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Updated: Feb 6, 2026

A Novel Method to Model Chronic Traumatic Encephalopathy in Drosophila
Published on: July 4, 2017
TGFβ1: Friend or Foe During Recovery in Encephalopathy
Brian H Kim1, Steven W Levison1
11 Department of Pharmacology, Physiology and Neuroscience, Rutgers University-New Jersey Medical School, Newark, NJ, USA.
Abstract:
The cytokine transforming growth factor (TGF)-β1 is highly induced after encephalopathic brain injury, with data showing that it can both contribute to the pathophysiology and aid in disease resolution. In the immature brain, sustained TGFβ-signaling after injury may prolong inflammation to both exacerbate acute stage damage and perturb the normal course of development. Yet in adult encephalopathy, elevated TGFβ1 may promote a reparative state. In this review, we highlight the context-dependent actions of TGFβ-signaling in the brain during resolution of encephalopathy and focus on neuronal survival mechanisms that are affected by TGFβ1. We discuss the mechanisms that contribute to the disparate actions of TGFβ1 toward elucidating the long-term neurological and neuropsychiatric consequences that follow encephalopathic injury.
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