Giuseppe
Emeritus
Alzheimer's disease gene signature says: beware of brain viral infections (Immunity and Ageing, BioMedCentral, abstract, edited)
[Source: Immunity and Ageing, BioMedCentral, full text: <cite cite="http://www.immunityageing.com/content/7/1/16">Abstract | Alzheimer's disease gene signature says: beware of brain viral infections</cite>. Abstract, edited.]
Alzheimer's disease gene signature says: beware of brain viral infections
Elisa Porcellini, Ilaria Carbone, Manuela Ianni and Federico Licastro
Immunity & Ageing 2010, 7:16
doi:10.1186/1742-4933-7-16
Published: 14 December 2010
Abstract (provisional)
Background
Recent findings from a genome wide association investigation in a large cohort of patients with Alzheimer's disease (AD) and non demented controls (CTR) showed that a limited set of genes was in a strong association (p > l0-5 ) with the disease.
Presentation of the hypothesis
In this report we suggest that the polymorphism association in 8 of these genes is consistent with a non conventional interpretation of AD etiology. Nectin-2 (NC-2), apolipoprotein E (APOE), glycoprotein carcinoembryonic antigen related cell adhesion molecule- 16 (CEACAM-16), B-cell lymphoma-3 (Bcl-3), translocase of outer mitochondrial membrane 40 homolog (T0MM-40), complement receptor-1 (CR-l), APOJ or clusterin and C-type lectin domain A family-16 member (CLEC-16A) result in a genetic signature that might affect individual brain susceptibility to infection by herpes virus family during aging, leading to neuronal loss, inflammation and amyloid deposition.
Implications of the hypothesis
We hypothesized that such genetic trait may predispose to AD via complex and diverse mechanisms each contributing to an increase of individual susceptibility to brain viral infections.
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[Source: Immunity and Ageing, BioMedCentral, full text: <cite cite="http://www.immunityageing.com/content/7/1/16">Abstract | Alzheimer's disease gene signature says: beware of brain viral infections</cite>. Abstract, edited.]
Alzheimer's disease gene signature says: beware of brain viral infections
Elisa Porcellini, Ilaria Carbone, Manuela Ianni and Federico Licastro
Immunity & Ageing 2010, 7:16
doi:10.1186/1742-4933-7-16
Published: 14 December 2010
Abstract (provisional)
Background
Recent findings from a genome wide association investigation in a large cohort of patients with Alzheimer's disease (AD) and non demented controls (CTR) showed that a limited set of genes was in a strong association (p > l0-5 ) with the disease.
Presentation of the hypothesis
In this report we suggest that the polymorphism association in 8 of these genes is consistent with a non conventional interpretation of AD etiology. Nectin-2 (NC-2), apolipoprotein E (APOE), glycoprotein carcinoembryonic antigen related cell adhesion molecule- 16 (CEACAM-16), B-cell lymphoma-3 (Bcl-3), translocase of outer mitochondrial membrane 40 homolog (T0MM-40), complement receptor-1 (CR-l), APOJ or clusterin and C-type lectin domain A family-16 member (CLEC-16A) result in a genetic signature that might affect individual brain susceptibility to infection by herpes virus family during aging, leading to neuronal loss, inflammation and amyloid deposition.
Implications of the hypothesis
We hypothesized that such genetic trait may predispose to AD via complex and diverse mechanisms each contributing to an increase of individual susceptibility to brain viral infections.
-
-----