Mitochondrial dysfunction in neurodegenerative diseases and drug targets via apoptotic signaling.

Mitochondrial dysfunction in neurodegenerative diseases and drug targets via apoptotic signaling.

Publication date: Jul 06, 2019

Mitochondrial dysfunction is becoming one of the most emerging pathological process in the etiology of neurological disorders. Other common etiologies of the neurological disorders are aging and oxidative stress. Neurodegenerative disorders for instance Huntington’s disease, Parkinson’s disease, Amyotrophic lateral sclerosis, Epilepsy, Schizophrenia, Multiple sclerosis, Neuropathic pain and Alzheimer’s disease involves mitochondrial dysfunction and is regarded as the core of their pathological processes. Most central pathological feature of the neurodegenerative diseases is apoptosis which is regulated by mitochondria. Altered signaling of the apoptotic mechanisms are involved in neurodegeneration. Abnormal levels of these molecular apoptotic proteins promotes the pathogenesis of neurological disorders. Mitochondria are also implicated in the production of reactive oxygen species (ROS). Raised ROS levels initiates the cascade leading to the non-apoptotic death of cells. ROS produced in cells acts as signaling molecules, but when produced in abundance will result in cellular consequences to deoxyribonucleic acid, proteins and lipids, decreased effectiveness of cellular mechanisms, initiation of inflammatory pathways, excitotoxicity, protein agglomeration and apoptosis. Protecting mitochondrial function has been identified as the most effective therapeutic approach to attenuate the pathogenesis of neurodegenerative diseases. This review aims to provide an insight into the mitochondrial dysfunction in the pathogenesis of neurological disorders, alteration in signaling cascades of apoptosis in mitochondrial dysfunction and the therapeutic strategies (both natural and synthetic drugs) targeting these mitochondrial apoptotic pathways and oxidative stress that holds great promise.

Wu, Y., Chen, M., and Jiang, J. Mitochondrial dysfunction in neurodegenerative diseases and drug targets via apoptotic signaling. 18550. 2019 Mitochondrion.

Concepts Keywords
Agglomeration Neurodegeneration
Aging Neuroprotection
Alzheimer Neurology
Amyotrophic Lateral Sclerosis Cell biology
Apoptosis Mitochondria
Apoptotic Branches of biology
Deoxyribonucleic Acid Senescence
Epilepsy Dysfunction neurodegenerative diseases
Etiologies Insight mitochondrial dysfunction
Etiology Pathogenesis neurodegenerative diseases
Excitotoxicity Mitochondrial dysfunction
Huntington Pain
Lipids Mitochondrion
Mitochondria Apoptosis
Mitochondrial Reactive oxygen species
Mitochondrion Oxidative stress
Multiple Sclerosis Apoptosis
Neurodegeneration
Neurodegenerative Diseases
Neurological Disorders
Neuropathic Pain
Oxidative Stress
Oxygen
Parkinson
Pathogenesis
ROS
Schizophrenia

Semantics

Type Source Name
gene UNIPROT RXFP2
disease MESH death
gene UNIPROT ROS1
drug DRUGBANK Rosoxacin
pathway BSID Apoptosis
disease MESH pathological processes
disease MESH Neuropathic pain
disease DOID Multiple sclerosis
disease MESH Multiple sclerosis
disease DOID Schizophrenia
disease MESH Schizophrenia
disease DOID Epilepsy
disease MESH Epilepsy
disease DOID Amyotrophic lateral sclerosis
disease MESH Amyotrophic lateral sclerosis
pathway BSID Oxidative Stress
disease MESH oxidative stress
pathway BSID Aging
disease MESH aging
disease MESH neurological disorders
pathway BSID Neurodegenerative Diseases
disease MESH neurodegenerative diseases

Original Article

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