Twins With Alzheimer's Disease

Cook, Robert H.; Schneck, Stuart A.; Clark, David B.

doi:10.1001/archneur.1981.00510050066011

Cited by 60 publications

(23 citation statements)

References 10 publications

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“…They may succumb to the same disease, but often the age of onset is years or even decades apart. An interesting example is a report of twins, both of whom developed histologically confirmed dementia of the Alzheimer's type; one had the diagnosis in her late 60s but the other was not diagnosed until age 83 (1). The conventional wisdom is that the bulk of these differences can be attributable to good or bad luck with one's environmental exposures, to the quality of medical and spousal care (or abuse), or to learned behavioral differences in how we exercise (perhaps mentally and physically) and what we eat, drink, or smoke, among myriad other possibilities.…”

mentioning

confidence: 99%

Epigenetic drift in aging identical twins

Martin

2005

Proc. Natl. Acad. Sci. U.S.A.

172

119

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confidence: 99%

Epigenetic drift in aging identical twins

Martin

2005

Proc. Natl. Acad. Sci. U.S.A.

172

119

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“…The most compelling evidence against to tally genetic inheritance is the discordance for AD among monozygotic twins [20,21], Cook et al [8] reported a pair of twins who were identical in appearance, both of whom developed AD that was documented by histopathology. The interesting aspect of this pair was that the age of onset of AD differed in the two cases by over 10 years.…”

Section: Discordance In Monozygotic Twinsmentioning

confidence: 99%

“…This is an arti fact which can arise because respondents of an affected person would be more motivated to seek out and recall similar cases in other family members than would be respondents of unaffected controls. (8) Rates of occur rence of AD in family members of probands should be compared to the rates in appro priate controls which takes into account the age and sex composition of the two groups.…”

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confidence: 99%

Inheritance of Alzheimer's Disease: Epidemiologic Evidence

Chandra

Schoenberg²

1989

Neuroepidemiology

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The available evidence suggests that there may be two subtypes of AD – inherited and noninherited. Inherited AD may have certain characteristics, e.g. younger age at onset and some clinical signs or symptoms, which distinguish them from noninherited cases. It is possible that the noninherited type of AD may also have a similar genetic defect as the inherited kind, the only difference being that in one case the defect is inherited from the parents and in the other the defect arises de novo during embryogenesis. An environmental factor operating during embryogenesis may be responsible for causing a genetic defect which later manifests as noninherited AD. Currently, however, there is no precise way to separate these two subtypes. The exact proportion of all cases of AD which are inherited on a genetic basis is not known, but it must be small. The mode of inheritance of genetic AD is not known. It must be emphasized that the subtypes of inherited and noninherited AD are not synonymous with the older categorization of AD into presenile and senile AD.

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“…On the other hand, when monozygotic twins are discordant for AD, differences in environmental exposure are likely to have determined the development of the disease [19]. In longitudinal studies, the onset of AD between monozygotic co-twins who eventually become concordant has varied by several years [14,20,21], indicating the contribution of environmental factors to the manifestation age of disease.…”

Section: Introductionmentioning

confidence: 99%

Regional Cerebral Glucose Metabolism in Monozygotic Twins Discordant for Alzheimer’s Disease

Järvenpää

Räihä

Kaprio

et al. 2003

Dement Geriatr Cogn Disord

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We investigated regional cerebral glucose metabolic rates (rCMRgluc) with positron emission tomography using 2-[¹⁸F]fluoro-2-deoxy-D-glucose (FDG) in 7 monozygotic twin pairs discordant for Alzheimer’s disease (AD). Ten healthy volunteers with comparable mean age and educational level served as controls. In the hippocampus, the mean ± SD rCMRgluc were 0.20 ± 0.03 µmol/ml/min for the demented twins, 0.21 ± 0.03 µmol/ml/min for their non-demented co-twins, and 0.23 ± 0.02 µmol/ml/min for the controls. The mean hippocampal rCMRgluc was reduced in the demented twins (p = 0.006), compared with the controls. In the lateral temporal cortex, the mean ± SD rCMRgluc were 0.27 ± 0.05, 0.28 ± 0.04, and 0.32 ± 0.02 µmol/ml/min, respectively. These mean rates were reduced both in the demented (p = 0.02) and the non-demented (p = 0.01) twins, compared with the controls. In conclusion, in the demented twins, the reduction of rCMRgluc was detected in the hippocampus and lateral temporal cortex, i.e. the 2 brain areas which show early changes in pathological and imaging studies in AD. Their non-demented co-twins showed milder reductions, which may be an indication of genetic susceptibility for dementia, and an early sign of a dementing illness in them.

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Twins With Alzheimer's Disease

Cited by 60 publications

References 10 publications

Epigenetic drift in aging identical twins

Epigenetic drift in aging identical twins

Inheritance of Alzheimer's Disease: Epidemiologic Evidence

Regional Cerebral Glucose Metabolism in Monozygotic Twins Discordant for Alzheimer’s Disease

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