Endurance exercise training promotes angiogenesis in the brain of chronic/progressive mouse model of Parkinson's Disease

Al-Jarrah, Muhammed; Jamous, Mohammad; Zailaey, Khalid Al; Bweir, Salameh

doi:10.3233/nre-2010-0574

Cited by 63 publications

(24 citation statements)

References 28 publications

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“…Other receptors that are known to be modulate spine loss in the context of DA-depletion, such as the L-type calcium channel may play a role in exercise mediated effects on spine density (Day et al, 2006). Finally, exercise may lead to changes in a number of factors affecting general brain health including the activation of astrocytes or microglia, alterations in the permeability of the blood brain barrier, increased vasculature (angiogenesis), and blood flow, all of which can influence neurotrophic factor expression or delivery and provide an environment promoting spine growth and spine maintenance (Li et al, 2005; Yang et al, 2007; Al-Jarrah et al, 2010; Kawanishi et al, 2010; Bernardi et al, 2013). …”

Section: Discussionmentioning

confidence: 99%

Treadmill exercise reverses dendritic spine loss in direct and indirect striatal medium spiny neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease

Toy

Petzinger

Leyshon

et al. 2014

Neurobiology of Disease

149

117

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Exercise has been shown to be beneficial for Parkinson’s disease (PD). A major interest in our lab has been to investigate how exercise modulates basal ganglia function and modifies disease progression. Dopamine (DA) depletion leads to loss of dendritic spines within the caudate nucleus and putamen (striatum) in PD and its animal models and contributes to motor impairments. Striatal medium spiny neurons (MSNs) can be delineated into two populations, the dopamine D1 receptor (DA-D1R)-containing MSNs of the direct pathway and dopamine D2 receptor (DA-D2R)-containing MSNs of the indirect pathway. There is evidence to suggest that the DA-D2R-indirect pathway MSNs may be preferentially affected after DA-depletion with a predominate loss of dendritic spine density when compared to MSNs of the DA-D1R-direct pathway in rodents; however, others have reported that both pathways may be affected in primates. The purpose of this study was to investigate the effects of intensive exercise on dendritic spine density and arborization in MSNs of these two pathways in the MPTP mouse model of PD. We found that MPTP led to a decrease in dendritic spine density in both DA-D1R-and DA-D2R-containing MSNs and 30 days of intensive treadmill exercise led to increased dendritic spine density and arborization in MSNs of both pathways. In addition, exercise increased the expression of synaptic proteins PSD-95 and synaptophysin. Taken together these findings support the potential effect of exercise in modifying synaptic connectivity within the DA-depleted striatum and in modifying disease progression in individuals with PD.

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Section: Discussionmentioning

confidence: 99%

Treadmill exercise reverses dendritic spine loss in direct and indirect striatal medium spiny neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease

Toy

Petzinger

Leyshon

et al. 2014

Neurobiology of Disease

149

117

View full text Add to dashboard Cite

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“…Furthermore, 4 weeks of running exercise prevented LPS-induced loss of DA neurons and motor dysfunction (Wu et al , 2011). Not surprisingly, treadmill exercise also promoted angiogenesis in the striatum of MPTP-treated mice (Al-Jarrah et al , 2010). It has been suggested that exercise may act to mitigate cortically-driven hyper-excitability in the basal ganglia (Gerecke et al , 2010; Petzinger et al , 2010).…”

Section: 0 Preconditioning Stimulimentioning

confidence: 99%

Preconditioning provides neuroprotection in models of CNS disease: Paradigms and clinical significance

