Mitochondria-targeted plastoquinone antioxidant SkQR1 has positive effect on memory of rats

Stelmashook, E. V.; Stavrovskaya, A. V.; Yamshchikova, N. G.; Ольшанский, А С; Kapay, N. A.; Попова, О. В.; Хаспеков, Л. Г.; Skrebitsky, V. G.; Isaev, N. K.

doi:10.1134/s0006297915050119

Cited by 8 publications

(3 citation statements)

References 18 publications

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“…It would therefore be desirable to know the time-course of oxidant production in a disease model so that initiation of direct antioxidant therapy can be optimally timed. Precursors of endogenous antioxidants, such glutathione (GSH) can be achieved by N-acetyl cysteine (NAC) which is approved for human use in acetaminophen toxicity but shows promise in many neurological diseases such as schizophrenia, HD and PD [40, 41]. …”

Section: Antioxidant Classesmentioning

confidence: 99%

Targeting Oxidative Stress in Central Nervous System Disorders

Patel

2016

Trends in Pharmacological Sciences

248

141

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There is widespread recognition that reactive oxygen species (ROS) play key roles in normal brain function and pathology in the context of neurological disease. Oxidative stress continues to remain a key therapeutic target for neurological diseases. In developing antioxidant therapies for neurological disease, special attention should be given to the brain’s unique vulnerability to oxidative insults and its architecture. Consideration of antioxidant therapy should be guided by a strong rationale for oxidative stress in the neurological disease. This review provides an overview of processes that can guide the development of antioxidant therapies in neurological diseases such as knowledge of basic redox mechanisms, unique features of brain pathophysiology, mechanisms and classes of antioxidants and desirable properties of drug candidates.

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Section: Antioxidant Classesmentioning

confidence: 99%

Targeting Oxidative Stress in Central Nervous System Disorders

Patel

2016

Trends in Pharmacological Sciences

248

141

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“…SkQ1 improved healthspan and lifespan in mitochondrial DNA (mtDNA) mutator mice [ 192 ]. Neuroprotective effects of SkQ1 were demonstrated in the senescence-accelerated OXYS rat, a model of aging featuring an overproduction of free radicals, lipid peroxidation, protein oxidation, DNA damage, and a variety of neurodegenerative features [ 193 , 194 , 195 , 196 ]. SkQ1 treatment in OXYS rats preserved hippocampal neuronal integrity, improved mitochondrial parameters, including increased enzymatic activity of ETC complexes I and IV, and reduced mitochondrial swelling and lipofuscin accumulation in the hippocampal CA1 neurons [ 197 ].…”

Section: Mitochondria-targeted Therapies In Admentioning

confidence: 99%

Disentangling Mitochondria in Alzheimer’s Disease

Johri

2021

IJMS

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Alzheimer’s disease (AD) is a major cause of dementia in older adults and is fast becoming a major societal and economic burden due to an increase in life expectancy. Age seems to be the major factor driving AD, and currently, only symptomatic treatments are available. AD has a complex etiology, although mitochondrial dysfunction, oxidative stress, inflammation, and metabolic abnormalities have been widely and deeply investigated as plausible mechanisms for its neuropathology. Aβ plaques and hyperphosphorylated tau aggregates, along with cognitive deficits and behavioral problems, are the hallmarks of the disease. Restoration of mitochondrial bioenergetics, prevention of oxidative stress, and diet and exercise seem to be effective in reducing Aβ and in ameliorating learning and memory problems. Many mitochondria-targeted antioxidants have been tested in AD and are currently in development. However, larger streamlined clinical studies are needed to provide hard evidence of benefits in AD. This review discusses the causative factors, as well as potential therapeutics employed in the treatment of AD.

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“…An early (2014) study by Stelmashook, et al, treated wild type Wistar rats with SkQ1 to deduce whether SkQ1 might affect memory or long-term potentiation [30]. A single i.p.…”

Section: Pre-clinical Studiesmentioning

confidence: 99%

Treating Neurodegenerative Disease with Antioxidants: Efficacy of the Bioactive Phenol Resveratrol and Mitochondrial-Targeted MitoQ and SkQ

Shinn

Lagalwar

2021

Preprint

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Growing evidence from neurodegenerative disease research supports an early pathogenic role for mitochondrial dysfunction in affected neurons that precedes morphological and functional deficits. Resulting oxidative stress and respiratory malfunction contribute to neuronal toxicity and may enhance the vulnerability of neurons to continued assault by aggregation-prone proteins. Consequently, targeting mitochondria with antioxidant therapy may be a non-invasive, inexpensive, and viable means of strengthening neuronal health and slowing disease progression, thereby extending quality of life. We review the pre-clinical and clinical findings available to date of the natural bioactive phenol resveratrol and two synthetic mitochondrial-targeted antioxidants MitoQ and SkQ.

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Mitochondria-targeted plastoquinone antioxidant SkQR1 has positive effect on memory of rats

Cited by 8 publications

References 18 publications

Targeting Oxidative Stress in Central Nervous System Disorders

Targeting Oxidative Stress in Central Nervous System Disorders

Disentangling Mitochondria in Alzheimer’s Disease

Treating Neurodegenerative Disease with Antioxidants: Efficacy of the Bioactive Phenol Resveratrol and Mitochondrial-Targeted MitoQ and SkQ

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