Harnessing the effects of endurance exercise to optimize cognitive health: Fundamental insights from Dr. Mark P. Mattson

Jachim, Sarah K.; Sakamoto, Ayumi; Zhang, Xu; Pearsall, Vesselina M.; Schafer, Marissa J.; LeBrasseur, Nathan K.

doi:10.1016/j.arr.2020.101147

Cited by 9 publications

(5 citation statements)

References 85 publications

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“…Cleavage of FNDC5 results in the formation of irisin. Although the roles of FNDC5/irisin in metabolic disorders have been documented, it is widely thought that these proteins have various functions in the central nervous system (CNS) [ 11 , 15 , 16 ]. In this respect, Hashemi [ 17 ] et al found that FNDC5 knockdown in neuroblasts could impair their differentiation into mature neurons, suggesting a critical role of FNDC5 in neuronal development.…”

Section: Introductionmentioning

confidence: 99%

FNDC5 prevents oxidative stress and neuronal apoptosis after traumatic brain injury through SIRT3-dependent regulation of mitochondrial quality control

Ge,

Wu,

Cai

et al. 2024

Cell Death Dis

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Mitochondrial dysfunction and oxidative stress are important mechanisms for secondary injury after traumatic brain injury (TBI), which result in progressive pathophysiological exacerbation. Although the Fibronectin type III domain-containing 5 (FNDC5) was reported to repress oxidative stress by retaining mitochondrial biogenesis and dynamics, its possible role in the secondary injury after TBI remain obscure. In present study, we observed that the level of serum irisin (the cleavage product of FNDC5) significantly correlated with the neurological outcomes of TBI patients. Knockout of FNDC5 increased the lesion volume and exacerbated apoptosis and neurological deficits after TBI in mice, while FNDC5 overexpression yielded a neuroprotective effect. Moreover, FNDC5 deficiency disrupted mitochondrial dynamics and function. Activation of Sirtuin 3 (SIRT3) alleviated FNDC5 deficiency-induced disruption of mitochondrial dynamics and bioenergetics. In neuron-specific SIRT3 knockout mice, FNDC5 failed to attenuate TBI-induced mitochondrial damage and brain injuries. Mechanically, FNDC5 deficiency led to reduced SIRT3 expression via enhanced ubiquitin degradation of transcription factor Nuclear factor erythroid 2-related factor 2 (NRF2), which contributed to the hyperacetylation and inactivation of key regulatory proteins of mitochondrial dynamics and function, including OPA1 and SOD2. Finally, engineered RVG29-conjugated nanoparticles were generated to selectively and efficiently deliver irisin to the brain of mice, which yielded a satisfactory curative effect against TBI. In conclusion, FNDC5/irisin exerts a protective role against acute brain injury by promoting SIRT3-dependent mitochondrial quality control and thus represents a potential target for neuroprotection after TBI.

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Section: Introductionmentioning

confidence: 99%

FNDC5 prevents oxidative stress and neuronal apoptosis after traumatic brain injury through SIRT3-dependent regulation of mitochondrial quality control

Ge,

Wu,

Cai

et al. 2024

Cell Death Dis

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“…PE also stimulated the ketone body D-β-hydroxybutyrate and cathepsin B to activate BDNF expression. Also, serotonin (Pietrelli et al, 2018) and several growth factors, including insulin growth factor-1 and vascular endothelial growth factor, were also induced by PE and exerted synergistic effects with BDNF in terms of neuroplasticity and neuroprotection (Jachim et al, 2020). Finally, neuroinflammation increases with aging and contributes to cognition decline, whereas PE was shown to attenuate this process (Huang et al, 2021).…”

Section: Discussionmentioning

confidence: 97%

Physical exercise frequency and cognition: a multicenter cross-sectional cohort study

Wen,

Gan,

Huang

et al. 2024

Front. Aging Neurosci.

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Background and aimsDementia imposes a heavy burden on society and families, therefore, effective drug treatments, exploring and preventing factors associated with dementia, are paramount. To provide reference points for the best frequency of physical exercise (physical exercise), we investigated the association between frequency of PE and cognition in Chinese old adults.Methods16,181 Chinese participants aged 65 years or older were included in this study. Associations between PE and cognition were estimated multivariate logistic and linear regression analyses. Associations were further investigated across dementia subtypes (Alzheimer dementia, vascular dementia, and other types of dementia). Subgroup analyses were performed in different age groups, in populations with and without stroke, and those with and without hypertension.ResultsPE associated with dementia after adjusting for full covariates (OR: 0.5414, 95% CI: 0.4536–0.6491, p < 0.001). Exercise performed at ≥3 times/week associated with lower risk of dementia (OR: 0.4794–0.6619, all p value <0.001). PE was associated with improved cognition (β: 12851, p < 0.001), and any PE frequency contributed to cognitive improvement (p values for exercise performed ≥1 time/week were <0.001). Similar conclusions were identified when we repeated analyses in different dementia subtypes and age groups. Subgroup analyses suggested that the cognition of individuals without hypertension also benefitted from exercising 1–2 times/week (OR: 0.6168, 95% CI: 0.4379–0.8668, p = 0.005).ConclusionThe best exercise frequency is exercising ≥3 times/week for individuals from different dementia subtypes and age groups. While for those without hypertension, PE at 1–2 times /week is also beneficial.

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“…Assim, exercitar-se contribui para uma melhora no desempenho das tarefas de memória do hipocampo, como recordação de histórias, listas de palavras e mnemônica discriminação em seres humanos. Ademais, atividades aeróbicas melhoram ainda mais a cognição e evitam reduções no volume cerebral associadas à idade em idosos 14 .…”

Section: Discussão Atividade Físicaunclassified

Relação do hormônio irisina liberado durante o exercício físico e a doença de Alzheimer: uma revisão da literatura

Gonçalves

Venturelli

Sarmento

et al. 2023

Rev. Med. (São Paulo)

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Com o aumento no número de idosos, observa-se também um aumento no aparecimento de algumas doenças, como a Doença de Alzheimer, caracterizada pela deterioração dos neurônios, com consequentes perdas significativas nas funções cerebrais. Durante o exercício físico, ocorre a liberação de mioquinas, dentre elas a irisina, produzida e ativada pelos músculos esqueléticos, promovendo efeitos benéficos na função cognitiva e na plasticidade geral do cérebro. Sendo assim, os exercícios físicos são um dos fatores conhecidos por retardar a neurodegeneração, desempenhando papel importante na vida dos idosos. Assim, este trabalho constitui uma revisão sistemática que busca apontar os benefícios trazidos pela prática de exercícios físicos na prevenção da patologia em questão.

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Harnessing the effects of endurance exercise to optimize cognitive health: Fundamental insights from Dr. Mark P. Mattson

Cited by 9 publications

References 85 publications

FNDC5 prevents oxidative stress and neuronal apoptosis after traumatic brain injury through SIRT3-dependent regulation of mitochondrial quality control

FNDC5 prevents oxidative stress and neuronal apoptosis after traumatic brain injury through SIRT3-dependent regulation of mitochondrial quality control

Physical exercise frequency and cognition: a multicenter cross-sectional cohort study

Relação do hormônio irisina liberado durante o exercício físico e a doença de Alzheimer: uma revisão da literatura

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