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Review
Neurosciences
Ilgiz Gareev et al.
Summary: Non-traumatic intracerebral hemorrhage (ICH) is the most common type of hemorrhagic stroke, often occurring between the ages of 45 and 60. Arterial hypertension is the primary cause of ICH, followed by other factors such as atherosclerosis, blood diseases, inflammation, intoxication and vitamin deficiencies. Mitochondrial dysfunction and dysregulated microRNAs (miRNAs) play important roles in ICH pathogenesis. Although miRNAs within the mitochondrial compartment challenge traditional signaling pathways, their potential as therapeutic targets and non-invasive diagnostic/prognostic biomarkers for ICH is still under-appreciated.
CURRENT NEUROPHARMACOLOGY
(2023)
Review
Neurosciences
Satyabrata Kundu et al.
Summary: Traumatic brain injury (TBI) is a global healthcare concern and a leading cause of death. TBI induces neuronal cell death independent of age, gender, and genetic background, resulting in long-term behavioral changes in TBI survivor patients. Various animal models, including rodents, zebrafish, and drosophila, have been developed to mimic TBI for understanding pathophysiology and evaluating therapeutic interventions.
CURRENT NEUROPHARMACOLOGY
(2023)
Review
Neurosciences
Md. Mominur Rahman et al.
Summary: Mitochondria are crucial for cellular homeostasis and metabolism in eukaryotes, especially in brain functions. Dysfunction of mitochondria is associated with neurodegenerative disorders such as Parkinson's disease, Alzheimer's disease, Huntington's disease, and amyotrophic lateral sclerosis. This review focuses on the mitochondrial disturbances in these disorders and discusses the potential use of mitochondrial drugs for their treatment and control, including mitochondrial antioxidants, mitochondrial permeability transition blockade, and mitochondrial gene therapy.
CURRENT NEUROPHARMACOLOGY
(2023)
Review
Neurosciences
Sheikh Arslan Sehgal et al.
Summary: With the development of novel drug discovery, biologically active compounds are used as pharmacological tools to understand complex biological mechanisms and find effective therapeutic agents. Mitochondria play a central role in various biological processes and dysfunction is associated with multiple pathologies. Targeting mitochondrial quality control mechanisms using pharmacological approaches is important, but there is a lack of biologically active molecules that can directly interact with mitochondria. Current chemical compounds used to induce mitophagy have limitations in understanding energy regulatory mechanisms. Efforts are being made to find molecules that can selectively remove defective mitochondria without affecting normal mitochondrial respiration. This report summarizes the recent progress in modulators of mitophagy.
CURRENT NEUROPHARMACOLOGY
(2023)
Review
Neurosciences
Mohannad A. A. Almikhlafi et al.
Summary: This article discusses the observation of abnormal mitochondrial morphology and metabolic dysfunction in neurodegenerative disorders. Mitochondrial dysfunction can be caused by aberrant mitochondrial DNA, mutant nuclear proteins, or unknown reasons. Considering the significant role of mitochondria in neurodegeneration, mitochondria-targeted therapies are a promising direction for the development of novel drug compounds. The review provides a brief description of how mitochondrial abnormalities contribute to various neurodegenerative disorders and explores the therapeutic effectiveness of mitochondria-directed antioxidants and mitochondrial gene therapy.
CURRENT NEUROPHARMACOLOGY
(2023)
Review
Neurosciences
Swati Dhasmana et al.
Summary: This review summarizes the mitochondrial dysfunction in the progression of ALS and emphasizes the potential of therapeutic candidates for restoring mitochondrial functions. The goals of mitochondrial therapies in ALS are to reduce ROS generation, enhance mitochondrial biogenesis, and inhibit apoptotic pathways. Combination therapy may hold the key to future ALS treatments.
CURRENT NEUROPHARMACOLOGY
(2023)
Review
Neurosciences
Mohammad Moshahid Khan et al.
Summary: Neurodegenerative and neurovascular disorders impact a large number of individuals globally and pose a significant health burden. Mitochondrial dysfunction plays a crucial role in the development of these disorders, making it an important target for potential disease-modifying treatments. Mitochondrial transplantation therapy (MTT) offers a new therapeutic intervention by replacing damaged mitochondria with healthy donor mitochondria. This review explores the significance of mitochondria and provides an overview of recent advances and developments in MTT for neurodegenerative and neurovascular disorders, focusing on Parkinson's disease, Alzheimer's disease, and stroke. MTT holds great promise as a disease-modifying intervention for these disorders.
CURRENT NEUROPHARMACOLOGY
(2023)
Review
Neurosciences
Abdullah Shaito et al.
Summary: Neurodegenerative disorders are neurological conditions that lead to the progressive loss of nerve cell functions and ultimately result in loss of movement, coordination, and mental functioning. The perturbation of mitochondrial function and dynamics has been shown to play a crucial role in the pathogenesis of these disorders, making mitochondrial biogenesis a potential therapeutic target.
CURRENT NEUROPHARMACOLOGY
(2023)
Review
Neurosciences
Showkat Ul Nabi et al.
Summary: Autism is a neurodevelopmental disorder that may be caused by a combination of environmental and genetic factors. Recent epidemiological studies have shown an increase in the prevalence of autism, with mitochondrial dysfunction playing a potential role in the progression of the disease. Limited research has focused on the association between mitochondrial dysfunction and autism, despite accumulating evidence suggesting its significance. This review aims to discuss the risk factors, role of mitochondria, genetic determinants, possible pathogenic pathways, and current therapeutic regimens for autism, as well as novel treatments being investigated in clinical trials.
CURRENT NEUROPHARMACOLOGY
(2023)
