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Novel therapeutic strategies targeting mitochondria as a gateway in neurodegeneration

期刊

NEURAL REGENERATION RESEARCH
卷 18, 期 5, 页码 991-995

出版社

WOLTERS KLUWER MEDKNOW PUBLICATIONS
DOI: 10.4103/1673-5374.355750

关键词

Alzheimer's disease; axon; energy homeostasis; glymphatic system; mitochondria; mitostasis; neurodegeneration; neuroregeneration; Parkinson's disease; therapeutical strategies

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Mitochondrial biology plays a crucial role in adult-onset neurodegenerative disorders, and the dysfunction of mitochondria can contribute to the progression of neuronal dysfunction and cellular death. Conversely, neurodegeneration can also affect mitochondrial health and function. Current research focuses on understanding the relationship between mitochondrial health and neuroregeneration, as well as developing therapeutic approaches to restore mitochondrial homeostasis.
In recent years, multiple disciplines have focused on mitochondrial biology and contributed to understanding its relevance towards adult-onset neurodegenerative disorders. These are complex dynamic organelles that have a variety of functions in ensuring cellular health and homeostasis. The plethora of mitochondrial functionalities confers them an intrinsic susceptibility to internal and external stressors (such as mutation accumulation or environmental toxins), particularly so in long-lived postmitotic cells such as neurons. Thus, it is reasonable to postulate an involvement of mitochondria in aging-associated neurological disorders, notably neurodegenerative pathologies including Alzheimer's disease and Parkinson's disease. On the other hand, biological effects resulting from neurodegeneration can in turn affect mitochondrial health and function, promoting a feedback loop further contributing to the progression of neuronal dysfunction and cellular death. This review examines state-of-the-art knowledge, focus on current research exploring mitochondrial health as a contributing factor to neuroregeneration, and the development of therapeutic approaches aimed at restoring mitochondrial homeostasis in a pathological setting.

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