Genetic stabilization of transthyretin, cerebrovascular disease, and life expectancy

44 Citationer (Scopus)

Abstract

Transthyretin can cause amyloidosis attributable to destabilization of transthyretin tetramers in plasma. We tested the hypothesis that genetic stabilization of transthyretin associates with reduced risk of vascular disease and increased life expectancy. APPROACH AND RESULTS: We included 68 602 participants from 2 prospective studies of the general population. We genotyped for 2 stabilizing genetic variants in the transthyretin gene (TTR), R104H and T119M, and determined the association of genotypes with plasma levels of transthyretin, measures of thyroid function, risk of vascular disease, and life expectancy. During a mean follow-up of 32 years, 10 636 participants developed vascular disease. We identified 321 heterozygotes for T119M (frequency, 0.47%); R104H was not detected. First, mean plasma transthyretin and thyroxine levels were increased by 17% (26 µg/mL) and 20% (19 nmol/L), respectively, in heterozygotes versus noncarriers (P=0.007 and P
OriginalsprogEngelsk
TidsskriftArteriosclerosis, Thrombosis, and Vascular Biology
Vol/bind33
Udgave nummer6
Sider (fra-til)1441-7
Antal sider7
ISSN1079-5642
DOI
StatusUdgivet - jun. 2013

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