Stetler

Leak

Gan

et al. 2014

Progress in Neurobiology

167

140

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Preconditioning is a phenomenon in which brief episodes of a sublethal insult induce robust protection against subsequent lethal injuries. Preconditioning has been observed in multiple organisms and can occur in the brain as well as other tissues. Extensive animal studies suggest that the brain can be preconditioned to resist acute injuries, such as ischemic stroke, neonatal hypoxia/ischemia, trauma, and agents that are used in models of neurodegenerative diseases, such as Parkinson’s disease and Alzheimer’s disease. Effective preconditioning stimuli are numerous and diverse, ranging from transient ischemia, hypoxia, hyperbaric oxygen, hypothermia and hyperthermia, to exposure to neurotoxins and pharmacological agents. The phenomenon of “cross-tolerance,” in which a sublethal stress protects against a different type of injury, suggests that different preconditioning stimuli may confer protection against a wide range of injuries. Research conducted over the past few decades indicates that brain preconditioning is complex, involving multiple effectors such as metabolic inhibition, activation of extra- and intracellular defense mechanisms, a shift in the neuronal excitatory/inhibitory balance, and reduction in inflammatory sequelae. An improved understanding of brain preconditioning should help us identify innovative therapeutic strategies that prevent or at least reduce neuronal damage in susceptible patients. In this review, we focus on the experimental evidence of preconditioning in the brain and systematically survey the models used to develop paradigms for neuroprotection, and then discuss the clinical potential of brain preconditioning. In a subsequent components of this two-part series, we will discuss the cellular and molecular events that are likely to underlie these phenomena.

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“…Among these activities, physical exercise has gained prominence due to its neuroprotective effects against dementia and other neurodegenerative diseases (Phillips et al, 2014;Vecchio et al, 2018). For instance, research has shown that regular exercise promoted hippocampal neurogenesis (Erickson et al, , 2011, local increases on the concentration of neurotrophins (such as BDNF; Leckie et al, 2014;Håkansson et al, 2017), neuroplasticity (Erickson and Kramer, 2009;Voss et al, 2013a,b;Erickson et al, 2014), angiogenesis (Bloor, 2005;Al-Jarrah et al, 2010), and adaptive changes in CBF (Dupuy et al, 2015;Jennings et al, 2015). Electrophysiological and neuroimaging studies have provided evidence that cardiorespiratory fitness is positively correlated with brain function, particularly in brain regions associated with the CAN, which has shown increased neuroplasticity after physical exercise interventions, improving both cardiovascular and cognitive control (Gomez-Pinilla and Hillman, 2013).…”

Section: Introductionmentioning

confidence: 99%

A Neurovisceral Integrative Study on Cognition, Heart Rate Variability, and Fitness in the Elderly

Matos

Vido

Garcia

et al. 2020

Front. Aging Neurosci.

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The association between physical fitness and cognitive performance has been widely investigated in the literature. However, the neurophysiological mechanisms underlying this relationship are not yet clear. Here, we aim to evaluate the interactions between executive function measures, heart rate variability (HRV), and physical fitness in the context of the neurovisceral integration (NVI) theory. Twenty-eight healthy elderly subjects (>60 years) were submitted to evaluation of executive performance with three computerized tests: the N-back test measured working memory capacity, the Stroop Color test evaluated inhibitory control and selective attention, and the Wisconsin Card Sorting Test (WCST) evaluated abstract reasoning and cognitive flexibility. We also used the Physical Testing Battery for the Elderly to measure aerobic capacity, dynamic balance, upper body flexibility, and handgrip strength. Our results confirm the relationship between executive function and physical fitness, particularly between working memory, cardiorespiratory fitness, and dynamic balance. We also demonstrate an association between executive performance and HRV in older people, corroborating previous results from other groups obtained in young adults. However, our regression models did not indicate that HRV mediates the relationship between cognition and physical fitness in the elderly, suggesting that age-related degeneration of autonomic control can affect aspects of NVI in this population.

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Endurance exercise training promotes angiogenesis in the brain of chronic/progressive mouse model of Parkinson's Disease

Cited by 63 publications

References 28 publications

Treadmill exercise reverses dendritic spine loss in direct and indirect striatal medium spiny neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease

Treadmill exercise reverses dendritic spine loss in direct and indirect striatal medium spiny neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease

Preconditioning provides neuroprotection in models of CNS disease: Paradigms and clinical significance

A Neurovisceral Integrative Study on Cognition, Heart Rate Variability, and Fitness in the Elderly

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