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Hannah E
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Hannah E

Reporter

AS SEEN ON
SaportaReport, National Review, MDPI

Preston's Summary

Hannah E is a Reporter at various esteemed publications. With a strong foundation in journalism and public policy from Georgia State University, she focuses on environmental issues, urban life, and storytelling, often covering topics related to Georgia, Atlanta, and NYC, as well as pressing issues like the Coronavirus. Hannah's work has been featured in notable outlets such as The Wall Street Journal, Newsweek, and the New York Daily News.

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Geo Focus

United States (National)

Coverage Attributes:

Beta
Cites Data: 21 %
Event Coverage: 16 %
Government Announcement: 11 %
Press Release: 11 %
Expert Commentary: 10 %

Themes Covered:

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Articles

MDPI

Obatoclax Rescues FUS-ALS Phenotypes in iPSC-Derived Neurons by Inducing Autophagy

Obatoclax Rescues FUS-ALS Phenotypes in iPSC-Derived Neurons by Inducing Autophagy

By: Maximina H.,, Marc, Pelucchi, Jared, Kristin, Castillo Bautista, Silvia, Hannah E., Cristina Marisol, Walters, Sterneckert, Mertens, Jerome, Gentzel, Yun, Eismann

Aging is associated with the disruption of protein homeostasis and causally contributes to multiple diseases, including amyotrophic lateral sclerosis (ALS). One strategy for restoring protein homeostasis and protecting neurons against age-dependent diseases such as ALS is to de-repress autophagy. BECN1 is a master regulator of autophagy; however, is repressed by BCL2 via a BH3 domain-mediated interaction. We used an induced pluripotent stem cell model of ALS caused by mutant FUS to identify a small molecule BH3 mimetic that disrupts the BECN1-BCL2 interaction. We identified obatoclax as a brain-penetrant drug candidate that rescued neurons at nanomolar concentrations by reducing cytoplasmic FUS levels, restoring protein homeostasis, and reducing degeneration. Proteomics data suggest that obatoclax protects neurons via multiple mechanisms. Thus, obatoclax is a candidate for repurposing as a possible ALS therapeutic and, potentially, for other age-associated disorders linked to defects in protein homeostasis.

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