Exercise benefits on Alzheimer’s disease: State-of-the-science

Valenzuela, Pedro L.; Castillo‐García, Adrián; Morales, Javier S.; Hampel, Harald; Emanuele, Enzo; Lista, Simone; Lucía, Alejandro

doi:10.1016/j.arr.2020.101108

Cited by 198 publications

(156 citation statements)

References 184 publications

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“…24 Third, using neuroimaging techniques, additional evidence for the impact of physical activity on brain function and structure is reported. 25e27 In this regard, physical activity/exercise might be a good predictor of long-term changes of brain structure, in particular brain volumes, 28 and risk for dementia, in particular for those who average more physical activity than their peers. 29 In addition, physical activity/exercise interventions have an important role in improving several noncognitive outcomes including disability, falls, and neuropsychiatric symptoms in participants affected by dementia.…”

Section: Discussionmentioning

confidence: 99%

Physical Activity and Exercise in Mild Cognitive Impairment and Dementia: An Umbrella Review of Intervention and Observational Studies

Demurtas

Schoene

Torbahn

et al. 2020

Journal of the American Medical Directors Association

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Section: Discussionmentioning

confidence: 99%

Physical Activity and Exercise in Mild Cognitive Impairment and Dementia: An Umbrella Review of Intervention and Observational Studies

Demurtas

Schoene

Torbahn

et al. 2020

Journal of the American Medical Directors Association

130

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“…In addition, exercise may improve insulin resistance, inflammation, and oxidative stress associated with impaired cognition. Furthermore, exercise produces myokines (cathepsin-B, irisin), which stimulate the production of brain-derived neurotrophic factor [71].…”

Section: Physical Inactivitymentioning

confidence: 99%

Nutrition Management in Older Adults with Diabetes: A Review on the Importance of Shifting Prevention Strategies from Metabolic Syndrome to Frailty

et al. 2020

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The increasing prevalence of older adults with diabetes has become a major social burden. Diabetes, frailty, and cognitive dysfunction are closely related to the mechanisms of aging. Insulin resistance, arteriosclerosis, chronic inflammation, oxidative stress, and mitochondrial dysfunction may be common mechanisms shared by frailty and cognitive impairment. Hyperglycemia, hypoglycemia, obesity, vascular factors, physical inactivity, and malnutrition are important risk factors for cognitive impairment and frailty in older adults with diabetes. The impact of nutrients on health outcomes varies with age; thus, shifting diet therapy strategies from the treatment of obesity/metabolic syndrome to frailty prevention may be necessary in patients with diabetes who are over 75 years of age, have frailty or sarcopenia, and experience malnutrition. For the prevention of frailty, optimal energy intake, sufficient protein and vitamin intake, and healthy dietary patterns should be recommended. The treatment of diabetes after middle age should include the awareness of proper glycemic control aimed at extending healthy life expectancy with proper nutrition, exercise, and social connectivity. Nutritional therapy in combination with exercise, optimal glycemic and metabolic control, and social participation/support for frailty prevention can extend healthy life expectancy and maintain quality of life in older adults with diabetes mellitus.

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“…Although no effective cure is yet available for MD, there is a rationale to support that regular physical exercise can be an adjuvant treatment to attenuate some phenotypic manifestations associated with these conditions, notably the decline in cardiorespiratory and muscle fitness that is commonly found in affected individuals (Cejudo et al, 2005;Taivassalo et al, 1996Taivassalo et al, , 1998Taivassalo et al, , 1999Taivassalo et al, , 2001Taivassalo et al, , 2006Adhihetty et al, 2007;Murphy et al, 2008;Jeppesen et al, 2006Jeppesen et al, , 2009Siciliano et al, 2000Siciliano et al, , 2012Bates et al, 2013;Fiuza-Luces et al, 2018a). Beyond its welldocumented fitness benefits for virtually all population groups, regular exercise might also have potential neuroprotective effects including improving central nervous system (CNS) blood flow and cognitive function, and preventing neurodegeneration and cognitive decline (Delezie and Handschin, 2018;Liu-Ambrose et al, 2018;Cabral et al, 2019;Valenzuela et al, 2020). While more research is needed, there is preliminary evidence supporting that exercise training might also attenuate, at least partly, the cerebellar degeneration associated with some diseases, and thus potentially alleviate ataxic symptoms (Aranca et al, 2016;Ayvat et al, 2018;Oliveira et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Exercise Training and Neurodegeneration in Mitochondrial Disorders: Insights From the Harlequin Mouse

et al. 2020

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AimCerebellar neurodegeneration is a main phenotypic manifestation of mitochondrial disorders caused by apoptosis-inducing factor (AIF) deficiency. We assessed the effects of an exercise training intervention at the cerebellum and brain level in a mouse model (Harlequin, Hq) of AIF deficiency.MethodsMale wild-type (WT) and Hq mice were assigned to an exercise (Ex) or control (sedentary [Sed]) group (n = 10–12/group). The intervention (aerobic and resistance exercises) was initiated upon the first symptoms of ataxia in Hq mice (∼3 months on average) and lasted 8 weeks. Histological and biochemical analyses of the cerebellum were performed at the end of the training program to assess indicators of mitochondrial deficiency, neuronal death, oxidative stress and neuroinflammation. In brain homogenates analysis of enzyme activities and levels of the oxidative phosphorylation system, oxidative stress and neuroinflammation were performed.ResultsThe mean age of the mice at the end of the intervention period did not differ between groups: 5.2 ± 0.2 (WT-Sed), 5.2 ± 0.1 (WT-Ex), 5.3 ± 0.1 (Hq-Sed), and 5.3 ± 0.1 months (Hq-Ex) (p = 0.489). A significant group effect was found for most variables indicating cerebellar dysfunction in Hq mice compared with WT mice irrespective of training status. However, exercise intervention did not counteract the negative effects of the disease at the cerebellum level (i.e., no differences for Hq-Ex vs. Hq-Sed). On the contrary, in brain, the activity of complex V was higher in both Hq mice groups in comparison with WT animals (p < 0.001), and post hoc analysis also revealed differences between sedentary and trained Hq mice.ConclusionA combined training program initiated when neurological symptoms and neuron death are already apparent is unlikely to promote neuroprotection in the cerebellum of Hq model of mitochondrial disorders, but it induces higher complex V activity in the brain.

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Exercise benefits on Alzheimer’s disease: State-of-the-science

Cited by 198 publications

References 184 publications

Physical Activity and Exercise in Mild Cognitive Impairment and Dementia: An Umbrella Review of Intervention and Observational Studies

Physical Activity and Exercise in Mild Cognitive Impairment and Dementia: An Umbrella Review of Intervention and Observational Studies

Nutrition Management in Older Adults with Diabetes: A Review on the Importance of Shifting Prevention Strategies from Metabolic Syndrome to Frailty

Exercise Training and Neurodegeneration in Mitochondrial Disorders: Insights From the Harlequin Mouse

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