Introduction: While animal models of exercise and PD have pushed the field forward, few studies have addressed exercise-induced neuroplasticity in human PD.
Method: As a first step toward promoting greater international collaboration on exercise-induced neuroplasticity in human PD, we present data on 8 human PD studies (published between 2008 and 2015) with 144 adults with PD of varying disease severity (Hoehn and Yahr stage 1 to stage 3), using various experimental (e.g., randomized controlled trial) and quasi-experimental designs on the effects of cognitive and physical activity on brain structure or function in PD. We focus on plasticity mechanisms of intervention-induced increases in maximal corticomotor excitability, exercise-induced changes in voxel-based gray matter volume changes and increases in exercise-induced serum levels of brain derived neurotrophic factor (BDNF). Finally, we provide a future perspective for promoting international, collaborative research on exercise-induced neuroplasticity in human PD.
Conclusion: An emerging body of evidence suggests exercise triggers several plasticity related events in the human PD brain including corticomotor excitation, increases and decreases in gray matter volume and changes in BDNF levels.
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http://dx.doi.org/10.1016/j.parkreldis.2015.09.030 | DOI Listing |
Background: Alzheimer's disease is the most dreaded multifactorial neurological illness for which there is currently no known treatment. Although the exact cause of AD is still unknown, several factors related to lifestyle, genetics, and environment are known to have a significant role in the disease's development. Alzheimer's disease is characterized by neuronal loss, neurofibrillary tangles, and senile plaques.
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December 2024
Laboratory of Molecular Biology, Institute of Physiotherapy and Health Sciences, Academy of Physical Education, Katowice, Poland.
Over the past couple of decades, it has become apparent that skeletal muscles might be engaged in endocrine signaling, mostly as a result of exercise or physical activity in general. The importance of this phenomenon is currently studied in terms of the impact that exercise- or physical activity -induced signaling factors have, in the interaction of the "muscle-brain crosstalk." So far, skeletal muscle-derived myokines were demonstrated to intercede in the connection between muscles and a plethora of various organs such as adipose tissue, liver, or pancreas.
View Article and Find Full Text PDFFASEB J
December 2024
Laboratory of Exercise Biochemistry and Neuroendocrinology, Institute of Health and Sport Sciences, University of Tsukuba, Tsukuba, Japan.
Exercise activates the dorsal hippocampus that triggers synaptic and cellar plasticity and ultimately promotes memory formation. For decades, these benefits have been explored using demanding and stress-response-inducing exercise at moderate-to-vigorous intensities. In contrast, our translational research with animals and humans has focused on light-intensity exercise (light exercise) below the lactate threshold (LT), which almost anyone can safely perform with minimal stress.
View Article and Find Full Text PDFExp Gerontol
December 2024
Departamento de Enfermería, Facultad de Enfermería, Universidad Nacional de Colombia, Sede Bogotá, Carrera 30 No. 45-03 Bogotá, D.C., Colombia. Electronic address:
Unlabelled: Chronic Non-Communicable Diseases (NCDs), including cardiovascular diseases, cancer, chronic respiratory diseases, and diabetes, are the leading global causes of mortality, accounting for 71 % of deaths annually. Metabolic Syndrome (MS), characterized by hypertension, obesity, insulin resistance, and dyslipidemia, is a significant risk factor for NCDs. Physical inactivity exacerbates these conditions, contributing to poor cardiovascular and mental health outcomes.
View Article and Find Full Text PDFNeuroscience
January 2025
Key Laboratory of Novel Targets and Drug Study for Neural Repair of Zhejiang Province, School of Medicine, Hangzhou City University, Hangzhou 310015, China. Electronic address:
Exercise-induced fatigue (EF) is characterized by a decline in maximal voluntary muscle force following prolonged physical activity, influenced by both peripheral and central factors. Central fatigue involves complex interactions within the central nervous system (CNS), where astrocytes play a crucial role. This study explores the impact of astrocytic calcium signals on EF.
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