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 exactly equivalent
portioning of cytoplasm (and thus mitochondrial genes) during the fissioning
process that produces MZ twins; MZ twins need not be genetically identical
with respect to mitochondrial genes. Monozygotic twins may be discordant for
many years for disorders arising via mitochondrial genetic mechanisms.3- 4
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Country-Specific Mortality and Growth Failure in Infancy and Yound Children and
Association With Material Stature
Use interactive graphics and maps to view and sort country-specific infant and early
dhildhood mortality and growth failure data and their association with maternal
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