Frontiers in Behavioral Neuroscience (Aug 2020)

The Reversal of Memory Deficits in an Alzheimer’s Disease Model Using Physical and Cognitive Exercise

  • Leticia R. Dare,
  • Alexandre Garcia,
  • Caroline B. Soares,
  • Luiza Lopes,
  • Ben-Hur S. Neves,
  • Daniel V. Dias,
  • Pâmela B. Mello-Carpes

DOI
https://doi.org/10.3389/fnbeh.2020.00152
Journal volume & issue
Vol. 14

Abstract

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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.

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