2016
DOI: 10.18632/aging.101054
|View full text |Cite
|
Sign up to set email alerts
|

An antioxidant specifically targeting mitochondria delays progression of Alzheimer’s disease-like pathology

Abstract: Mitochondrial aberrations are observed in human Alzheimer's disease (AD) and in medical conditions that increase the risk of this disorder, suggesting that mitochondrial dysfunction may contribute to pathophysiology of AD. Here, using OXYS rats that simulate key characteristics of sporadic AD, we set out to determine the role of mitochondria in the pathophysiology of this disorder. OXYS rats were treated with a mitochondria-targeted antioxidant SkQ1 from age 12 to 18 months, that is, during active progression … Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1

Citation Types

3
54
0
2

Year Published

2017
2017
2022
2022

Publication Types

Select...
6
2
1

Relationship

1
8

Authors

Journals

citations
Cited by 61 publications
(59 citation statements)
references
References 66 publications
(97 reference statements)
3
54
0
2
Order By: Relevance
“…ROS are major contributors to loss of neuronal apoptosis. Many antioxidant compounds have been demonstrated to protect the brain from Aβ neurotoxicity [42]. Given that serious adverse effects are related to synthetic antioxidants, recent research has been focused on natural products with antioxidant properties.…”
Section: Discussionmentioning
confidence: 99%
“…ROS are major contributors to loss of neuronal apoptosis. Many antioxidant compounds have been demonstrated to protect the brain from Aβ neurotoxicity [42]. Given that serious adverse effects are related to synthetic antioxidants, recent research has been focused on natural products with antioxidant properties.…”
Section: Discussionmentioning
confidence: 99%
“…Much like ubiquinone, plastiquinone acts as an antioxidant by quenching superoxide. Using a rat model with an inherited over production of free radicals that present AD like pathology (OXYS model), SkQ1 supplemented via the diet was found to accumulate in neuronal mitochondria [172] . Furthermore, SkQ1 supplementation reduces A levels and tau hyperphosporylation in addition to improving memory and learning behaviours [172,173] .…”
Section: Toxin Induced Models Of Admentioning
confidence: 99%
“…This rat model simulates key characteristics of AD including tau protein hyper-phosphorylation, synaptic losses, neuronal cell death, behavioral alterations, and a decrease in cognitive functions on the background of increase in APP levels, enhanced accumulation of Aβ, and formation of amyloid plaques in the brain.The genome of OXYS rats lacking the mutations in the App, Psen1, and Psen2 genes, which are specific for the early form of AD, also speaks in favor of the this model matching the particular criteria of sporadic AD . According to our data, the development and progression of AD-like pathology in OXYS rats may be caused by mitochondrial dysfunction -2016, Kolosova et al, 2017, Tyumentsev et al, 2018). Here we summarize our evidence supporting the validity of this assertion.…”
mentioning
confidence: 50%
“…The key role of mitochondrial dysfunction in the pathophysiology of AD is confirmed by the ability of mitochondria-targeted antioxidant SkQ1 to alleviate the neurodegenerative alterations via improvement of structural and functional state of mitochondria in OXYS rats. Namely, SkQ1 prevents the neuronal loss and synaptic damage, enhances neurotrophic supply, and decreases the amounts of toxic forms of Aβ and tau hyperphosphorylation in the hippocampus of OXYS rats, thereby resulting in improvement of cognitive function (Stefanova et al, , 2016Kolosova et al, 2017). Collectively, these data allow us to conclude that mitochondrial dysfunction appears at least to mediate or possibly even initiate pathological molecular cascades of AD-like pathology in OXYS rats.…”
mentioning
confidence: 99%