Molecular and Cellular Basis of Misfolded Proteins in Neurodegenerative Diseases
نویسندگان
1 Functional Neurosurgery Research Center, Shohada Tajrish Comprehensive Neurosurgical Center of Excellence, Shahid Beheshti University of Medical Sciences, Tehran, Iran
2 Functional Neurosurgery Research Center, Shohada Tajrish Comprehensive Neurosurgical Center of Excellence, Shahid Beheshti University of Medical Sciences, Tehran, Iran
3 Functional Neurosurgery Research Center, Shohada Tajrish Comprehensive Neurosurgical Center of Excellence, Shahid Beheshti University of Medical Sciences, Tehran, Iran
4 Functional Neurosurgery Research Center, Shohada Tajrish Comprehensive Neurosurgical Center of Excellence, Shahid Beheshti University of Medical Sciences, Tehran, Iran
doi
39176چکیده
Neurodegeneration is characterized by a progressive loss of nerve structure and function which lead to cognitive impairment such as dementia. Neurodegenerative diseases (NDs) are partially caused by neuronal cell death and glial homeostasis. NDs such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) can develop with aging. As well, in Huntington’s disease (HD) and amyotrophic lateral sclerosis (ALS), genetic mutations can affect CNS cell function. NDs occur through important processes including, protein misfolding and aggregation of misfolded proteins. These processes cause neurofibrillary tangles and plaques that result in neuronal cytotoxicity. Here, our intention is to shed light on some of the key roles of protein misfolding and aggregation in NDs. This review focuses specifically on understanding the molecular and cell-based mechanisms of protein misfolding and aggregation involved in the development of NDs.
