ArticleJournal of neurochemistry2017
Exercise and BDNF reduce Aβ production by enhancing α-secretase processing of APP.
Article in Journal of neurochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 1 of them a synthesis that pooled it.
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Who cites it
98 citing papers in PubMed, 1 synthesis or guideline pooled it, 180 citations in OpenAlex.
- Effectiveness of Resistance Exercise on Cognitive Function in Animal Models of Alzheimer Disease: A Systematic Review and Meta-Analysis.The journal of prevention of Alzheimer's disease · 2024Pooled it
- Irisin-BDNF axis mediates muscle-brain communication: a complete molecular cascade and potential bidirectional feedback from peripheral activation to central protection.Biogerontology · 2026Review
- Effects of metformin and exercise on Alzheimer's model induced by D-galactose in the rats: A behavioral, histological and BDNF gene study.Biochemistry and biophysics reports · 2026Article
- Neuronal HDAC9: A key regulator of cognitive and synaptic aging, rescuing Alzheimer's disease-related phenotypes.Molecular psychiatry · 2026Article
- Exercise mimetics: molecular mechanisms, biological and therapeutic effects.Molecular biomedicine · 2026Review
- Exercise-induced GPLD1 is associated with neuroprotection and improvement of hippocampal dysfunction in an Alzheimer's disease model.Metabolic brain disease · 2026Article
- Lifestyle strategies and mechanistic implications for slowing neurodegeneration.npj metabolic health and disease · 2026Review
- The impact of nutritional and exercise interventions on Alzheimer's disease pathophysiology via modulation of the microbiota-gut-brain-axis.Nutritional neuroscience · 2026Review
- The Role of Transcranial Magnetic Stimulation for the Treatment of Alzheimer's Disease: A Narrative Review.Life (Basel, Switzerland) · 2026Review
- BDNF-amyloid-Frontiers in molecular neuroscience · 2026Review
- Beyond Estrogen: Unraveling the Complexities of Hormonal Signaling Pathways in Alzheimer's Disease and Their Implications for Precision Therapy.Molecular neurobiology · 2025Review
- Exercise training enhances myokine release and reduces brain insulin resistance: insights into muscle-CNS metabolic cross-talk.Metabolic brain disease · 2025Review
- Serum BDNF and progression to MCI in cognitively normal older adults: A prospective cohort study.The journal of prevention of Alzheimer's disease · 2025Article
- Lifetime walking and Alzheimer's pathology: A longitudinal study in older adults.The journal of prevention of Alzheimer's disease · 2025Article
- Enhanced Neuroprotection by Diosgenin and Pterostilbene Combination Against Neurotoxicity Induced by Amyloid-Β 1-42 in SH-SY5Y Differentiated Cell Models.Annals of neurosciences · 2025Article
- The Clock and the Brain: Circadian Rhythm and Alzheimer's Disease.Current issues in molecular biology · 2025Review
- Brain derived neurotrophic factor and secreted amyloid precursor protein-α response to moderate and high intensity exercise.Physiological reports · 2025Article
- Mechanism study of exercise intervention on circadian disruption in Alzheimer's disease.Frontiers in neuroscience · 2025Review
- AnCurrent Alzheimer research · 2025Article
- Enhancing sleep quality in synucleinopathies through physical exercise.Frontiers in cellular neuroscience · 2025Review
38 more citing papers are in PubMed but not listed here.
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6 authors at 2 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by aggregation of toxic forms of amyloid β peptide (Aβ). Treatment strategies have largely been focused on inhibiting the enzymes (β- and γ-secretases) that liberate Aβ from the amyloid precursor protein (APP). While evidence suggests that individuals who exercise regularly are at reduced risk for AD and studies of animal models demonstrate that running can ameliorate brain Aβ pathology and associated cognitive deficits, the underlying mechanisms are unknown. However, considerable evidence suggests that brain-derived neurotrophic factor (BDNF) mediates beneficial effects of exercise on neuroplasticity and cellular stress resistance. Here, we tested the hypothesis that BDNF promotes non-amyloidogenic APP processing. Using a transgenic mouse model of Alzheimer's disease and cultured human neural cells, we demonstrate that exercise and BDNF reduce production of toxic Aβ peptides through a mechanism involving enhanced α-secretase processing of APP. This anti-amyloidogenic APP processing involves subcellular redistribution of α-secretase and an increase in intracellular neuroprotective APP peptides capable of binding and inhibiting β-secretase. Moreover, our results suggest that BDNF's ability to promote neurite outgrowth is primarily exerted through pathways other than APP processing. Exercise and other factors that enhance BDNF signaling may therefore have both therapeutic and prophylactic value in the battle against AD. Read the Editorial Highlight for this article on page 191.
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