The analysis of mitochondrial diseases has recently been given substance by:
 
1) the characterization of the natural history and assessment of prognostic criteria of diseases due to large size deletions of the mitochondrial DNA (Auré et al, 2007),
 
2) the description of the clinical features and natural history of diseases due to alteration of the ferritin light chain gene (FTL1) (Chinnery et al, 2007).
 
3) and the description of secondary coenzyme Q10 deficiencies in ataxia with oculomotor apraxia (Le Ber et al, 2007).
 
4) We have evaluated the cellular models brought by patients skin fibroblasts immortalized with the telomerase gene (hTERT) (Auré et al, 2007).

 

5) and we have demonstrated the presence and provoking factors of apoptosis in muscle tissue with a mitochondrial DNA alteration (Fayet et al, 2006).