Filtered By:
Source: Molecular Neurobiology
Condition: Mitochondrial Disease

This page shows you your search results in order of date.

Order by Relevance | Date

Total 7 results found since Jan 2013.

Investigation of Mitochondrial Related Variants in a Cerebral Small Vessel Disease Cohort
AbstractMonogenic forms of cerebral small vessel disease (CSVD) can be caused by both variants in nuclear DNA and mitochondrial DNA (mtDNA). Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is known to have a phenotype similar to Cerebral Autosomal Dominant Arteriopathy with Sub-cortical Infarcts and Leukoencephalopathy (CADASIL), and can be caused by variants in the mitochondrial genome and in several nuclear-encoded mitochondrial protein (NEMP) genes. The aim of this study was to screen for variants in the mitochondrial genome and NEMP genes in aNOTCH3-negative CADASIL cohort, to identify a...
Source: Molecular Neurobiology - August 25, 2022 Category: Neurology Source Type: research

Mitochondrial Quality and Quantity Control: Mitophagy Is a Potential Therapeutic Target for Ischemic Stroke
AbstractIschemic stroke is a cerebrovascular disease with high mortality and disability, which seriously affects the health and lives of people around the world. Effective treatment for ischemic stroke has been limited by its complex pathological mechanisms. Increasing evidence has indicated that mitochondrial dysfunction plays an essential role in the occurrence, development, and pathological processes of ischemic stroke. Therefore, strict control of the quality and quantity of mitochondria via mitochondrial fission and fusion as well as mitophagy is beneficial to the survival and normal function maintenance of neurons. U...
Source: Molecular Neurobiology - March 9, 2022 Category: Neurology Source Type: research

Brain Photobiomodulation Therapy: a Narrative Review
This article reviews the state-of-the-art preclinical and clinical evidence regarding the efficacy of brain PBM therapy.
Source: Molecular Neurobiology - January 11, 2018 Category: Neurology Source Type: research

Mitochondrial Quality Control and Disease: Insights into Ischemia-Reperfusion Injury
AbstractMitochondria are key regulators of cell fate during disease. They control cell survival via the production of ATP that fuels cellular processes and, conversely, cell death via the induction of apoptosis through release of pro-apoptotic factors such as cytochrome C. Therefore, it is essential to have stringent quality control mechanisms to ensure a healthy mitochondrial network. Quality control mechanisms are largely regulated by mitochondrial dynamics and mitophagy. The processes of mitochondrial fission (division) and fusion allow for damaged mitochondria to be segregated and facilitate the equilibration of mitoch...
Source: Molecular Neurobiology - April 11, 2017 Category: Neurology Source Type: research

The Neuro-Immune Pathophysiology of Central and Peripheral Fatigue in Systemic Immune-Inflammatory and Neuro-Immune Diseases
Abstract Many patients with systemic immune-inflammatory and neuro-inflammatory disorders, including depression, rheumatoid arthritis, systemic lupus erythematosus, Sjögren’s disease, cancer, cardiovascular disorder, Parkinson’s disease, multiple sclerosis, stroke, and chronic fatigue syndrome/myalgic encephalomyelitis, endure pathological levels of fatigue. The aim of this narrative review is to delineate the wide array of pathways that may underpin the incapacitating fatigue occurring in systemic and neuro-inflammatory disorders. A wide array of immune, inflammatory, oxidative and nitrosative stress (O&...
Source: Molecular Neurobiology - January 20, 2015 Category: Neurology Source Type: research

Cofilin Inhibition Restores Neuronal Cell Death in Oxygen–Glucose Deprivation Model of Ischemia
Abstract Ischemia is a condition associated with decreased blood supply to the brain, eventually leading to death of neurons. It is associated with a diverse cascade of responses involving both degenerative and regenerative mechanisms. At the cellular level, the changes are initiated prominently in the neuronal cytoskeleton. Cofilin, a cytoskeletal actin severing protein, is known to be involved in the early stages of apoptotic cell death. Evidence supports its intervention in the progression of disease states like Alzheimer’s and ischemic kidney disease. In the present study, we have hypothesized the possible i...
Source: Molecular Neurobiology - December 20, 2014 Category: Neurology Source Type: research