<p>This review synthesizes current evidence on the psychological and neurological benefits of physical activity, with emphasis on mental health, Parkinson’s disease (PD), and Alzheimer’s disease (AD). Physical inactivity is increasingly recognized as a modifiable risk factor that may exacerbate neuroinflammatory and metabolic dysfunctions associated with these conditions. Structured exercise has been shown to activate muscle–brain signaling pathways, including neurotrophic factors (BDNF, IGF-1, VEGF), immune modulation (IL-6, IL-10), metabolic regulators (PGC-1α, SIRT1), and peripheral mediators such as myokines and gut-brain axis components. For mental health, exercise is associated with reductions in depressive, anxiety, and stress-related symptoms, potentially through HPA-axis recalibration, neurotransmitter remodeling (serotonin, dopamine), and enhanced endocannabinoid signaling. These changes are supported by fMRI and EEG studies showing improved prefrontal–limbic connectivity and cognitive resilience. In PD, exercise interventions are linked to improvements in motor control, balance, and mood, likely mediated by dopaminergic integrity, neurotrophic support, and anti-inflammatory effects, with multimodal programs (aerobic, resistance, and dance-based) often demonstrating superior outcomes. In AD, mid-life physical activity has been associated with reduced dementia risk in epidemiological studies; proposed mechanisms include enhanced amyloid/tau clearance, glymphatic function, and synaptic adaptation, with some RCTs reporting hippocampal volume preservation and improved network connectivity. Shared mechanisms across conditions include neurotrophic upregulation and anti-inflammatory effects, whereas distinct pathways involve dopaminergic circuit remodeling in PD and glymphatic facilitation in AD. Clinical translation through FITT principles (frequency, intensity, time, type) requires personalized prescriptions, strong adherence strategies, and multidisciplinary integration. Despite methodological heterogeneity and limitations in the existing trials, structured physical activity emerges as a scalable, non-pharmacological intervention with potential for prevention, symptom management, and neuroprotection. Larger, well-designed studies are needed to optimize its application and clarify long-term disease-modifying effects.</p>

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Psychological and neurological benefits of physical activity: impact on mental health, Parkinson’s disease, and Alzheimer’s disease

  • Gang Li,
  • Yating Li

摘要

This review synthesizes current evidence on the psychological and neurological benefits of physical activity, with emphasis on mental health, Parkinson’s disease (PD), and Alzheimer’s disease (AD). Physical inactivity is increasingly recognized as a modifiable risk factor that may exacerbate neuroinflammatory and metabolic dysfunctions associated with these conditions. Structured exercise has been shown to activate muscle–brain signaling pathways, including neurotrophic factors (BDNF, IGF-1, VEGF), immune modulation (IL-6, IL-10), metabolic regulators (PGC-1α, SIRT1), and peripheral mediators such as myokines and gut-brain axis components. For mental health, exercise is associated with reductions in depressive, anxiety, and stress-related symptoms, potentially through HPA-axis recalibration, neurotransmitter remodeling (serotonin, dopamine), and enhanced endocannabinoid signaling. These changes are supported by fMRI and EEG studies showing improved prefrontal–limbic connectivity and cognitive resilience. In PD, exercise interventions are linked to improvements in motor control, balance, and mood, likely mediated by dopaminergic integrity, neurotrophic support, and anti-inflammatory effects, with multimodal programs (aerobic, resistance, and dance-based) often demonstrating superior outcomes. In AD, mid-life physical activity has been associated with reduced dementia risk in epidemiological studies; proposed mechanisms include enhanced amyloid/tau clearance, glymphatic function, and synaptic adaptation, with some RCTs reporting hippocampal volume preservation and improved network connectivity. Shared mechanisms across conditions include neurotrophic upregulation and anti-inflammatory effects, whereas distinct pathways involve dopaminergic circuit remodeling in PD and glymphatic facilitation in AD. Clinical translation through FITT principles (frequency, intensity, time, type) requires personalized prescriptions, strong adherence strategies, and multidisciplinary integration. Despite methodological heterogeneity and limitations in the existing trials, structured physical activity emerges as a scalable, non-pharmacological intervention with potential for prevention, symptom management, and neuroprotection. Larger, well-designed studies are needed to optimize its application and clarify long-term disease-modifying effects.