Abstract
Traumatic brain injury (TBI) and brain ischemia/reperfusion cause neurodegenerative processes that can continue after the acute stage with the development of severe brain atrophy with dementia. In this case, the long-term neurodegeneration of the brain is similar to the neurodegeneration characteristic of Alzheimer’s disease (AD) and is associated with the accumulation of beta amyloid and tau protein. In the pathogenesis of AD as well as in the pathogenesis of cerebral ischemia and TBI oxidative stress, progressive inflammation, glial activation, blood–brain barrier dysfunction, and excessive activation of autophagy are involved, which implies the presence of many targets that can be affected by neuroprotectors. That is, multivariate cascades of nerve tissue damage represent many potential targets for therapeutic interventions. One of such substances that can be used in multi-purpose therapeutic strategies is methylene blue (MB). This drug can have an antiapoptotic and anti-inflammatory effect, activate autophagy, inhibit the aggregation of proteins with an irregular shape, inhibit NO synthase, and bypass impaired electron transfer in the respiratory chain of mitochondria. MB is a well-described treatment for methemoglobinemia, malaria, and encephalopathy caused by ifosfamide. In recent years, this drug has attracted great interest as a potential treatment for a number of neurodegenerative disorders, including the effects of TBI, ischemia, and AD.
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Research ethics: Not applicable.
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Informed consent: Not applicable..
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Author contributions: Nickolay K. Isaev: conceptualization, search and analysis of articles, preparation of figures, supervision for article, writing original draft, review & editing; Elena V. Stelmashook, Elizaveta E. Genrikhs: search and analysis of articles, writing original draft, review & editing, writing help, and review & editing. The authors have accepted responsibility for the entire content of this manuscript and approved its submission.
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Competing interests: The authors declare that they have no conflict of interest.
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Research funding: This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
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Data availability: The data of the paper are available upon request from the corresponding author.
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© 2024 Walter de Gruyter GmbH, Berlin/Boston
Artikel in diesem Heft
- Frontmatter
- Dendritic spines and their role in the pathogenesis of neurodevelopmental and neurological disorders
- Mitochondria and MICOS – function and modeling
- The role of long noncoding RNAs in amyotrophic lateral sclerosis
- Current potential pathogenic mechanisms of copper-zinc superoxide dismutase 1 (SOD1) in amyotrophic lateral sclerosis
- Analysis of radiological features in patients with post-stroke depression and cognitive impairment
- Impact of carotid stenosis on the outcome of stroke patients submitted to reperfusion treatments: a narrative review
- Methylene blue and its potential in the treatment of traumatic brain injury, brain ischemia, and Alzheimer’s disease
Artikel in diesem Heft
- Frontmatter
- Dendritic spines and their role in the pathogenesis of neurodevelopmental and neurological disorders
- Mitochondria and MICOS – function and modeling
- The role of long noncoding RNAs in amyotrophic lateral sclerosis
- Current potential pathogenic mechanisms of copper-zinc superoxide dismutase 1 (SOD1) in amyotrophic lateral sclerosis
- Analysis of radiological features in patients with post-stroke depression and cognitive impairment
- Impact of carotid stenosis on the outcome of stroke patients submitted to reperfusion treatments: a narrative review
- Methylene blue and its potential in the treatment of traumatic brain injury, brain ischemia, and Alzheimer’s disease