Journal
NEUROBIOLOGY OF AGING
Volume 95, Issue -, Pages 161-167Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2020.06.020
Keywords
Alzheimer's disease; Amyloid beta; TDP-43; TARDBP; Amyotrophic lateral sclerosis; Limbic-predominant age-related TDP-43 encephalopathy; Protein oligomers; Comorbidity
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Funding
- National Research Foundation of Korea [NRF-2020R1A2B5B01002463]
- Gachon University [2018-0682]
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder that results from the accumulation of plaques by cleaved A beta(42) peptides as well as neurofibrillary tangles of tau proteins. This accumulation triggers a complex cascade of cytotoxic, neuroinflammatory, and oxidative stresses that lead to neuronal death throughout the progression of the disease. Much of research in AD focused on the 2 pathologic proteins. Interestingly, another form of dementia with similar clinical manifestations of AD, but preferentially affected much older individuals, was termed as limbic-predominant age-related transactive response DNA-binding protein 43 (TDP-43) encephalopathy (LATE) and involved the cytotoxic intraneuronal deposition of phosphorylated TDP-43. TDP-43 proteinopathy was also found to be involved in AD pathology leading to the possibility that AD and LATE may share a common upstream etiology. This paper discusses the roles molecular pathways known in AD may have on influencing TDP-43 proteinopathy and the development of AD, LATE, or the 2 being comorbid with each other. (C) 2020 Elsevier Inc. All rights reserved.
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