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Epigenetic Regulation of Ferroptosis in Central Nervous System Diseases
AbstractFerroptosis, a newly identified form of cell death, is characterized by iron overload and accumulation of lipid reactive oxygen species. Inactivation of pathways, such as glutathione/glutathione peroxidase 4, NAD(P)H/ferroptosis suppressor protein 1/ubiquinone, dihydroorotate dehydrogenase/ubiquinol, or guanosine triphosphate cyclohydrolase-1/6(R)-l-erythro-5,6,7,8-tetrahydrobiopterin pathways, have been found to induce ferroptosis. The accumulating data suggest that epigenetic regulation can determine cell sensitivity to ferroptosis at both the transcriptional and translational levels. While many of the effectors ...
Source: Molecular Neurobiology - May 28, 2023 Category: Neurology Source Type: research

Gene Therapy Approach with an Emphasis on Growth Factors: Theoretical and Clinical Outcomes in Neurodegenerative Diseases
This article mainly focu ses on the delivering modes of genetic materials in the CNS, which includes viral and non-viral vectors and their application in gene therapy. Despite the many clinical trials conducted so far, data have shown disappointing outcomes. The efforts done to improve outcomes, efficacy, and safety in the identification of targets in various neurological disorders are also discussed here. Adapting gene therapy as a new therapeutic approach for treating neurological disorders seems to be promising, with early detection and delivery of therapy before the neuron is lost, helping a lot the development of new ...
Source: Molecular Neurobiology - October 15, 2021 Category: Neurology Source Type: research

Ferrostatin-1 Alleviates White Matter Injury Via Decreasing Ferroptosis Following Spinal Cord Injury
AbstractSpinal cord injury (SCI), a devastating neurological impairment, usually imposes a long-term psychological stress and high socioeconomic burden for the sufferers and their family. Recent researchers have paid arousing attention to white matter injury and the underlying mechanism following SCI. Ferroptosis has been revealed to be associated with diverse diseases including stroke, cancer, and kidney degeneration. Ferrostatin-1, a potent inhibitor of ferroptosis, has been illustrated to curb ferroptosis in neurons, subsequently improving functional recovery after traumatic brain injury (TBI) and SCI. However, the role...
Source: Molecular Neurobiology - October 12, 2021 Category: Neurology Source Type: research

Obscure Involvement of MYC in Neurodegenerative Diseases and Neuronal Repair
AbstractMYC is well known as a potent oncogene involved in regulating cell cycle and metabolism. Augmented MYC expression leads to cell cycle dysregulation, intense cell proliferation, and carcinogenesis. Surprisingly, its increased expression in neurons does not induce their proliferation, but leads to neuronal cell death and consequent development of a neurodegenerative phenotype. Interestingly, while cancer and neurodegenerative diseases such as Alzheimer ’s disease are placed at the opposite sides of cell division spectrum, both start with cell cycle dysregulation and stimulation of proliferation. It seems that MYC a...
Source: Molecular Neurobiology - May 5, 2021 Category: Neurology Source Type: research

Exosomes in Acquired Neurological Disorders: New Insights into Pathophysiology and Treatment
AbstractExosomes are endogenous nanovesicles that play critical roles in intercellular signaling by conveying functional genetic information and proteins between cells. Exosomes readily cross the blood-brain barrier and have promise as therapeutic delivery vehicles that have the potential to specifically deliver molecules to the central nervous system (CNS). This unique feature also makes exosomes attractive as biomarkers in diagnostics, prognostics, and therapeutics in the context of multiple significant public health conditions, including acquired neurological disorders. The purpose of this review is to summarize the sta...
Source: Molecular Neurobiology - October 26, 2018 Category: Neurology Source Type: research

MMP-12, a Promising Therapeutic Target for Neurological Diseases
AbstractThe role of matrix metalloproteinase-12 (MMP-12) in the pathogenesis of several inflammatory diseases such as chronic obstructive pulmonary disease, emphysema, and asthma is well established. Several new studies and recent reports from our laboratory and others highlighted the detrimental role of MMP-12 in the pathogenesis of several neurological diseases. In this review, we discuss in detail the pathological role of MMP-12 and the possible underlying molecular mechanisms that contribute to disease pathogenesis in the context of central nervous system diseases such as stroke, spinal cord injury, and multiple sclero...
Source: Molecular Neurobiology - February 1, 2017 Category: Neurology Source Type: research

Direct Conversion of Somatic Cells into Induced Neurons
AbstractThe progressive loss and degeneration of neurons in the central nervous system (CNS), as a result of traumas or diseases including Alzheimer ’s, Parkinson’s, Huntington’s disease, stroke, and traumatic injury to the brain and spinal cord, can usually have devastating effects on quality of life. The current strategies available for treatments are described including drug delivery, surgery, electrical stimulation, and cell-based tiss ue engineering approaches. However, apart from cell-based therapy, other attempts are limited in improving clinical outcomes. Recently, stem cell and neural stem cell (NSC) in part...
Source: Molecular Neurobiology - December 15, 2016 Category: Neurology Source Type: research

N -Palmitoylethanolamine and Neuroinflammation: a Novel Therapeutic Strategy of Resolution
Abstract Inflammation is fundamentally a protective cellular response aimed at removing injurious stimuli and initiating the healing process. However, when prolonged, it can override the bounds of physiological control and becomes destructive. Inflammation is a key element in the pathobiology of chronic pain, neurodegenerative diseases, stroke, spinal cord injury, and neuropsychiatric disorders. Glia, key players in such nervous system disorders, are not only capable of expressing a pro-inflammatory phenotype but respond also to inflammatory signals released from cells of immune origin such as mast cells. Chronic ...
Source: Molecular Neurobiology - June 8, 2015 Category: Neurology Source Type: research