Mutations in mitochondrial DNA appear to be responsible for a number of neurological disorders, including myoclonic epilepsy and ragged-red fiber disease, Leber's hereditary optic neuropathy, and Kearns-Sayre syndrome. In each case, the disease phenotype is expressed when the ratio of mutant to wild-type mitochondria exceeds a threshold peculiar to each disease, but usually in the 60 to 95 percent range. Given that these are debilitating conditions, why has no cure been developed?

a. The defective mitochondria would need to be corrected for a cure to be achieved, and that appears to be technologically impossible at this time.
b. The defective mitochondria would need to be identified for a cure to be achieved, and that appears to be technologically impossible at this time.
c. The defective mitochondria would need to be corrected for a cure to be achieved, and that appears to be very expensive.
d. The defective mitochondria would need to be corrected for a cure to be achieved, and that may cause damage to the whole organism.

Can you suggest a general approach that might be used to treat, or perhaps even cure, these disorders?

a. Suppress the replication of mutant mitochondria and favor the replication of normal mitochondria.
b. Suppress the replication of normal mitochondria and favor the replication of mutant mitochondria.
c. Favor the replication of both mutant and normal mitochondria.
d. Suppress the replication of both mutant and normal mitochondria.

Compared with the vast number of mitochondria in an embryo, the number of mitochondria in an ovum is relatively small. Might such an ooplasmic mitochondrial bottleneck present an opportunity for therapy or cure?

a. It may be possible to cure it by increasing mitochondria number in any way.
b. It may be possible to alter the heteroplasmic ratio by favoring replication of mitochondria.
c. It may be possible to alter the heteroplasmic ratio by microinjection of mitochondria.
d. No, there is no opportunity.