Journal
ELIFE
Volume 7, Issue -, Pages -Publisher
ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.36768
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Funding
- Parkinson's Foundation Stanley Fahn Junior Faculty Maxime [PF-JFA-1762]
- UCB Pharma
- Robert A. and Renee E. Belfer Family Foundation
- Huffington Foundation
- Howard Hughes Medical Institute
- Intellectual and Developmental Disabilities Research Center NIH [U54 HD083092]
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [U54HD083092] Funding Source: NIH RePORTER
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Alzheimer's and Parkinson's disease are late onset neurodegenerative diseases that will require therapy over decades to mitigate the effects of disease-driving proteins such tau and asynuclein (alpha-Syn). Previously we found that TRIM28 regulates the levels and toxicity of alpha-Syn and tau (Rousseaux et at, 2016). However, it was not clear how TRIM28 regulates alpha-Syn and it was not known if its chronic inhibition later in life was safe. Here, we show that TRIM28 may regulate alpha-Syn and tau levels via SUMOylation, and that genetic suppression of Trim28 in adult mice is compatible with life. We were surprised to see that mice lacking Trim28 in adulthood do not exhibit behavioral or pathological phenotypes, and importantly, adult reduction of TRIM28 results in a decrease of alpha-Syn and tau levels. These results suggest that deleterious effects from TRIM28 depletion are limited to development and that its inhibition adulthood provides a potential path for modulating alpha-Syn and tau levels.
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