Effect of treadmill exercise on PI3K/AKT/mTOR, autophagy, and Tau hyperphosphorylation in the cerebral cortex of NSE/htau23 transgenic mice

Kang, Eun-Bum; Cho, Joon-Yong

doi:10.5717/jenb.2015.19.3.199

Cited by 2 publications

(1 citation statement)

References 29 publications

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“…Beneficial effects can result from facilitating cerebellar reserve both in terms of activation of neuroprotective mechanisms, and of stimulation of circuit maturation. It is worth noting that the impact of motor exercise on autophagy regulation with neuroprotective effects has been shown also in other neurological pathologies [175][176][177]. Autophagy modulation can therefore add to the numerous mechanistic substrates through which experience-including exercise-molds the brain.…”

Section: Cellular Mechanisms Underlying Functional Cerebellar Reservementioning

confidence: 97%

Consensus Paper. Cerebellar Reserve: From Cerebellar Physiology to Cerebellar Disorders

et al. 2019

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Cerebellar reserve refers to the capacity of the cerebellum to compensate for tissue damage or loss of function resulting from many different etiologies. When the inciting event produces acute focal damage (e.g., stroke, trauma), impaired cerebellar function may be compensated for by other cerebellar areas or by extracerebellar structures (i.e., structural cerebellar reserve). In contrast, when pathological changes compromise cerebellar neuronal integrity gradually leading to cell death (e.g., metabolic and immune-mediated cerebellar ataxias, neurodegenerative ataxias), it is possible that the affected area itself can compensate for the slowly evolving cerebellar lesion (i.e., functional cerebellar reserve). Here, we examine cerebellar reserve from the perspective of the three cornerstones of clinical ataxiology: control of ocular movements, coordination of voluntary axial and appendicular movements, and cognitive functions. Current evidence indicates that cerebellar reserve is potentiated by environmental enrichment through the mechanisms of autophagy and synaptogenesis, suggesting that cerebellar reserve is not rigid or fixed, but exhibits plasticity potentiated by experience. These conclusions have therapeutic implications. During the period when cerebellar reserve is preserved, treatments should be directed at stopping disease progression and/or limiting the pathological process. Simultaneously, cerebellar reserve may be potentiated using multiple approaches. Potentiation of cerebellar reserve may lead to compensation and restoration of function in the setting of cerebellar diseases, and also in disorders primarily of the cerebral hemispheres by enhancing cerebellar mechanisms of action. It therefore appears that cerebellar reserve, and the underlying plasticity of cerebellar microcircuitry that enables it, may be of critical neurobiological importance to a wide range of neurological/neuropsychiatric conditions.

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Section: Cellular Mechanisms Underlying Functional Cerebellar Reservementioning

confidence: 97%

Consensus Paper. Cerebellar Reserve: From Cerebellar Physiology to Cerebellar Disorders

et al. 2019

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CDKL3 Promotes Non-small Cell Lung Cancer by Suppressing Autophagy Via Activation of PI3K/Akt/mTOR Pathway

Chai

Lei

et al. 2023

Mol Biotechnol

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Effect of treadmill exercise on PI3K/AKT/mTOR, autophagy, and Tau hyperphosphorylation in the cerebral cortex of NSE/htau23 transgenic mice

Abstract: Eun-Bum Kang and Joon-Yong Cho. Effect of treadmill exercise on PI3K/AKT/mTOR, autophagy, and Tau hyperphosphorylation in the cerebral cortex of NSE/htau23 transgenic mice.

Cited by 2 publications

References 29 publications

Consensus Paper. Cerebellar Reserve: From Cerebellar Physiology to Cerebellar Disorders

Consensus Paper. Cerebellar Reserve: From Cerebellar Physiology to Cerebellar Disorders

CDKL3 Promotes Non-small Cell Lung Cancer by Suppressing Autophagy Via Activation of PI3K/Akt/mTOR Pathway

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