Protective effects of different exercise modalities in an Alzheimer’s disease-like model

Özbeyli, Dilek; Sarı, Gülce; Özkan, Naziye; Karademir, Betül; Yüksel, Meral; Kaya, Özlem; Çakır, Özgür Kasımay

doi:10.1016/j.bbr.2017.03.044

Cited by 43 publications

(15 citation statements)

References 73 publications

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“…Voss et al [76] was the first study that demonstrated the existence of exercise-induced functional plasticity in large-scale brain systems in the aging brain. Analogous results were found by Ozbeyi et al [82] who compared varying exercise models (aerobic, resistance, combined: aerobic + resistance), and noted that exercise may have protective effects in the development stage of AD by improving the antioxidant system and brain plasticity.…”

Section: Mechanistic Action Of Pa On Adsupporting

confidence: 80%

Physical Activity and Alzheimer’s Disease: A Narrative Review

et al. 2019

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Although age is a dominant risk factor for Alzheimer’s disease (AD), epidemiological studies have shown that physical activity may significantly decrease age-related risks for AD, and indeed mitigate the impact in existing diagnosis. The aim of this study was to perform a narrative review on the preventative, and mitigating, effects of physical activity on AD onset, including genetic factors, mechanism of action and physical activity typology. In this article, we conducted a narrative review of the influence physical activity and exercise have on AD, utilising key terms related to AD, physical activity, mechanism and prevention, searching the online databases; Web of Science, PubMed and Google Scholar, and, subsequently, discuss possible mechanisms of this action. On the basis of this review, it is evident that physical activity and exercise may be incorporated in AD, notwithstanding, a greater number of high-quality randomised controlled trials are needed, moreover, physical activity typology must be acutely considered, primarily due to a dearth of research on the efficacy of physical activity types other than aerobic.

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Section: Mechanistic Action Of Pa On Adsupporting

confidence: 80%

Physical Activity and Alzheimer’s Disease: A Narrative Review

et al. 2019

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“…Outside of direct modulation of important cellular cascades such as those targeted in the present work, circulating IGF-1 levels have been implicated in the clearance of β-amyloid. In animal models, higher circulating IGF-1 levels have been associated with increased mobilization of clearing proteins-such as albumin and transthyretin-along with lower amyloid deposition and increased release of intracellular amyloid that may ultimately translate to decreased amyloid burden [39,40]. Thus, exercise modulation of hippocampal and circulating IGF-1 may play other important ancillary roles in preventing accretion of β-amyloid oligomers.…”

Section: Discussionmentioning

confidence: 99%

“…Importantly, this finding closely parallels one of only several reports that β-amyloid levels were regulated by RT in AD. For example, Özbeyli et al found a significant increase in hippocampal IGF-1 expression in conjunction with a decrease in β-amyloid following six weeks of ladder climbing in an AD rodent model [40]. Perhaps the reduction in β-amyloid load in RT represents a complementary adaptive response driven by the high force output and intermittent periods of rest.…”

Section: Discussionmentioning

confidence: 99%

Hippocampal Growth Factor and Myokine Cathepsin B Expression following Aerobic and Resistance Training in 3xTg-AD Mice

Pena

Paez

Johnson

et al. 2020

International Journal of Chronic Diseases

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Aerobic training (AT) can support brain health in Alzheimer’s disease (AD); however, the role of resistance training (RT) in AD is not well established. Aside from direct effects on the brain, exercise may also regulate brain function through secretion of muscle-derived myokines. Aims. This study examined the effects of AT and RT on hippocampal BDNF and IGF-1 signaling, β-amyloid expression, and myokine cathepsin B in the triple transgenic (3xTg-AD) model of AD. 3xTg-AD mice were assigned to one of the following groups: sedentary (Tg), aerobic trained (Tg+AT, 9 wks treadmill running), or resistance trained (Tg+RT, 9 wks weighted ladder climbing) (n=10/group). Rotarod latency and strength were assessed pre- and posttraining. Hippocampus and skeletal muscle were collected after training and analyzed by high-resolution respirometry, ELISA, and immunoblotting. Tg+RT showed greater grip strength than Tg and Tg+AT at posttraining (p<0.01). Only Tg+AT improved rotarod peak latency (p<0.01). Hippocampal IGF-1 concentration was ~15% greater in Tg+AT and Tg+RT compared to Tg (p<0.05); however, downstream signals of p-IGF-1R, p-Akt, p-MAPK, and p-GSK3β were not altered. Cathepsin B, hippocampal p-CREB and BDNF, and hippocampal mitochondrial respiration were not affected by AT or RT. β-Amyloid was ~30% lower in Tg+RT compared to Tg (p<0.05). This data suggests that regular resistance training reduces β-amyloid in the hippocampus concurrent with increased concentrations of IGF-1. Both types of training offered distinct benefits, either by improving physical function or by modifying signals in the hippocampus. Therefore, inclusion of both training modalities may address central defects, as well as peripheral comorbidities in AD.

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“…Individuals who practice regular physical activity have a 30-40% reduced risk of AD development in comparison to physically inactive individuals (Aarsland et al, 2010;Williams et al, 2010). Several studies have demonstrated that aerobic PE, such as running or swimming exercise, improved memory in rats with Aβ-induced AD (Kim et al, 2014;Özbeyli et al, 2017;Prado Lima et al, 2018;Rossi Dare et al, 2019). Exercise-induced factors, including neurogenesis, synaptic plasticity, and increased cerebral blood flow, seem to promote beneficial effects on the brain (Tari et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

The Reversal of Memory Deficits in an Alzheimer’s Disease Model Using Physical and Cognitive Exercise

Daré

Garcia

Soares

et al. 2020

Front. Behav. Neurosci.

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Alzheimer's disease (AD) is the leading cause of dementia in the world, accounting for 50-75% of cases. Currently, there is limited treatment for AD. The current pharmacological therapy minimizes symptom progression but does not reverse brain damage. Studies focused on nonpharmacological treatment for AD have been developed to act on brain plasticity and minimize the neurotoxicity caused by the amyloid-beta (Aβ) peptide. Using a neurotoxicity model induced by Aβ in rats, the present study shows that physical (PE) and cognitive exercise (CE) reverse recognition memory deficits (with a prominent effect of long-term object recognition memory), decrease hippocampal lipid peroxidation, restore the acetylcholinesterase activity altered by Aβ neurotoxicity, and seems to reverse, at least partially, hippocampal tissue disorganization.

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Protective effects of different exercise modalities in an Alzheimer’s disease-like model

Cited by 43 publications

References 73 publications

Physical Activity and Alzheimer’s Disease: A Narrative Review

Physical Activity and Alzheimer’s Disease: A Narrative Review

Hippocampal Growth Factor and Myokine Cathepsin B Expression following Aerobic and Resistance Training in 3xTg-AD Mice

The Reversal of Memory Deficits in an Alzheimer’s Disease Model Using Physical and Cognitive Exercise

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