Mitochondrial dysfunction is common in the CNS with stroke, SCI, TBI, ALS, MS, Huntington's disease and Alzheimer's disease (Mecocci et al., 1996; Mattiazzi et al., 2002; Wiedemann et al., 2002; Korde et al., 2005, 2007; Vijayvergiya et al., 2005; Dutta et al., 2006; Singh et al., 2006; Sullivan et al., 2007; Robertson et al., 2007; Regenold et al., 2008; Vyshkina et al., 2008; Martin et al., 2009; Pandya et al., 2009; Patel et al., 2009; Readnower et al., 2011; Sauerbeck et al., 2011; Zhao et al., 2011; Lunnon et al., 2012). In these conditions, mitochondrial dysfunction correlates with cell death, functional impairment, and cognitive deficit. This is intuitively obvious since energy production by mitochondria is essential for survival of all cells, including neurons (Nicholls and Budd, 2000; Stephans et al., 2002; Borland et al., 2008). Oligodendrocytes also have high energy demands since they must maintain large amounts of plasma membrane as myelin. Damage to oligodendrocyte mitochondria impairs energy metabolism resulting in reduced myelin production and compaction, and ultimately hypo-myelination or complete axon demyelination (Kalman et al., 1997). Accordingly, finding new therapies that protect mitochondria should help protect neurons and oligodendrocytes in most, if not all, forms of CNS disease.
