Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/83587
Title: The small molecule AUTEN-99 (autophagy enhancer-99) prevents the progression of neurodegenerative symptoms
Authors: Kovács, Tibor
Billes, Viktor
Komlós, Marcell
Hotzi, Bernadette
Manzéger, Anna
Tarnóci, Anna
Papp, Diána
Szikszai, Fanni
Szinyákovics, Janka
Rácz, Ákos
Noszál, Béla
Veszelka, Szilvia
Walter, Fruzsina R.
Deli, Mária A.
Hackler, Laszlo
Alfoldi, Robert
Huzian, Orsolya
Puskas, Laszlo G.
Liliom, Hanna
Tárnok, Krisztián
Schlett, Katalin
Borsy, Adrienn
Welker, Ervin
Kovács, Attila L.
Pádár, Zsolt
Erdős, Attila
Legradi, Adam
Bjelik, Annamaria
Gulya, Károly
Gulyás, Balázs
Vellai, Tibor
Keywords: Drug discovery
Diseases
Issue Date: 2017
Source: Kovács, T., Billes, V., Komlós, M., Hotzi, B., Manzéger, A., Tarnóci, A., et al. (2017). The small molecule AUTEN-99 (autophagy enhancer-99) prevents the progression of neurodegenerative symptoms. Scientific Reports, 7, 42014-.
Series/Report no.: Scientific Reports
Abstract: Autophagy functions as a main route for the degradation of superfluous and damaged constituents of the cytoplasm. Defects in autophagy are implicated in the development of various age-dependent degenerative disorders such as cancer, neurodegeneration and tissue atrophy, and in accelerated aging. To promote basal levels of the process in pathological settings, we previously screened a small molecule library for novel autophagy-enhancing factors that inhibit the myotubularin-related phosphatase MTMR14/Jumpy, a negative regulator of autophagic membrane formation. Here we identify AUTEN-99 (autophagy enhancer-99), which activates autophagy in cell cultures and animal models. AUTEN-99 appears to effectively penetrate through the blood-brain barrier, and impedes the progression of neurodegenerative symptoms in Drosophila models of Parkinson’s and Huntington’s diseases. Furthermore, the molecule increases the survival of isolated neurons under normal and oxidative stress-induced conditions. Thus, AUTEN-99 serves as a potent neuroprotective drug candidate for preventing and treating diverse neurodegenerative pathologies, and may promote healthy aging.
URI: https://hdl.handle.net/10356/83587
http://hdl.handle.net/10220/42675
ISSN: 2045-2322
DOI: 10.1038/srep42014
Schools: Lee Kong Chian School of Medicine (LKCMedicine) 
Rights: © 2017 The Author(s) (Nature Publishing Group). This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:LKCMedicine Journal Articles

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