Journal
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
Volume 12, Issue 2, Pages 363-373Publisher
WILEY
DOI: 10.1111/j.1582-4934.2008.00276.x
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Funding
- NIA NIH HHS [K99 AG029729, AG029729A, R00 AG029729] Funding Source: Medline
- NATIONAL INSTITUTE ON AGING [K99AG029729, R00AG029729] Funding Source: NIH RePORTER
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Accumulation of proteins is a recurring event in many neurodegenerative diseases, including Alzheimer's disease (AD).Evidence has suggested that protein accumulation may result from a dysfunction in the ubiquitin proteasome system (UPS). Indeed, there is clear genetic and biochemical evidence of an involvement of the ubiquitin proteasome system in AD. This review summarizes the data supporting an involvement of the UPS in the pathogenesis of AD, focusing on the data showing the relationship between A beta and tau, the two hallmark lesions of AD, and the UPS.
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