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The Emerging Role of Autophagy-Associated lncRNAs in the Pathogenesis of Neurodegenerative Diseases

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MDPI
DOI: 10.3390/ijms24119686

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lncRNA; autophagy; neurodegenerative disease; Alzheimer's disease; Parkinson's disease

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Neurodegenerative diseases are a major global health problem, and identifying molecular markers related to neurodegenerative processes is urgently important. Defects in autophagy, the process of removing aggregate-prone proteins in neurons, are often associated with the development of neurodegenerative diseases. Aberrant regulation of long non-coding RNAs (lncRNAs) also plays a role in neurological disorders. This review summarizes the recent progress in studying lncRNAs and autophagy in the context of neurodegenerative disorders, particularly Alzheimer's disease (AD) and Parkinson's disease (PD), providing guidance for future research in this field.
Neurodegenerative diseases (NDDs) have become a significant global public health problem and a major societal burden. The World Health Organization predicts that NDDs will overtake cancer as the second most common cause of human mortality within 20 years. Thus, it is urgently important to identify pathogenic and diagnostic molecular markers related to neurodegenerative processes. Autophagy is a powerful process for removing aggregate-prone proteins in neurons; defects in autophagy are often associated with the pathogenesis of NDDs. Long non-coding RNAs (lncRNAs) have been suggested as key regulators in neurodevelopment; aberrant regulation of lncRNAs contributes to neurological disorders. In this review, we summarize the recent progress in the study of lncRNAs and autophagy in the context of neurodegenerative disorders, especially Alzheimer's disease (AD) and Parkinson's disease (PD). The information presented here should provide guidance for future in-depth investigations of neurodegenerative processes and related diagnostic molecular markers and treatment targets.

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