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Role of mitochondrial dysfunction in the pathogenesis of Huntingtons disease

For example, astrocyte-specific expression of SOCS3 in AD mouse models was shown to suppress not only GFAP induction and morphological hypertrophy but also neuroprotective and neurotoxic associated markers while simultaneously improving amyloid burden, synaptic function and cognition

The sum of the activity of all CYP3As is the total CYP3A activity, which is responsible for metabolizing 50% of all clinically relevant drugs (Guengerich, 1999