ironjustice
2011-12-31 00:29:18 UTC
"Iron overload may be a causative factor "
Transferrin and HFE genes interact in Alzheimer's disease risk: the
Epistasis Project.
Lehmann DJ,Schuur M, Warden DR, Hammond N, Belbin O, Kölsch H, Lehmann
MG, Wilcock GK, Brown K, Kehoe PG, Morris CM,
Coto E, Barker R, Alvarez V, Deloukas P, Mateo I, Gwilliam R,
Combarros O, Arias-Vásquez A, Aulchenko YS, Ikram MA, Breteler MM, van
Duijn CM, Oulhaj A, Heun R, Cortina-Borja M, Morgan K, Robson K,Smith
AD
Oxford Project to Investigate Memory and Ageing (OPTIMA),
University Department of Physiology, Anatomy and Genetics, Oxford, UK.
Neurobiology of Aging [2012, 33(1):202.e1-202.e13]
Abstract
Iron overload may contribute to the risk of Alzheimer's disease (AD).
In the Epistasis Project, with 1757 cases of AD and 6295 controls, we
studied 4 variants in 2 genes of iron metabolism: hemochromatosis
(HFE) C282Y and H63D, and transferrin (TF) C2 and -2G/A.
We replicated the reported interaction between HFE 282Y and TF C2 in
the risk of AD: synergy factor, 1.75 (95% confidence interval,
1.1-2.8, p = 0.02) in Northern Europeans.
The synergy factor was 3.1 (1.4-6.9; 0.007) in subjects with the
APOEε4 allele.
We found another interaction, between HFE 63HH and TF -2AA, markedly
modified by age.
Both interactions were found mainly or only in Northern Europeans.
The interaction between HFE 282Y and TF C2 has now been replicated
twice, in altogether 2313 cases of AD and 7065 controls, and has also
been associated with increased iron load.
We therefore suggest that iron overload may be a causative factor in
the development of AD.
Treatment for iron overload might thus be protective in some cases.
(PMID:20817350)
DOI: 10.1016/j.neurobiolaging.2010.07.018
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Tom
Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
Transferrin and HFE genes interact in Alzheimer's disease risk: the
Epistasis Project.
Lehmann DJ,Schuur M, Warden DR, Hammond N, Belbin O, Kölsch H, Lehmann
MG, Wilcock GK, Brown K, Kehoe PG, Morris CM,
Coto E, Barker R, Alvarez V, Deloukas P, Mateo I, Gwilliam R,
Combarros O, Arias-Vásquez A, Aulchenko YS, Ikram MA, Breteler MM, van
Duijn CM, Oulhaj A, Heun R, Cortina-Borja M, Morgan K, Robson K,Smith
AD
Oxford Project to Investigate Memory and Ageing (OPTIMA),
University Department of Physiology, Anatomy and Genetics, Oxford, UK.
Neurobiology of Aging [2012, 33(1):202.e1-202.e13]
Abstract
Iron overload may contribute to the risk of Alzheimer's disease (AD).
In the Epistasis Project, with 1757 cases of AD and 6295 controls, we
studied 4 variants in 2 genes of iron metabolism: hemochromatosis
(HFE) C282Y and H63D, and transferrin (TF) C2 and -2G/A.
We replicated the reported interaction between HFE 282Y and TF C2 in
the risk of AD: synergy factor, 1.75 (95% confidence interval,
1.1-2.8, p = 0.02) in Northern Europeans.
The synergy factor was 3.1 (1.4-6.9; 0.007) in subjects with the
APOEε4 allele.
We found another interaction, between HFE 63HH and TF -2AA, markedly
modified by age.
Both interactions were found mainly or only in Northern Europeans.
The interaction between HFE 282Y and TF C2 has now been replicated
twice, in altogether 2313 cases of AD and 7065 controls, and has also
been associated with increased iron load.
We therefore suggest that iron overload may be a causative factor in
the development of AD.
Treatment for iron overload might thus be protective in some cases.
(PMID:20817350)
DOI: 10.1016/j.neurobiolaging.2010.07.018
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk