ReviewAmerican journal of physiology. Regulatory, integrative and comparative physiology2017
Filling the void: a role for exercise-induced BDNF and brain amyloid precursor protein processing.
Review in American journal of physiology. Regulatory, integrative and comparative physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 36 citations in OpenAlex.
- Brain derived neurotrophic factor and secreted amyloid precursor protein-α response to moderate and high intensity exercise.Physiological reports · 2025Article
- Effect of Baduanjin exercise in a blended online-offline model on cognitive function and peripheral blood BDNF levels in older adults.Frontiers in physiology · 2025Article
- The Brain-Gut-Bone Axis in Neurodegenerative Diseases: Insights, Challenges, and Future Prospects.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Influence of Exercise and Genistein to Mitigate the Deleterious Effects of High-Fat High-Sugar Diet on Alzheimer's Disease-Related Markers in Male Mice.International journal of molecular sciences · 2024Article
- The dissolution, reassembly and further clearance of amyloid-β fibrils by tailor-designed dissociable nanosystem for Alzheimer's disease therapy.Exploration (Beijing, China) · 2024Article
- Aniracetam: An Evidence-Based Model for Preventing the Accumulation of Amyloid-β Plaques in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2024Article
- Exercise Intervention for Alzheimer's Disease: Unraveling Neurobiological Mechanisms and Assessing Effects.Life (Basel, Switzerland) · 2023Review
- Four anti-aging drugs and calorie-restricted diet produce parallel effects in fat, brain, muscle, macrophages, and plasma of young mice.GeroScience · 2023Article
- Cap-independent translation of GPLD1 enhances markers of brain health in long-lived mutant and drug-treated mice.Aging cell · 2022Article
- Voluntary wheel running alters markers of amyloid-beta precursor protein processing in an ovarian hormone depleted model.Frontiers in endocrinology · 2022Article
- Exercise and estrogen: common pathways in Alzheimer's disease pathology.American journal of physiology. Endocrinology and metabolism · 2021Review
- A study protocol for MindMoves: A lifestyle physical activity and cognitive training intervention to prevent cognitive impairment in older women with cardiovascular disease.Contemporary clinical trials · 2021Article
- Examination of BDNF Treatment on BACE1 Activity and Acute Exercise on Brain BDNF Signaling.Frontiers in cellular neuroscience · 2021Article
- Acute exercise and brain BACE1 protein content: a time course study.Physiological reports · 2019Article
- The 2019 New Investigator Review Awards.American journal of physiology. Regulatory, integrative and comparative physiology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inactivity, obesity, and insulin resistance are significant risk factors for the development of Alzheimer's disease (AD). Several studies have demonstrated that diet-induced obesity, inactivity, and insulin resistance exacerbate the neuropathological hallmarks of AD. The aggregation of β-amyloid peptides is one of these hallmarks. β-Site amyloid precursor protein-cleaving enzyme 1 (BACE1) is the rate-limiting enzyme in amyloid precursor protein (APP) processing, leading to β-amyloid peptide formation. Understanding how BACE1 content and activity are regulated is essential for establishing therapies aimed at reducing and/or slowing the progression of AD. Exercise training has been proven to reduce the risk of AD as well as decrease β-amyloid production and BACE1 content and/or activity. However, these long-term interventions also result in improvements in adiposity, circulating metabolites, glucose tolerance, and insulin sensitivity making it difficult to determine the direct effects of exercise on brain APP processing. This review highlights this large void in our knowledge and discusses our current understanding of the direct of effect of exercise on β-amyloid production. We have concentrated on the central role that brain-derived neurotrophic factor (BDNF) may play in mediating the direct effects of exercise on reducing brain BACE1 content and activity as well as β-amyloid production. Future studies should aim to generate a greater understanding of how obesity and exercise can directly alter APP processing and AD-related pathologies. This knowledge could provide evidence-based hypotheses for designing therapies to reduce the risk of AD and dementia.
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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.