A Review of Exercise-Induced Neuroplasticity in Ischemic Stroke: Pathology and Mechanisms

Xing, Ying; Bai, Yulong

doi:10.1007/s12035-020-02021-1

Cited by 87 publications

(61 citation statements)

References 130 publications

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“…211 Remarkably, human and animal studies strongly link aerobic exercise training with amplified BDNF signaling as well as synaptic proteins, such as growth-associated protein-43, and angiogenic factors, such as IGF-1 and VEGF. 210,[212][213][214] Evidence suggests that increased serum levels of BDNF are most consistently observed following aerobic exercise sessions that last more than 30 min and at a frequency of 4 days per week, 215 which is very similar to 150 min weekly recommended by clinical practice guidelines. 216 In animal models of stroke, exercise promotes angiogenesis, synaptic plasticity, and even neurogenesis via VEGF and BDNF signaling pathways that are highly dependent on NO signaling.…”

Section: Modulating Aberrant Immune Responsesmentioning

confidence: 82%

“…209 The poststroke functional recovery phase is characterized by the resolution of inflammation coupled with coordinated neurotrophic and angiogenic processes. 210 As outlined above, BDNF plays a central role in increased poststroke neuroplasticity along with its receptor tyrosine kinase B. BDNF coordinates structural remodeling at synaptic, axonal, and dendritic levels with the participation of downstream synaptic and endothelial targets. 211 Remarkably, human and animal studies strongly link aerobic exercise training with amplified BDNF signaling as well as synaptic proteins, such as growth-associated protein-43, and angiogenic factors, such as IGF-1 and VEGF.…”

Section: Modulating Aberrant Immune Responsesmentioning

confidence: 99%

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Diabetes, stroke, and neuroresilience: looking beyond hyperglycemia

Krinock

Singhal

2021

Annals of the New York Academy of Sciences

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Ischemic stroke is a leading cause of morbidity and mortality among type 2 diabetic patients. Preclinical and translational studies have identified critical pathophysiological mediators of stroke risk, recurrence, and poor outcome in diabetic patients, including endothelial dysfunction and inflammation. Most clinical trials of diabetes and stroke have focused on treating hyperglycemia alone. Pioglitazone has shown promise in secondary stroke prevention for insulin-resistant patients; however, its use is not yet widespread. Additional research into clinical therapies directed at diabetic pathophysiological processes to prevent stroke and improve outcome for diabetic stroke survivors is necessary. Resilience is the process of active adaptation to a stressor. In patients with diabetes, stroke recovery is impaired by insulin resistance, endothelial dysfunction, and inflammation, which impair key neuroresilience pathways maintaining cerebrovascular integrity, resolving poststroke inflammation, stimulating neural plasticity, and preventing neurodegeneration. Our review summarizes the underpinnings of stroke risk in diabetes, the clinical consequences of stroke in diabetic patients, and proposes hypotheses and new avenues of research for therapeutics to stimulate neuroresilience pathways and improve stroke outcome in diabetic patients.

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Section: Modulating Aberrant Immune Responsesmentioning

confidence: 82%

Section: Modulating Aberrant Immune Responsesmentioning

confidence: 99%

Diabetes, stroke, and neuroresilience: looking beyond hyperglycemia

Krinock

Singhal

2021

Annals of the New York Academy of Sciences

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“…The term "neuroplasticity" is a novel concept referring to the potential ability of the nervous system to modify its structural and functional characteristics answering to altered demands and environments [68]. Neuroplasticity is a dynamic process involving changes in the number of brain nuclei and structures, numerous functions (learning, memory, movement) and various interactions [69]. Evidence from both human and animal studies have suggested that PA has a facilitating effect on neuroplasticity; regular PA stimulates angiogenesis, synaptogenesis, neurogenesis as well as the synthesis of neurotransmitters in various cerebral areas [70][71][72][73][74][75].…”

