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To the Editor: Dr Tanner and colleagues¹ investigated potential genetic contributions to the cause of sporadic Parkinson disease (PD) through the ascertainment of PD in monozygotic (MZ) and dizygotic (DZ) twin pairs and found that concordance for PD was low and was equivalent in MZ and DZ pairs. They concluded that heredity is not a major causal component in most cases of PD.

While this study argues strongly against a role for conventional Mendelian (chromosomal) genetic mechanisms in PD, it does not argue against all genetic mechanisms since it fails to evaluate mitochondrial genetics. Mitochondrial genes are inherited cytoplasmically and maternally and do not follow the rules of Mendelian inheritance upon which the study by Tanner et al is predicated. Mutations in mitochondrial genes are known to cause human diseases that do not follow Mendelian patterns.² Unlike the case with nuclear genes, there is no a priori basis for assuming . . . [Full Text of this Article]

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Parkinson Disease in Twins: An Etiologic Study
Caroline M. Tanner, Ruth Ottman, Samuel M. Goldman, Jonas Ellenberg, Piu Chan, Richard Mayeux, and J. William Langston
JAMA. 1999;281(4):341-346.
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