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Bad luck An unappreciated limitation in the interpretation of twin studies.

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American Journal of Medical Genetics Part B (Neuropsychiatric Genetics) 141B:681 (2006)
Letter to the Editor
Bad Luck: An Unappreciated Limitation in the
Interpretation of Twin Studies
Please cite this article as follows: Hardy J. 2006. Bad
Luck: An Unappreciated Limitation in the Interpretation of Twin Studies. Am J Med Genet Part B 141B:681.
To the Editor:
The study of concordance and discordance rates for twin has
been, and continues to be, a central methodology in the
dissecting of the influences of nature and nurture in biology
[Martin et al., 1997]. However, an assumption is often drawn
from the analyses of concordance rates in monozygotic
twins that the variance not attributable to genetic influence
must be attributable to environmental influences. This belief
pervades the genetic literature and especially the literature of
psychiatric genetics. However, it is not so. If a biological
process is both stochastic and self-sustaining, it could occur in
one identical twin, but not the other even if their environment
was the same. While this might be thought of as a rather
esoteric limitation of the methodology, in fact there are several
processes that may plausibly fit this description. For example,
synaptic strengthening is self sustaining [Malenka and Bear,
2004] and may underlie psychiatric disorders and permissive
templating, which almost certainly underlies prion disease
pathogenesis [Hill and Collinge, 2003] and may underlie other
amyloid deposition diseases including Alzheimer’s and Parkinson’s disease [Walker et al., 2002; Hardy, 2005] also has the
potential to be both stochastic in initiation and self sustaining
*Correspondence to: John Hardy, Laboratory of Neurogenetics,
National Institute on Aging, Porter Neuroscience Building, 35,
Convent Drive, Bethesda, MD 20892.
E-mail: hardyj@mail.nih.gov
Received 11 March 2006; Accepted 3 April 2006
DOI 10.1002/ajmg.b.30353
ß 2006 Wiley-Liss, Inc.
in propagation. In diseases such as these, and doubtless in
others, one should not interpret lack of complete concordance
in monozygotic twins as necessarily signifying a role for
environmental factors. However unsatisfying it may seem,
bad luck may have an important but unappreciated role in the
initiation of disease.
John Hardy*
Laboratory of Neurogenetics
National Institute on Aging
Bethesda, Maryland
REFERENCES
Hardy J. 2005. Expression of normal sequence pathogenic proteins for
neurodegenerative disease contributes to disease risk: ‘Permissive
templating’ as a general mechanism underlying neurodegeneration.
Biochem Soc Trans 33:578–581.
Hill AF, Collinge J. 2003. Subclinical prion infection. Trends Microbiol
11:578–584.
Malenka RC, Bear MF. 2004. LTP and LTD: an embarrassment of riches.
Neuron 44:5–21.
Martin N, Boomsma D, Machin G. 1997. A twin-pronged attack on complex
traits. Nat Genet 17:387–392.
Walker LC, Callahan MJ, Bian F, Durham RA, Roher AE, Lipinski WJ.
2002. Exogenous induction of cerebral beta-amyloidosis in betaAPPtransgenic mice. Peptides 23:1241–1247.
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