Treadmill Exercise Attenuates Aβ-Induced Mitochondrial Dysfunction and Enhances Mitophagy Activity in APP/PS1 Transgenic Mice

Zhao, Na; Qu, Yan; Xia, Jie; Zhang, Xianliang; Li, Baixia; Yin, Lingyu; Xu, Bo

doi:10.1007/s11064-020-03003-4

Cited by 42 publications

(35 citation statements)

References 46 publications

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“…Studies that evaluated potential neuroprotective agents in AD models that ameliorate neurodegeneration via enhancement of Parkin-mediated mitophagy (Wang et al, 2018 ; Fang et al, 2019 ; Hirano et al, 2019 ; Gao et al, 2020 ; Han et al, 2020 ; Sun et al, 2020 ; Xiong et al, 2020 ; Yang et al, 2020 ; Zhao et al, 2020 , 2021 ). The studies used both in vivo and in vitro models of AD, and the outcomes mainly included increased the Parkin level or related proteins.…”

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…Twelve weeks of treadmill exercise for APP/PS1 mice upregulated Parkin, enhanced mitophagy, and decreased Aβ levels (Zhao et al, 2020 ). However, PINK1 alteration patterns were not consistent with the rest (Zhao et al, 2020 ). NAD-dependent deacetylase sirtuin-1 (SIRT1) is an interesting protein with several protective roles in the body.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Insights Into Parkin-Mediated Mitophagy in Alzheimer's Disease: A Systematic Review

Goudarzi

Hosseini

Abdollahi

et al. 2021

Front. Aging Neurosci.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Insights Into Parkin-Mediated Mitophagy in Alzheimer's Disease: A Systematic Review

Goudarzi

Hosseini

Abdollahi

et al. 2021

Front. Aging Neurosci.

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“…Mitophagy is an essential cell activity to degrade and remove damaged mitochondria or excess mitochondria, which participates in the adjustment of the functional integrity of the mitochondrial network and cell survival [ 83 ]. Mitochondrial Ca 2+ dysregulation also interferes with mitophagy [ 84 ], which further aggravates the generation of Aβ aggregates and AD pathological development, forming a vicious cycle between Aβos and mitochondrial disability [ 85 , 86 ].…”

Section: The Neurotoxicological Mechanisms Of Aβosmentioning

confidence: 99%

The Toxicity and Polymorphism of β-Amyloid Oligomers

Huang

Liu

2020

IJMS

100

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It is widely accepted that β-amyloid oligomers (Aβos) play a key role in the progression of Alzheimer’s disease (AD) by inducing neuron damage and cognitive impairment, but Aβos are highly heterogeneous in their size, structure and cytotoxicity, making the corresponding studies tough to carry out. Nevertheless, a number of studies have recently made remarkable progress in the describing the characteristics and pathogenicity of Aβos. We here review the mechanisms by which Aβos exert their neuropathogenesis for AD progression, including receptor binding, cell membrane destruction, mitochondrial damage, Ca2+ homeostasis dysregulation and tau pathological induction. We also summarize the characteristics and pathogenicity such as the size, morphology and cytotoxicity of dimers, trimers, Aβ*56 and spherical oligomers, and suggest that Aβos may play a different role at different phases of AD pathogenesis, resulting in differential consequences on neuronal synaptotoxicity and survival. It is warranted to investigate the temporal sequence of Aβos in AD human brain and examine the relationship between different Aβos and cognitive impairment.

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“…A loss of intracellular Ca 2+ homeostasis causes mitochondrial Ca 2+ overload and mitochondrial dysfunction with the production of reactive oxygen species inducing membrane-lipid peroxidation, failure in the respiratory chain and in bioenergetics, increased mitochondria permeability and activation of Ca 2+ -dependent proteases such as calpains, finally leading to neuronal cell death [ 127 , 128 , 129 ]. Calcium dysregulation at mitochondrial levels also interferes with mitophagy, which is an essential process to remove damaged mitochondria, which plays a key role in the adjustment of the functional integrity of the mitochondrial network and cell survival [ 130 , 131 ]. This further contributes to the generation of Aβ oligomers and AD progression, creating a vicious circle between Aβ and mitochondria dysfunction [ 132 , 133 ].…”

Section: Calcium Homeostasis and Oligomer-mediated Synaptotoxicitymentioning

confidence: 99%

An Unbalanced Synaptic Transmission: Cause or Consequence of the Amyloid Oligomers Neurotoxicity?

Sciaccaluga

Megaro

Bellomo

et al. 2021

IJMS

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Amyloid-β (Aβ) 1-40 and 1-42 peptides are key mediators of synaptic and cognitive dysfunction in Alzheimer’s disease (AD). Whereas in AD, Aβ is found to act as a pro-epileptogenic factor even before plaque formation, amyloid pathology has been detected among patients with epilepsy with increased risk of developing AD. Among Aβ aggregated species, soluble oligomers are suggested to be responsible for most of Aβ’s toxic effects. Aβ oligomers exert extracellular and intracellular toxicity through different mechanisms, including interaction with membrane receptors and the formation of ion-permeable channels in cellular membranes. These damages, linked to an unbalance between excitatory and inhibitory neurotransmission, often result in neuronal hyperexcitability and neural circuit dysfunction, which in turn increase Aβ deposition and facilitate neurodegeneration, resulting in an Aβ-driven vicious loop. In this review, we summarize the most representative literature on the effects that oligomeric Aβ induces on synaptic dysfunction and network disorganization.

show abstract

Treadmill Exercise Attenuates Aβ-Induced Mitochondrial Dysfunction and Enhances Mitophagy Activity in APP/PS1 Transgenic Mice

Cited by 42 publications

References 46 publications

Insights Into Parkin-Mediated Mitophagy in Alzheimer's Disease: A Systematic Review

Insights Into Parkin-Mediated Mitophagy in Alzheimer's Disease: A Systematic Review

The Toxicity and Polymorphism of β-Amyloid Oligomers

An Unbalanced Synaptic Transmission: Cause or Consequence of the Amyloid Oligomers Neurotoxicity?

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