise training to prevent deficits in recognition memory related to Aβ neurotoxicity. Methods: We subjected Wistar rats to multicomponent training (including aerobic and anaerobic physical exercise and cognitive exercise) and then infused amyloid-β peptide into their hippocampus. Results: We show that long-term multicomponent training prevents the amyloid-β-associated neurotoxicity in the hippocampus. It reduces hippocampal lipid peroxidation, restores antioxidant capacity, and increases glutathione levels, finally preventing recognition memory deficits. Conclusion: Multicomponent training avoids memory deficits related to amyloid-β neurotoxicity on an animal model.
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