Section: Improved Neuronal Plasticitymentioning

confidence: 99%

“…Age-related reductions in the concentrations of NAA have been found especially throughout late life, meanwhile, higher NAA levels were associated with better working memory performance; additionally, in older adults, higher aerobic fitness levels offset an age-related decline in NAA giving increased neuronal viability [89]. Finally, an important role in promoting exercise-related synaptic plasticity is played by neurotrophins, including insulin-like growth factor (IGF-1) and brain-derived neurotrophic factor (BDNF) [69]. Rodent models have shown that short-term periods of increased PA are sufficient to upregulate central and peripheral factors that support the brain, and promote synaptic plasticity through increased expression of mRNA for BDNF and IGF-1 but also for Nerve growth factor (NGF), and tropomyosin receptor kinase B (TrkB) [78,92].…”

Section: Improved Neuronal Plasticitymentioning

confidence: 99%

“…It is well known the role carried out by exercise in mediating the recovery of post-stroke damage. PA can contribute to the functional compensation of surviving brain areas involved in limb function: the possible mechanisms include enhanced activity and axonal growth of the pyramidal and extrapyramidal systems in the ipsi-lesional and contralesional hemispheres [69]. Despite the intriguing pathophysiological context and the numerous experimental data available, only a few studies have attempted to ascertain the vascular and anti-ischemic protection role played by PA before that an ischemic cerebral accident occurs.…”

Section: Anti-ischemic Effects Of Physical Activitymentioning

confidence: 99%

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Role of Regular Physical Activity in Neuroprotection against Acute Ischemia

Raimondo

Rizzo

Musiari

et al. 2020

IJMS

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One of the major obstacles that prevents an effective therapeutic intervention against ischemic stroke is the lack of neuroprotective agents able to reduce neuronal damage; this results in frequent evolution towards a long-term disability with limited alternatives available to aid in recovery. Nevertheless, various treatment options have shown clinical efficacy. Neurotrophins such as brain-derived neurotrophic factor (BDNF), widely produced throughout the brain, but also in distant tissues such as the muscle, have demonstrated regenerative properties with the potential to restore damaged neural tissue. Neurotrophins play a significant role in both protection and recovery of function following neurological diseases such as ischemic stroke or traumatic brain injury. Unfortunately, the efficacy of exogenous administration of these neurotrophins is limited by rapid degradation with subsequent poor half-life and a lack of blood–brain-barrier permeability. Regular exercise seems to be a therapeutic approach able to induce the activation of several pathways related to the neurotrophins release. Exercise, furthermore, reduces the infarct volume in the ischemic brain and ameliorates motor function in animal models increasing astrocyte proliferation, inducing angiogenesis and reducing neuronal apoptosis and oxidative stress. One of the most critical issues is to identify the relationship between neurotrophins and myokines, newly discovered skeletal muscle-derived factors released during and after exercise able to exert several biological functions. Various myokines (e.g., Insulin-Like Growth Factor 1, Irisin) have recently shown their ability to protects against neuronal injury in cerebral ischemia models, suggesting that these substances may influence the degree of neuronal damage in part via inhibiting inflammatory signaling pathways. The aim of this narrative review is to examine the main experimental data available to date on the neuroprotective and anti-ischemic role of regular exercise, analyzing also the possible role played by neurotrophins and myokines.

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Multimodal Sensing in Stroke Motor Rehabilitation

Zhao

Wang

et al. 2023

Advanced Sensor Research

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Applying sensors in biomedical institutions and home‐based stroke rehabilitation is now a global research focus. In this review paper, the relationship between stroke diseases’ physiology mechanism and diverse sensors’ functionalities is detailed explained. The review starts by interpreting how stroke influences motion abilities and then introduces broadly adopted physical training methods. After, the working principles of sensors and their use to objectively provide patients’ body information for stroke rehabilitation status are discussed. The content of the paper aims to not only review the state‐of‐the‐art works of developing sensors for assisting in evaluating stroke patients’ status but also bridging the gap between medical staff and engineers.

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A Review of Exercise-Induced Neuroplasticity in Ischemic Stroke: Pathology and Mechanisms

Cited by 87 publications

References 130 publications

Diabetes, stroke, and neuroresilience: looking beyond hyperglycemia

Diabetes, stroke, and neuroresilience: looking beyond hyperglycemia

Role of Regular Physical Activity in Neuroprotection against Acute Ischemia

Multimodal Sensing in Stroke Motor Rehabilitation

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