Abstract
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.
Highlights
According to the World Health Organization, Alzheimer’s disease (AD) is a global public health priority (Lane et al, 2018)
Our results demonstrate that physical exercise (PE) and cognitive exercise (CE) can reverse memory deficits, hippocampal oxidative imbalance, and some hippocampal morphological alterations related to Aβinduced neurotoxicity model (Aβ) neurotoxicity
The present results show that physical and CEs can promote recognition, short and long-term memory (LTM) consolidation in animals with memory deficits induced by Aβ neurotoxicity
Summary
According to the World Health Organization, Alzheimer’s disease (AD) is a global public health priority (Lane et al, 2018). This neurodegenerative disease is the most common form of dementia, accounting for 50–75% of cases (Prince et al, 2015). The current pharmacological therapies only minimize the progression of the symptoms; they do not reverse brain damage (Habtemariam, 2019). In this sense, research focused on nonpharmacological treatment has been developed (Zucchella et al, 2018).
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