Exercise as Medicine for the Treatment of Brain Dysfunction: Evidence for Cortical Stroke, Cerebellar Ataxia, and Parkinson’s Disease

This review addresses the role of exercise as an intervention for treating neurological disease. It focuses on three major neurological diseases that either present in acute or neurodegenerative forms—Parkinson’s disease, cerebellar ataxia, and cortical stroke. Each of the diseases affects primarily different brain structures, namely the basal ganglia, the cerebellum, and the cerebrum. These structures are all known to be involved in motor control, and the dysfunction of each structure leads to distinct movement deficits. The review summarizes current knowledge on how exercise can aid rehabilitation or therapeutic efforts. In addition, it addresses the role of robotic devices in enhancing available therapies by reviewing how robot-aided therapies may promote the recovery for stroke survivors. It highlights recent scientific evidence in support of exercise as a treatment for brain dysfunction, but also outlines the still open challenges for unequivocally demonstrating the benefits of exercise.

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Neurotoxic and Neuroprotective Role of Exosomes in Parkinson’s Disease

Current Pharmaceutical Design ◽

10.2174/1381612825666191113103537 ◽

2020 ◽

Vol 25 (42) ◽

pp. 4510-4522 ◽

Cited By ~ 5

Author(s):

Biancamaria Longoni ◽

Irene Fasciani ◽

Shivakumar Kolachalam ◽

Ilaria Pietrantoni ◽

Francesco Marampon ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Potential Role ◽

Current Knowledge ◽

Biological Fluids ◽

Cell Communication ◽

Target Cells ◽

Cellular Debris ◽

The Brain

: Exosomes are extracellular vesicles produced by eukaryotic cells that are also found in most biological fluids and tissues. While they were initially thought to act as compartments for removal of cellular debris, they are now recognized as important tools for cell-to-cell communication and for the transfer of pathogens between the cells. They have attracted particular interest in neurodegenerative diseases for their potential role in transferring prion-like proteins between neurons, and in Parkinson’s disease (PD), they have been shown to spread oligomers of α-synuclein in the brain accelerating the progression of this pathology. A potential neuroprotective role of exosomes has also been equally proposed in PD as they could limit the toxicity of α-synuclein by clearing them out of the cells. Exosomes have also attracted considerable attention for use as drug vehicles. Being nonimmunogenic in nature, they provide an unprecedented opportunity to enhance the delivery of incorporated drugs to target cells. In this review, we discuss current knowledge about the potential neurotoxic and neuroprotective role of exosomes and their potential application as drug delivery systems in PD.

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Hypoxia, Acidification and Inflammation: Partners in Crime in Parkinson’s Disease Pathogenesis?

Immuno ◽

10.3390/immuno1020006 ◽

2021 ◽

Vol 1 (2) ◽

pp. 78-90

Author(s):

Johannes Burtscher ◽

Grégoire P. Millet

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Neurodegenerative Diseases ◽

Current Knowledge ◽

Cell Types ◽

Brain Cell ◽

Special Focus ◽

Molecular Alterations ◽

Research Fields

Like in other neurodegenerative diseases, protein aggregation, mitochondrial dysfunction, oxidative stress and neuroinflammation are hallmarks of Parkinson’s disease (PD). Differentiating characteristics of PD include the central role of α-synuclein in the aggregation pathology, a distinct vulnerability of the striato-nigral system with the related motor symptoms, as well as specific mitochondrial deficits. Which molecular alterations cause neurodegeneration and drive PD pathogenesis is poorly understood. Here, we summarize evidence of the involvement of three interdependent factors in PD and suggest that their interplay is likely a trigger and/or aggravator of PD-related neurodegeneration: hypoxia, acidification and inflammation. We aim to integrate the existing knowledge on the well-established role of inflammation and immunity, the emerging interest in the contribution of hypoxic insults and the rather neglected effects of brain acidification in PD pathogenesis. Their tight association as an important aspect of the disease merits detailed investigation. Consequences of related injuries are discussed in the context of aging and the interaction of different brain cell types, in particular with regard to potential consequences on the vulnerability of dopaminergic neurons in the substantia nigra. A special focus is put on the identification of current knowledge gaps and we emphasize the importance of related insights from other research fields, such as cancer research and immunometabolism, for neurodegeneration research. The highlighted interplay of hypoxia, acidification and inflammation is likely also of relevance for other neurodegenerative diseases, despite disease-specific biochemical and metabolic alterations.

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Environment, Genetics and Idiopathic Parkinson's Disease

Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques ◽

10.1017/s0317167100031334 ◽

1991 ◽

Vol 18 (1) ◽

pp. 70-76 ◽

Cited By ~ 16

Author(s):

Judes Poirier ◽

Sandra Kogan ◽

Serge Gauthier

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Current Knowledge ◽

Idiopathic Parkinson’S Disease ◽

Parkinsonian Syndromes ◽

Idiopathic Parkinson's Disease ◽

Radical Generation ◽

Review Current ◽

Aging Factor

ABSTRACT:Since Idiopathic Parkinson's disease (IPD) was first described more than 170 years ago, there have been major advances in the understanding of the etiology of the disease as well as in its treatment. This article will review current knowledge concerning the role of the environment, genetic hypotheses and the aging factor in the etiology of IPD and proposes a complex interaction involving all these factors. Hypotheses regarding mitochondrial inhibition and free radical generation in IPD are discussed in relation to the mechanism of action of neurotoxins known to produce parkinsonian syndromes.

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Functional Role of the Cerebellum in Parkinson Disease: A PET Study

Neurology ◽

10.1212/wnl.0000000000012036 ◽

2021 ◽

pp. 10.1212/WNL.0000000000012036

Author(s):

Audrey Riou ◽

Jean-François Houvenaghel ◽

Thibaut Dondaine ◽

Sophie Drapier ◽

Paul Sauleau ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Multiple Testing ◽

Principal Component ◽

Brain Structures ◽

Cognitive Domain ◽

Metabolic Imaging ◽

Crus I ◽

The Right

OBJECTIVES:To test for cerebellar involvement in motor and nonmotor impairments in Parkinson’s disease (PD), and to determine patterns of metabolic correlations with supratentorial brain structures, we correlated clinical motor, cognitive and psychiatric scales with cerebellar metabolism.METHODS:We included 90 patients with PD. Motor, cognitive and psychiatric domains were assessed, and resting-state 18FDG-PET metabolic imaging was performed. The motor, cognitive and psychiatric scores were entered separately in a principal component analysis. We looked for correlations between these three principal components and cerebellar metabolism. Furthermore, we extracted the mean glucose metabolism value for each significant cerebellar cluster and looked for patterns of cerebrum-cerebellum metabolic correlations.RESULTS:Severity of impairment was correlated with increased metabolism in the anterior lobes and vermis (motor domain), and the right Crus I, Crus II, and declive (cognitive domain), and the right Crus I and Crus II (psychiatric domain). There were no results surviving multiple testing corrections regarding the psychiatric domain. Moreover, we found distributed and overlapping - but not identical- patterns of metabolic correlations for motor and cognitive domains. Specific supratentorial structures (cortical structures, basal ganglia, and thalamus) were strongly correlated with each of the cerebellar clusters.CONCLUSIONS:These results confirm the role of the cerebellum in nonmotor domains of Parkinson’s disease, with differential but overlapping patterns of metabolic correlations suggesting the involvement of cerebello-thalamo-striatal-cortical loops.

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