期刊
NEUROBIOLOGY OF DISEASE
卷 138, 期 -, 页码 -出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2020.104784
关键词
Apolipoprotein E; Immunomodulation; Oligomers; Early onset AD; Therapy; Peptoids; Pathological chaperone; Beta amyloid; Interaction
资金
- NIH [NS073502, AG008051]
- Bluesand Foundation
- Edward and Della L. Thome Memorial Foundation
- Dementia Australia
Alzheimer's disease (AD) is a devastating neurodegenerative disorder that is growing in prevalence globally. It is the only major cause of death without any effective pharmacological means to treat or slow progression. Inheritance of the epsilon 4 allele of the Apolipoprotein (APO) E gene is the strongest genetic risk factor for late-onset AD. The interaction between APOE and amyloid beta (A beta) plays a key role in AD pathogenesis. The APOE-A beta interaction regulates A beta aggregation and clearance and therefore directly influences the development of amyloid plaques, congophilic amyloid angiopathy and subsequent tau related pathology. Relatively few AD therapeutic approaches have directly targeted the APOE-A beta interaction thus far. Here we review the critical role of APOE in the pathogenesis of AD and some of the most promising therapeutic approaches that focus on the APOE-A beta interaction.
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