Mitochondrial Transcription Factor A (TFAM) is a key activator of mitochondrial (mt) DNA transcription as well as a participant in mitochondrial genome replication. mtDNA is highly susceptible to oxidative stress leading to mitochondrial dysfunction. Overexpression of TFAM has been implicated in the amelioration of age dependent impairment of brain functions through the prevention of oxidative stress and mitochondrial dysfunction in microglia (Hayashi et al., 2008). More recently, TFAM overexpression has been shown to potentially reduce oxidative stress in motor neurons and delay onset of amyotrophic lateral sclerosis (ALS) in ALS model mice (Morimoto et al., 2012).
