Authors:

David Yin

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About Paper:

Oxidative stress plays a significant role in functional loss after spinal cord injury(SCI). As a factor of oxidative stress, lipid-peroxidation releases acrolein, one of the most destructive aldehydes, which damages proteins, lipids, and DNA. Mitochondrial aldehyde dehydrogenase 2(ALDH2) is a critical enzyme that detoxifies acrolein endogenously. However, around 600 million people have mutations, primarily known as "Asian flush," that lower the enzymatic activity of ALDH2. In spinal cord injury, individuals that carry this mutation could lead to the accumulation of acrolein and other toxic aldehydes, worsening the pathological damage associated with the secondary injury and recovery. The first aim of this study is to determine ALDH2*2 mutants' susceptibility to acrolein accumulation and poor recovery after SCI. The ultimate goal of this study is to validate the acrolein- clearing and neuroprotective role of ALDH2 in SCI. By using the transgenic (TG) ALDH2*2 deficiency mouse model that recapitulates the real genetic condition that exists in humans, we observed a more exaggerated acrolein build-up, inflammatory response in the spinal cord, and behavioral dysfunctions when compared to the wild type (WT) after SCI. We also planned to implement an ALDH2 enzyme agonist to alleviate such dysfunctions by rescuing the ALDH2 activity and reducing the level of acrolein.

Source:

Purdue University / 2023

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Co-authors:

David Yin