Exercise‐Induced Protection Against Aging and Neurodegenerative Diseases

Marques‐Aleixo, Inês; Santos‐Alves, Estela; Moreira, Paula I.; Oliveira, Paulo J.; Magalhães, José; Ascensão, António

doi:10.1002/9781118840634.ch26

Cited by 2 publications

(2 citation statements)

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“…As mentioned, the proposed efficacy of chronical forms of PE at antagonizing the harmful consequences of aging and the associated NDD seems to be related, at least partially, to the powerful effects in the boosting of antioxidant systems and the downregulation of the enhanced ROS generation characterizing these physiopathological conditions. PE seems to mitigate the levels of oxidative stress, and improve the deleterious consequences on mitochondrial biogenesis and OXPHOS activity commonly occurring in the different NDD (17,113,118). Despite mitochondrial-redox changes are accepted as crucial beneficial features of an exercise-related protective phenotype that are able to mitigate the development and symptoms of NDD (Fig.…”

Section: Does Exercise Antagonize Age-related Neurodegenerative Diseases Through Redoxmediated Mechanisms?mentioning

confidence: 99%

“…In contrast to the acute severe single exercise bouts, the ability of the regular exercise to induce more resistant phenotypes against harmful stress conditions, such as age-related NDD have been widely accepted (118). Among distinct neuronal sources of ROS production, mitochondria have been considered as one of the most relevant (7), being also important potential target substructures for exercise-induced adaptation in the context of aging and NDD.…”

Section: Does Exercise Antagonize Age-related Neurodegenerative Diseases Through Redoxmediated Mechanisms?mentioning

confidence: 99%

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Preventive and Therapeutic Potential of Physical Exercise in Neurodegenerative Diseases

Marques‐Aleixo

Beleza

Sampaio

et al. 2021

Antioxidants & Redox Signaling

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The prevalence and incidence of age-related neurodegenerative diseases (NDD), tend to increase along with the enhanced average of the world life expectancy. NDD are a major cause of morbidity and disability, affecting the healthcare, social and economic systems with a significant impact. Critical Issues and Recent Advances:Despite the worldwide burden of NDD and the ongoing research efforts to increase the underlying molecular mechanisms involved in NDD pathophysiologies, pharmacological therapies have been presenting merely narrow benefits.On the other hand, absent of detrimental side effects but growing merits, regular physical exercise has been considered a prone pleiotropic non-pharmacological alternative able to modulate brain structure and function, thereby stimulating a healthier and "fitness" neurological phenotype.Future Directions: This review summarizes the state-of-the-art of some peripheral and central-related mechanisms that underlie the impact of physical exercise on brain plasticity as well as its relevance for the prevention and/or treatment of NDD. Nevertheless, further studies are needed in order to better clarify the molecular signaling pathways associated with muscle contractions-related myokines release and its plausible positive effects in the brain.

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Section: Does Exercise Antagonize Age-related Neurodegenerative Diseases Through Redoxmediated Mechanisms?mentioning

confidence: 99%

Section: Does Exercise Antagonize Age-related Neurodegenerative Diseases Through Redoxmediated Mechanisms?mentioning

confidence: 99%

Preventive and Therapeutic Potential of Physical Exercise in Neurodegenerative Diseases

Marques‐Aleixo

Beleza

Sampaio

et al. 2021

Antioxidants & Redox Signaling

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Mixed Models Quantify Annual Volume Change; Linear Regression Determines Thalamic Volume as the Best Subcortical Structure Volume Predictor in Alzheimer’s Disease and Aging

Leger¹,

Herbert

Stevens

et al. 2022

Preprint

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Background: Thalamus-hippocampus-putamen and thalamus-cerebellar interconnections are dense. The extent this connectivity is paralleled by each structure's volume impact on another is unquantified in Alzheimer's disease (AD). Mixed model quantification of annual volume change in AD is scarce and absent inclusive of the cerebellum, hippocampus, putamen and lateral ventricles and thalamus. Among these structures, autopsy evidence of early-stage AD seems largely but not entirely restricted to the hippocampus and thalamus. Objective: Variation in annual volume related to time and baseline age was assessed for the hippocampus, putamen, cerebellum, lateral ventricles and thalamus. Which subcortical structure's volume had the largest explanatory effect of volume variation in other subcortical structures was also determined. Method: The intraclass correlation coefficient was used to assess test-retest reliability of structure automated segmentation. Linear regression (N = 45) determined which structure's volume most impacted volume of other structures. Finally, mixed models (N = 36; 108 data points) quantified annual structure volume change from baseline to 24-months. Results: High test-retest reliability was indicated by a mean ICC score of .989 (SD = .012). Thalamic volume consistently had the greatest explanatory effect of hippocampal, putamen, cerebellar and lateral ventricular volume. The group variable proxy for AD significantly contributed to the best-fitting hippocampal linear regression model, hippocampal and thalamic longitudinal mixed models, and approached significance in the longitudinal lateral ventricular mixed model. Mixed models determined time (1 year) had a negative effect on hippocampal, cerebellar and thalamic volume, no effect on putamen volume, and a positive effect on lateral ventricular volume. Baseline age had a negative effect on hippocampal and thalamic volume, no effect on cerebellar or putamen volume and a positive effect on lateral ventricular volume. Interpretation: Linear regression determined thalamic volume as a virtual centralized index of hippocampal, cerebellar, putamen, and lateral ventricular volume. Relative to linear regression, longitudinal mixed models had greater sensitivity to detect contribution of early AD, or potential AD pathology (MCI), via the group variable not just to volume reduction in the hippocampus but also in the thalamus.

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Exercise‐Induced Protection Against Aging and Neurodegenerative Diseases

Cited by 2 publications

References 109 publications

Preventive and Therapeutic Potential of Physical Exercise in Neurodegenerative Diseases

Preventive and Therapeutic Potential of Physical Exercise in Neurodegenerative Diseases

Mixed Models Quantify Annual Volume Change; Linear Regression Determines Thalamic Volume as the Best Subcortical Structure Volume Predictor in Alzheimer’s Disease and Aging

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