Pathophysiology of amyotrophic lateral ]sclerosi using aipha-tocopherol transfer protein gene knockout mouse.

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1) MDA and HNE modifications in the brain of aTTP null mouse were increased and improved by vitamin E supplementation.2) HNE-modified protein is SOD. This modification disturbed the radical scavenge function of SOD, resulting in enhance the oxidative stress by vitamin E deficiency.3) Dopamine content in the striatum of aTTP null mouse was decreased after administration of MPTP, indicating dopamine decrease in Parkinson disease is related to oxidative stress.4) Onset of symptom in G93ASOD1 TgM crossed with aTTP null mouse is accelerated with more marked degeneration of anterior horn cell, indicating pathophysiology of ALS is affected by oxidative stress,