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Mitochondrial Dysfunction And Oxidative Stress In Neurodegenerative Diseases Pdf

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Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases

Mitochondria play a pivotal role in bioenergetics and respiratory functions, which are essential for the numerous biochemical processes underpinning cell viability. Mitochondrial morphology changes rapidly in response to external insults and changes in metabolic status via fission and fusion processes so-called mitochondrial dynamics that maintain mitochondrial quality and homeostasis. Damaged mitochondria are removed by a process known as mitophagy, which involves their degradation by a specific autophagosomal pathway. Recent research suggests that restoration of mitochondrial function by physical exercise, an antioxidant diet, or therapeutic approaches can delay the onset and slow the progression of AD. In this review, we focus on recent progress that highlights the crucial role of alterations in mitochondrial function and oxidative stress in the pathogenesis of AD, emphasizing a framework of existing and potential therapeutic approaches.

Mitochondria dysfunction in the pathogenesis of Alzheimer’s disease: recent advances

Neurodegenerative diseases are characterized by the progressive deterioration of neuronal function in the central or peripheral nervous system and ultimately the death of nerve cells. There is a big evidence that oxidative stress is an essential mediator implicated in neurodegenerative processes and may be a key event triggering various forms of cell death. Here, we review the hypothesis that neuronal loss resulted from oxidative stress may be initiated by a drastic decrease in the antioxidant molecule glutathione GSH. GSH plays a vital role in cellular redox homeostasis in the nervous system and protects neurons against a variety of oxidative insults. GSH depletion can enhance oxidative stress and may increase protein aggregation leading to initiate cell death in distinct neuronal populations. During the past thirty to forty years, and along with the global rise in life expectancy, neurodegenerative diseases of the brain that affect the elderly in particular have become a burden on society more and more. Thus, the scientists place a special focus on age-related neurodegenerative diseases ADD research.

Metrics details. Under the microscope, neuronal accumulation of abnormal tau proteins and amyloid plaques are two pathological hallmarks in affected brain regions. Although the detailed mechanism of the pathogenesis of AD is still elusive, a large body of evidence suggests that damaged mitochondria likely play fundamental roles in the pathogenesis of AD. It is believed that a healthy pool of mitochondria not only supports neuronal activity by providing enough energy supply and other related mitochondrial functions to neurons, but also guards neurons by minimizing mitochondrial related oxidative damage. In this regard, exploration of the multitude of mitochondrial mechanisms altered in the pathogenesis of AD constitutes novel promising therapeutic targets for the disease. In this review, we will summarize recent progress that underscores the essential role of mitochondria dysfunction in the pathogenesis of AD and discuss mechanisms underlying mitochondrial dysfunction with a focus on the loss of mitochondrial structural and functional integrity in AD including mitochondrial biogenesis and dynamics, axonal transport, ER-mitochondria interaction, mitophagy and mitochondrial proteostasis. The major symptom presents as deterioration of cognition and memory functions due to the progressive and selective loss of neurons in forebrain and other brain areas.

The Role of Oxidative Stress in Alzheimer Disease

The nuclear factor erythroid-derived 2 NF-E2 -related factor 2 Nrf2 is a transcription factor well-known for its function in controlling the basal and inducible expression of a variety of antioxidant and detoxifying enzymes. As part of its cytoprotective activity, increasing evidence supports its role in metabolism and mitochondrial bioenergetics and function. Neurodegenerative diseases are excellent candidates for Nrf2-targeted treatments. Together with them, mitochondrial dysfunction is implicated in the pathogenesis of most neurodegenerative disorders.

Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Many lines of evidence suggest that mitochondria have a central role in ageing-related neurodegenerative diseases.

Mitochondrial Dysfunction and Oxidative Stress in Alzheimer’s Disease

These pathological conditions are characterized by progressive loss of neuron cells, compromised motor or cognitive functions, and accumulation of abnormally aggregated proteins. Mitochondrial dysfunction is one of the main features of the aging process, particularly in organs requiring a high-energy source such as the heart, muscles, brain, or liver.

Neurodegenerative Diseases: Potential Effect of Glutathione

Author contributions: Xueping Chen is responsible for designing and writing the manuscript. Chunyan Guo helps to revise the manuscript. Jiming Kong is responsible for manuscript oversight and instruction. The mitochondrial respiratory chain and enzymatic reactions by various enzymes are endogenous sources of reactive oxygen species. Exogenous reactive oxygen species -inducing stressors include ionizing radiation, ultraviolet light, and divergent oxidizing chemicals.

Markesbery WR. Arch Neurol. Increasing evidence demonstrates that oxidative stress causes damage to cell function with aging and is involved in a number of age-related disorders including atherosclerosis, arthritis, and neurodegenerative disorders. In the neurodegenerative diseases, oxidative stress has been implicated in amyotrophic lateral sclerosis, Parkinson disease, Huntington disease, and Alzheimer disease AD. The neurodegenerative disorder receiving the most attention has been AD, in which an increase occurs in oxidation of brain lipids, carbohydrates, proteins, and DNA. Some of the products of oxidation have been found in the major histopathologic alterations in AD: the neurofibrillary tangles NFTs and senile plaques reviewed in Markesbery and Carney 1 and Ceballos-Picot 2.

Interestingly, the mitochondria have been also implicated as central executioners of cell death. This is a preview of subscription content, access via your institution. Rent this article via DeepDyve. Frandsen, A. Excitatory amino acid-mediated cytotoxicity and calcium homeostasis in cultured neurons. Tymianski, M.

Oxidative Stress in Neurodegenerative Diseases: From a Mitochondrial Point of View

Background

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Oxidative stress and mitochondrial dysfunction-linked neurodegenerative disorders

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