Possible Neuroprotective Mechanisms of Physical Exercise in Neurodegeneration

Mahalakshmi, B.; Maurya, Nancy; Lee, Shin-Da; Velmurugan, Bharath Kumar

doi:10.3390/ijms21165895

Cited by 163 publications

(113 citation statements)

References 122 publications

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“…It is for these patterns in changes according to genotype, age and exercise that we have chosen the tibialis anterior muscle to measure the expression of COL1A1 and MT-CO1; which allowed us to make a correlation between the genotype-dependent changes in muscle weight and power and the corresponding changes in the expression of these two proteins, depending on SPARC expression. Additionally, the decrease in brain weight percentage with ageing correlates with age-related neurodegeneration and related diseases [87,88], which are improved by exercise [89][90][91] and that, also, correlate with our data, showing an increase (trend) in the brain weight percentage with exercise.…”

Section: Body and Tissue Weights (Table 3)supporting

confidence: 89%

Exercise Training of Secreted Protein Acidic and Rich in Cysteine (Sparc) KO Mice Suggests That Exercise-Induced Muscle Phenotype Changes Are SPARC-Dependent

et al. 2020

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We previously identified secreted protein acidic and rich in cysteine (Sparc) as an exercise-induced gene in young and elderly individuals. Via this animal experiment, we aim to identify selected implications of SPARC mainly within the muscle in the contexts of exercise. Mice were divided into eight groups based on three variables (age, genotype and exercise): Old (O) or young (Y) × Sparc knock-out (KO) or wild-type (WT) × sedentary (Sed) or exercise (Ex). The exercised groups were trained for 12 weeks at the lactate threshold (LT) speed (including 4 weeks of adaptation period) and all mice were sacrificed afterwards. Body and selected tissues were weighed, and lactate levels in different conditions measured. Expression of skeletal muscle (SM) collagen type I alpha 1 chain (COL1A1) and mitochondrially encoded cytochrome c oxidase I (MT-CO1) in addition to SM strength (grip power) were also measured. Ageing increased the body and white adipose tissue (WAT) weights but decreased SM weight percentage (to body weight) and MT-CO1 expression (in WT). Exercise increased SM COL1A1 in WT mice and MT-CO1 expression, as well as weight percentage of the tibialis anterior muscle, and decreased WAT weight (trend). Compared to WT mice, Sparc KO mice had lower body, muscle and WAT weights, with a decrease in SM MT-CO1 and COL1A1 expression with no genotype effect on lactate levels in all our blood lactate measures. Sparc KO effects on body composition, adiposity and metabolic patterns are toward a reduced WAT and body weight, but with a negative metabolic and functional phenotype of SM. Whereas such negative effects on SM are worsened with ageing, they are relatively improved by exercise. Importantly, our data suggest that the exercise-induced changes in the SM phenotype, in terms of increased performance (metabolic, strength and development), including lactate-induced changes, are SPARC-dependent.

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Section: Body and Tissue Weights (Table 3)supporting

confidence: 89%

Exercise Training of Secreted Protein Acidic and Rich in Cysteine (Sparc) KO Mice Suggests That Exercise-Induced Muscle Phenotype Changes Are SPARC-Dependent

et al. 2020

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“…Physical exercise affects many mechanisms at the cellular and molecular levels. It improves the production of neurotrophic factors, neurotransmitters, and hormones and promotes neuronal survival and neuroplasticity (Mahalakshmi et al, 2020). However, evidence that short-term, singlecomponent exercise interventions promote cognitive function and prevent cognitive decline or dementia in older adults is largely insufficient (Brasure et al, 2018).…”

Section: Role Of Non-pharmacological Interventionsmentioning

confidence: 99%

Overview of Meta-Analyses of Five Non-pharmacological Interventions for Alzheimer's Disease

Wang

Pei

Zhan

et al. 2020

Front. Aging Neurosci.

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Background: Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive memory deficits, cognitive decline, and spatial disorientation. Non-pharmacological interventions to treat AD have been reported in many meta-analyses (MAs), but robust conclusions have not been made because of variations in the scope, quality, and findings of these reviews.Objective: This work aimed to review existing MAs to provide an overview of existing evidence on the effects of five non-pharmacological interventions in AD patients on three outcomes: Mini-Mental State Examination (MMSE), activities of daily living (ADL), and Alzheimer's Disease Assessment Scale-cognitive section (ADAS-cog).Methods: The databases PubMed, Cochrane Library, Embase, and Web of Science were searched to collect MAs of non-pharmacological interventions for AD. Two reviewers independently conducted literature screening, data extraction, and quality assessment. We assessed the quality of MAs with the Measurement Tool to Assess Systematic Reviews (AMSTAR) 2 and assessed the evidence quality for significant outcomes using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system.Results: We found 10 eligible MAs, which included between three (133 patients) and 15 randomized trials (1,217 patients), and five non-pharmacological interventions, namely, acupuncture therapy (40%), exercise intervention (30%), music therapy (10%), cognitive intervention (10%), and repetitive transcranial magnetic stimulation (rTMS) (10%). All the included MAs were critically low to low quality by AMSTAR 2. Acupuncture therapy and exercise intervention showed the preliminary potential to improve ADL and MMSE. rTMS and acupuncture therapy show benefits in decreasing ADAS-cog, and there were some evidence of improved MMSE with cognitive intervention. All these outcomes scored very low quality to moderate quality of evidence on the GRADE system.Conclusions: Non-pharmacological therapy shows promise for the treatment of AD, but there is still a lack of high-quality evidence. In the future, the quality of the original research needs to be improved, and strictly designed MAs should be carried out following methodological requirements.

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“…For instance, the neuroprotective mechanism of flavonoids, is thought to proceed via multiple mechanisms including suppression of lipid peroxidation, inhibition of inflammatory mediators, modulation of gene expressions and improvement of the activity of antioxidant enzymes [ 18 ]. Combined with regular physical exercise [ 20 ], increasing the intake of fruits containing bioactive antioxidants is suggested to delay or inhibit neurodegeneration and correlated diseases [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

New Neuroprotective Effect of Lemon IntegroPectin on Neuronal Cellular Model

et al. 2021

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Lemon IntegroPectin obtained via hydrodynamic cavitation of organic lemon processing waste in water shows significant neuroprotective activity in vitro, as first reported in this study investigating the effects of both lemon IntegroPectin and commercial citrus pectin on cell viability, cell morphology, reactive oxygen species (ROS) production, and mitochondria perturbation induced by treatment of neuronal SH-SY5Y human cells with H2O2. Mediated by ROS, including H2O2 and its derivatives, oxidative stress alters numerous cellular processes, such as mitochondrial regulation and cell signaling, propagating cellular injury that leads to incurable neurodegenerative diseases. These results, and the absence of toxicity of this new pectic substance rich in adsorbed flavonoids and terpenes, suggest further studies to investigate its activity in preventing, retarding, or even curing neurological diseases.

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Possible Neuroprotective Mechanisms of Physical Exercise in Neurodegeneration

Cited by 163 publications

References 122 publications

Exercise Training of Secreted Protein Acidic and Rich in Cysteine (Sparc) KO Mice Suggests That Exercise-Induced Muscle Phenotype Changes Are SPARC-Dependent

Exercise Training of Secreted Protein Acidic and Rich in Cysteine (Sparc) KO Mice Suggests That Exercise-Induced Muscle Phenotype Changes Are SPARC-Dependent

Overview of Meta-Analyses of Five Non-pharmacological Interventions for Alzheimer's Disease

New Neuroprotective Effect of Lemon IntegroPectin on Neuronal Cellular Model

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