Genetic stabilization of transthyretin, cerebrovascular disease, and life expectancy

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Standard

Genetic stabilization of transthyretin, cerebrovascular disease, and life expectancy. / Hornstrup, Louise S; Frikke-Schmidt, Ruth; Nordestgaard, Børge G; Tybjærg-Hansen, Anne.

I: Arteriosclerosis, Thrombosis, and Vascular Biology, Bind 33, Nr. 6, 06.2013, s. 1441-7.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Hornstrup, LS, Frikke-Schmidt, R, Nordestgaard, BG & Tybjærg-Hansen, A 2013, 'Genetic stabilization of transthyretin, cerebrovascular disease, and life expectancy', Arteriosclerosis, Thrombosis, and Vascular Biology, bind 33, nr. 6, s. 1441-7. https://doi.org/10.1161/ATVBAHA.113.301273

APA

Hornstrup, L. S., Frikke-Schmidt, R., Nordestgaard, B. G., & Tybjærg-Hansen, A. (2013). Genetic stabilization of transthyretin, cerebrovascular disease, and life expectancy. Arteriosclerosis, Thrombosis, and Vascular Biology, 33(6), 1441-7. https://doi.org/10.1161/ATVBAHA.113.301273

Vancouver

Hornstrup LS, Frikke-Schmidt R, Nordestgaard BG, Tybjærg-Hansen A. Genetic stabilization of transthyretin, cerebrovascular disease, and life expectancy. Arteriosclerosis, Thrombosis, and Vascular Biology. 2013 jun.;33(6):1441-7. https://doi.org/10.1161/ATVBAHA.113.301273

Author

Hornstrup, Louise S ; Frikke-Schmidt, Ruth ; Nordestgaard, Børge G ; Tybjærg-Hansen, Anne. / Genetic stabilization of transthyretin, cerebrovascular disease, and life expectancy. I: Arteriosclerosis, Thrombosis, and Vascular Biology. 2013 ; Bind 33, Nr. 6. s. 1441-7.

Bibtex

@article{2440f6a5e10c4bc89c2ceda55579e06a,
title = "Genetic stabilization of transthyretin, cerebrovascular disease, and life expectancy",
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",
author = "Hornstrup, {Louise S} and Ruth Frikke-Schmidt and Nordestgaard, {B{\o}rge G} and Anne Tybj{\ae}rg-Hansen",
year = "2013",
month = jun,
doi = "10.1161/ATVBAHA.113.301273",
language = "English",
volume = "33",
pages = "1441--7",
journal = "Arteriosclerosis, Thrombosis, and Vascular Biology",
issn = "1079-5642",
publisher = "Lippincott Williams & Wilkins",
number = "6",

}

RIS

TY - JOUR

T1 - Genetic stabilization of transthyretin, cerebrovascular disease, and life expectancy

AU - Hornstrup, Louise S

AU - Frikke-Schmidt, Ruth

AU - Nordestgaard, Børge G

AU - Tybjærg-Hansen, Anne

PY - 2013/6

Y1 - 2013/6

N2 - 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

AB - 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

U2 - 10.1161/ATVBAHA.113.301273

DO - 10.1161/ATVBAHA.113.301273

M3 - Journal article

C2 - 23580146

VL - 33

SP - 1441

EP - 1447

JO - Arteriosclerosis, Thrombosis, and Vascular Biology

JF - Arteriosclerosis, Thrombosis, and Vascular Biology

SN - 1079-5642

IS - 6

ER -

ID: 48539695