Editing Autophagy
Warning: You are not logged in. Your IP address will be publicly visible if you make any edits. If you log in or create an account, your edits will be attributed to your username, along with other benefits.
The edit can be undone.
Please check the comparison below to verify that this is what you want to do, and then save the changes below to finish undoing the edit.
Latest revision | Your text | ||
Line 11: | Line 11: | ||
''The most prevalent pathological features of many neurodegenerative diseases are the aggregation of misfolded proteins and the loss of certain neuronal populations. Autophgy, as major intracellular machinery for degrading aggregated proteins and damaged organelles, has been reported to be involved in the occurance of pathological changes in many neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis. In this review, we summarized most recent research progress in this topic and provide a new perspective regarding autophagy regulation on the pathogenesis of neurodegenerative diseases. Finally, we further discussed the signaling molecules in autophagy-related pathways as therapeutic targets for the treatment of these diseases. ''' {{#pmid:28703923|guo2017}} | ''The most prevalent pathological features of many neurodegenerative diseases are the aggregation of misfolded proteins and the loss of certain neuronal populations. Autophgy, as major intracellular machinery for degrading aggregated proteins and damaged organelles, has been reported to be involved in the occurance of pathological changes in many neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis. In this review, we summarized most recent research progress in this topic and provide a new perspective regarding autophagy regulation on the pathogenesis of neurodegenerative diseases. Finally, we further discussed the signaling molecules in autophagy-related pathways as therapeutic targets for the treatment of these diseases. ''' {{#pmid:28703923|guo2017}} | ||
− | |||
− | |||
== References == | == References == |