Homeostasis of carbohydrates and reactive oxygen species is critically changed in the brain of middle-aged mice: Molecular mechanisms and functional reasons

Bayliak, Maria M.; Gospodaryov, Dmytro V.; Lushchak, Volodymyr I.

doi:10.1016/j.bbadva.2023.100077

Cited by 10 publications

(5 citation statements)

References 161 publications

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“…The brain uses about 20% more oxygen than other organs, making it more exposed to reactive oxygen species (ROS) and reactive nitrogen species (RNS) [ 26 , 27 ]. Both ROS and RNS are very unstable structures due to the unpaired electron present within their molecules.…”

Section: Ad Pathomechanismsmentioning

confidence: 99%

“…Similar to thalidomide, it inhibits the activation of CNS phagocytes and impairs the process of tau protein phosphorylation [ 207 ]. In addition to TNF-α, the treatment of Alzheimer’s disease can also involve the inhibition of other pro-inflammatory factors [ 27 ]. Interleukins, including pro-inflammatory IL-12 and IL-23, may be targets for the treatment of AD.…”

Section: Treatment Of Inflammation In Admentioning

confidence: 99%

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Inflammatory Processes in Alzheimer’s Disease—Pathomechanism, Diagnosis and Treatment: A Review

Twarowski

Herbet

2023

IJMS

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Alzheimer’s disease is one of the most commonly diagnosed cases of senile dementia in the world. It is an incurable process, most often leading to death. This disease is multifactorial, and one factor of this is inflammation. Numerous mediators secreted by inflammatory cells can cause neuronal degeneration. Neuritis may coexist with other mechanisms of Alzheimer’s disease, contributing to disease progression, and may also directly underlie AD. Although much has been established about the inflammatory processes in the pathogenesis of AD, many aspects remain unexplained. The work is devoted in particular to the pathomechanism of inflammation and its role in diagnosis and treatment. An in-depth and detailed understanding of the pathomechanism of neuroinflammation in Alzheimer’s disease may help in the development of diagnostic methods for early diagnosis and may contribute to the development of new therapeutic strategies for the disease.

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Section: Ad Pathomechanismsmentioning

confidence: 99%

Section: Treatment Of Inflammation In Admentioning

confidence: 99%

Inflammatory Processes in Alzheimer’s Disease—Pathomechanism, Diagnosis and Treatment: A Review

Twarowski

Herbet

2023

IJMS

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“…However, in the normal state, these levels are minimal due to the antioxidants present in the mitochondria. According to the available knowledge, a disturbance of complex I will disrupt this homeostasis, and a dramatic increase in reactive oxygen species will occur [ 87 ]. One consequence is mitochondrial instability, which will trigger a negative cycle of increasing ROS production, damage, and mitochondrial malfunction.…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial Dysfunction in Sporadic Amyotrophic Lateral Sclerosis Patients: Insights from High-Resolution Respirometry

Parvanovova,

Evinova,

Grofik

et al. 2024

Biomedicines

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Amyotrophic lateral sclerosis is a severe neurodegenerative disease whose exact cause is still unclear. Currently, research attention is turning to the mitochondrion as a critical organelle of energy metabolism. Current knowledge is sufficient to confirm the involvement of the mitochondria in the pathophysiology of the disease, since the mitochondria are involved in many processes in the cell; however, the exact mechanism of involvement is still unclear. We used peripheral blood mononuclear cells isolated from whole fresh blood from patients with amyotrophic lateral sclerosis for measurement and matched an age- and sex-matched set of healthy subjects. The group of patients consisted of patients examined and diagnosed at the neurological clinic of the University Hospital Martin. The set of controls consisted of healthy individuals who were actively searched, and controls were selected on the basis of age and sex. The group consisted of 26 patients with sporadic forms of ALS (13 women, 13 men), diagnosed based on the definitive criteria of El Escorial. The average age of patients was 54 years, and the average age of healthy controls was 56 years. We used a high-resolution O2K respirometry method, Oxygraph-2k, to measure mitochondrial respiration. Basal respiration was lower in patients by 29.48%, pyruvate-stimulated respiration (respiratory chain complex I) was lower by 29.26%, and maximal respiratory capacity was lower by 28.15%. The decrease in succinate-stimulated respiration (respiratory chain complex II) was 26.91%. Our data confirm changes in mitochondrial respiration in ALS patients, manifested by the reduced function of complex I and complex II of the respiratory chain. These defects are severe enough to confirm this disease’s hypothesized mitochondrial damage. Therefore, research interest in the future should be directed towards a deeper understanding of the involvement of mitochondria and respiratory complexes in the pathophysiology of the disease. This understanding could develop new biomarkers in diagnostics and subsequent therapeutic interventions.

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“…ROSmediated oxidation of certain cysteine residues of the cytosolic protein, KEAP1, results in increased levels of Nrf2. Nrf2 then localizes to the nucleus where it upregulates the expression of many genes encoding antioxidant enzymes as well as antiinflammatory system components (Lushchak, 2015;Bayliak et al, 2023).…”

Section: Effects Of Cellular Hydrogen Peroxidementioning

confidence: 99%

Potential oxidative stress related targets of mitochondria-focused therapy of PTSD

Kmita,

Pinna,

Lushchak

2023

Front. Physiol.

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Post-traumatic stress disorder (PTSD) remains a highly prevalent, under-diagnosed, and under-treated psychiatric disorder that often deteriorates over time, and is highly comorbid with major depressive disorder, suicidality, and substance use disorder. Several biomarkers have been proposed but have yet to be implemented into clinical practice. Treatments, including selective serotonin reuptake inhibitors, are efficacious in only a small number of patients, which underscores the need to develop novel, efficient treatments. Mitochondrial dysfunction resulting from chronic oxidative stress has been linked with both altered neurotransmitter signaling and the inflammatory response. Hereinafter, we discuss mechanisms by which mitochondrial dysfunction may contribute to the development of PTSD symptoms, and how these may even increase PTSD susceptibility. We also highlight possible therapeutic targets to reduce oxidative stress to prevent or treat PTSD symptoms.

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Homeostasis of carbohydrates and reactive oxygen species is critically changed in the brain of middle-aged mice: Molecular mechanisms and functional reasons

Cited by 10 publications

References 161 publications

Inflammatory Processes in Alzheimer’s Disease—Pathomechanism, Diagnosis and Treatment: A Review

Inflammatory Processes in Alzheimer’s Disease—Pathomechanism, Diagnosis and Treatment: A Review

Mitochondrial Dysfunction in Sporadic Amyotrophic Lateral Sclerosis Patients: Insights from High-Resolution Respirometry

Potential oxidative stress related targets of mitochondria-focused therapy of PTSD

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