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No association between the alpha2-macroglobulin (A2M) deletion and Alzheimer's disease, and no change in A2M mRNA, protein, or protein expression.

Artikel i vetenskaplig tidskrift
Författare Kaj Blennow
Anne Ricksten
J A Prince
A J Brookes
T Emahazion
Carina Wasslavik
N Bogdanovic
Niels Andreasen
S Båtsman
J Marcusson
K Nägga
Anders Wallin
Björn Regland
H Olofsson
Camilla Hesse
Pia Davidsson
L Minthon
Ann Jansson
Lars Palmqvist
Lars Rymo
Publicerad i Journal of neural transmission (Vienna, Austria : 1996)
Volym 107
Nummer/häfte 8-9
Sidor 1065-79
ISSN 0300-9564
Publiceringsår 2000
Publicerad vid Institutionen för klinisk neurovetenskap
Institutionen för klinisk neurovetenskap, Sektionen för laborativ neurovetenskap
Institutionen för laboratoriemedicin, Avdelningen för klinisk kemi/transfusionsmedicin
Sidor 1065-79
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Aged, Alzheimer Disease, genetics, pathology, Apolipoprotein E4, Apolipoproteins E, genetics, Base Sequence, Blotting, Western, Electrophoresis, Polyacrylamide Gel, European Continental Ancestry Group, genetics, Female, Gene Deletion, Gene Expression, Gene Frequency, Genetic Predisposition to Disease, Genotype, Humans, Male, Molecular Sequence Data, Plaque, Amyloid, pathology, Polymorphism, Genetic, RNA, Messenger, metabolism, Reverse Transcriptase Polymerase Chain Reaction, Sequence Analysis, DNA, alpha-Macroglobulins, analysis, cerebrospinal fluid, genetics
Ämneskategorier Klinisk laboratoriemedicin, Neurologi

Sammanfattning

A polymorphism consisting of a deletion near the 5' splice site of exon 18 on the alpha2-macroglobulin (A2M) gene (A2M-2) has been suggested to be associated with Alzheimer's disease (AD) in family-based studies. We studied the A2M-2 allele together with the ApoE alleles in a large series on patients with AD (n = 449) and age-matched controls (n = 349). Neuropathologically confirmed diagnoses were available in 199 cases (94 AD and 107 control cases). We found no increase in A2M-2 genotype or allele frequencies in AD (27.5% and 14.6%) versus controls (26.4% and 14.9%). In contrast, a marked increase (p < 0.0001) in ApoE epsilon4 genotype or allele frequencies was found in AD (66.6% and 41.2%) as compared with controls (29.8% and 16.5%), suggesting sufficient statistical power in our sample. No relation was found between the A2M-2 and the ApoE epsilon4 allele. No change in A2M exon 17-18 mRNA size or sequence or A2M protein size was found in cases carrying the A2M-2 deletion, suggesting that there is no biological consequences of the A2M intronic deletion. No change in A2M protein level in cerebrospinal fluid was found in AD, suggesting that the A2M-2 allele does not effect the A2M protein expression in the brain. The lack of an association between the A2M-2 allele and AD in the present study, and the lack of abnormalities in the A2M mRNA or protein suggest that the A2M-2 allele is not associated with AD.

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