ArticleFrontiers in behavioral neuroscience2020
The Reversal of Memory Deficits in an Alzheimer's Disease Model Using Physical and Cognitive Exercise.
Article in Frontiers in behavioral neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Physical exercise as a therapeutic strategy in animal models of Alzheimer's disease: Molecular, behavioral, and histopathological evidence.Biochemistry and biophysics reports · 2026Review
- Ferroptosis in Neuropsychiatric and Neurodegenerative Disorders: Shared Mechanisms and Disease-Specific Signatures.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Targeting ferroptosis for neuroprotection: potential therapeutic avenues in neurodegenerative and neuropsychiatric diseases.Frontiers in physiology · 2025Review
- Analysis of Effect of Intensity of Aerobic Exercise on Cognitive and Motor Functions and Neurotrophic Factor Expression Patterns in an Alzheimer's Disease Rat Model.Journal of personalized medicine · 2023Article
- Effect of a combined program of running exercise and environmental enrichment on memory function and neurogenesis markers in amyloid-beta-induced Alzheimer-like model.Iranian journal of basic medical sciences · 2023Article
- Does Preoperative Cognitive Optimization Improve Postoperative Outcomes in the Elderly?Journal of clinical medicine · 2022Review
- Editorial: Molecular mechanisms of Alzheimer's disease: From top to bottom.Frontiers in aging · 2022Article
- Understanding How Physical Exercise Improves Alzheimer's Disease: Cholinergic and Monoaminergic Systems.Frontiers in aging neuroscience · 2022Review
- The effect of URB597, exercise or their combination on the performance of 6-OHDA mouse model of Parkinson disease in the elevated plus maze, tail suspension test and step-down task.Metabolic brain disease · 2021Article
- Lipid Peroxidation and Antioxidant Supplementation in Neurodegenerative Diseases: A Review of Human Studies.Antioxidants (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.