期刊
PHARMACOLOGY & THERAPEUTICS
卷 172, 期 -, 页码 22-33出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pharmthera.2016.11.010
关键词
Alzheimer's disease; Parkinson's disease; ALS; Tau; alpha-synuclein; TDP-43
资金
- Ministry of Education Japan Society for the Promotion of Science KAKENHI Grant [23228004]
- Ministry of Health, Labor, and Welfare of Japan [12946221]
- Research Committee on Establishment of Novel Treatments for Amyotrophic Lateral Sclerosis
- Brain Mapping by Integrated Neurotechnologies for Disease Studies (Brain/MINDS) from Japan Agency for Medical Research and Development, AMED
- Grants-in-Aid for Scientific Research [23228004] Funding Source: KAKEN
Prion-like propagation of abnormal intracytoplasmic proteins, which are the defining features of major neurodegenerative disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS), has been proposed. A growing body of evidence strongly suggests that abnormal tau, alpha-synuclein and TDP-43 have prion-like properties, convert the corresponding normal proteins into abnormal forms, and are transmitted from cell to cell, spreading throughout the brain. This idea is extremely important not only for understanding the pathogenesis and progression of these diseases, but also for the development of molecular therapies. Since the distributions and spreading of the abnormal proteins are closely associated with disease symptoms and progression, gain-of-toxic-function of these proteins may affect the neurons and glial cells either directly or indirectly, or both. It is essential to regulate the aggregation of abnormal intracellular proteins and their cell-to-cell transmission in order to stop, or at least slow, the progression of these diseases. (C) 2016 Elsevier Inc. All rights reserved.
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