TY  - GEN
T1  - Beta-blockers reduce intestinal permeability and early mortality following traumatic brain injury in Drosophila
AU  - Scharenbrock, Amanda R
AU  - Katzenberger, Rebeccah J
AU  - Fischer, Megan C
AU  - Ganetzky, Barry
AU  - Wassarman, David A
DO  - 10.17912/micropub.biology.000461
UR  - http://beta.micropublication.org/journals/biology/micropub-biology-000461/
AB  - Traumatic brain injury (TBI) is a substantial public health problem with treatment made difficult by unique neurological sequelae of individual cases (Johnson and Griswold 2017; Pavlovic et al. 2019). Pathological processes evolve over time after TBI and are associated with complex changes in neurotransmitter systems (McGuire et al. 2019). Relevant neurotransmitters include catecholamines such as norepinephrine, epinephrine, and dopamine that target adrenergic receptors (Jenkins et al. 2016). Elevated levels of circulating catecholamines in plasma, in particular epinephrine, at the time of hospital admission after TBI are associated with increased risk of worse functional outcomes and mortality (Woolf et al. 1987; Rizoli et al. 2017). Furthermore, retrospective and prospective studies show that TBI patients treated with beta-blockers, agents that block binding of epinephrine to its receptor, have a significantly reduced risk of mortality (Cotton et al. 2007; Schroeppel et al. 2010; Alali et al. 2014; Mohseni et al. 2015; Ko et al. 2016; Khalini et al. 2020; Florez-Perdomo et al. 2021). Beta-blockers appear to act on trauma-induced signals from the brain, since non-head trauma patients treated with beta-blockers do not have a reduced risk of mortality (Hendrick et al. 2016).
PY  - 2021
JO  - microPublication Biology
ER  -