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Am J Psychiatry 1995; 152:164-172
Copyright © 1995 by American Psychiatric Association
Unstable genes--unstable mind?
A Petronis and JL Kennedy
Department of Neurogenetics, Clarke Institute of Psychiatry, Toronto, Ont., Canada.
OBJECTIVE: Over the past 3 years, reports of DNA alteration in myotonic
dystrophy, fragile X syndrome (types A and E), Kennedy's disease,
Huntington's disease, spinocerebellar ataxia type 1, and dentatorubral-
pallidoluysian atrophy have identified a new class of human mutation,
referred to as trinucleotide repeat amplification. All available evidence
suggests that this unstable trinucleotide repeat DNA is the biological
basis of the clinical phenomenon of genetic anticipation. Two components of
anticipation, greater severity and earlier age at onset in subsequent
generations, have been widely observed in schizophrenia and bipolar
affective disorder. Thus, a reanalysis of the genetics of major psychosis
from the perspective of unstable DNA is of significant interest. METHOD:
The authors reviewed the available literature on anticipation and related
phenomena in major psychosis and reevaluated the family, twin, and adoption
study data. RESULTS: The unstable DNA concept competes well with the
traditional multifactorial polygenic theory; many deviations from a single
gene mode of inheritance in psychiatric twin and family studies, which
previously served as strong proof for more than one etiologic gene, can be
easily explained by the non-Mendelian behavior of unstable DNA. In
addition, this new paradigm provides a simple explanation for unclear
issues in the genetics of major psychosis, such as the identical rate of
psychosis in the offspring of discordant monozygotic twins. CONCLUSIONS:
The major advantage of the unstable DNA hypothesis over the multifactorial
polygenic theory lies in the possibility of falsifying the unstable DNA
hypothesis by two independent laboratory strategies: a classical linkage
analysis and a set of novel methods for the direct detection of unstable
DNA sites.
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