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Apolipoprotein E gene promoter polymorphisms in Alzheimer's disease.
Microsc Res Tech 2000; 50(4):261-7MR

Abstract

Alzheimer's disease, the most frequent form of senile dementia, presents in the vast majority of cases as a multifactorial trait, where a series of genetic and environmental risk factors converge. The increasing body of data, both epidemiological and functional, is strengthening the evidence that apolipoprotein E (APOE, gene; apoE, protein) is a true susceptibility factor for the onset of the common form of Alzheimer's disease. The E4 isoform of apoE remains to date as the main genetic risk factor for the disease, although the mechanisms responsible for this association are not well understood. It is also clear that apoE4 is not necessary or sufficient to cause the disease, indicating that other risk and protecting factors exist. ApoE is upregulated in response to nervous system injury, suggesting that it could have a neuroprotective role; on the other hand, there is evidence indicating that apoE is neurotoxic when present at high levels. Thus, apoE levels seem to be relevant for the functionality of the protein. The APOE proximal promoter hosts numerous regulatory elements, raising the possibility that polymorphisms in this region could produce variation in apoE levels by altering APOE transcriptional activity, which could finally result in AD susceptibility. We will review here the current evidence on the relationship between APOE proximal promoter polymorphisms, APOE gene transcriptional activity and apoE protein levels, and risk for AD.

Authors+Show Affiliations

Departamento de Biología Molecular and Centro de Biología Molecular Severo Ochoa (C.S.I.C.-U.A.M.), Universidad Autónoma de Madrid, 28049 Madrid, Spain. mjbullido@cbm.uam.esNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

10936877

Citation

Bullido, M J., and F Valdivieso. "Apolipoprotein E Gene Promoter Polymorphisms in Alzheimer's Disease." Microscopy Research and Technique, vol. 50, no. 4, 2000, pp. 261-7.
Bullido MJ, Valdivieso F. Apolipoprotein E gene promoter polymorphisms in Alzheimer's disease. Microsc Res Tech. 2000;50(4):261-7.
Bullido, M. J., & Valdivieso, F. (2000). Apolipoprotein E gene promoter polymorphisms in Alzheimer's disease. Microscopy Research and Technique, 50(4), pp. 261-7.
Bullido MJ, Valdivieso F. Apolipoprotein E Gene Promoter Polymorphisms in Alzheimer's Disease. Microsc Res Tech. 2000 Aug 15;50(4):261-7. PubMed PMID: 10936877.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Apolipoprotein E gene promoter polymorphisms in Alzheimer's disease. AU - Bullido,M J, AU - Valdivieso,F, PY - 2000/8/11/pubmed PY - 2000/10/7/medline PY - 2000/8/11/entrez SP - 261 EP - 7 JF - Microscopy research and technique JO - Microsc. Res. Tech. VL - 50 IS - 4 N2 - Alzheimer's disease, the most frequent form of senile dementia, presents in the vast majority of cases as a multifactorial trait, where a series of genetic and environmental risk factors converge. The increasing body of data, both epidemiological and functional, is strengthening the evidence that apolipoprotein E (APOE, gene; apoE, protein) is a true susceptibility factor for the onset of the common form of Alzheimer's disease. The E4 isoform of apoE remains to date as the main genetic risk factor for the disease, although the mechanisms responsible for this association are not well understood. It is also clear that apoE4 is not necessary or sufficient to cause the disease, indicating that other risk and protecting factors exist. ApoE is upregulated in response to nervous system injury, suggesting that it could have a neuroprotective role; on the other hand, there is evidence indicating that apoE is neurotoxic when present at high levels. Thus, apoE levels seem to be relevant for the functionality of the protein. The APOE proximal promoter hosts numerous regulatory elements, raising the possibility that polymorphisms in this region could produce variation in apoE levels by altering APOE transcriptional activity, which could finally result in AD susceptibility. We will review here the current evidence on the relationship between APOE proximal promoter polymorphisms, APOE gene transcriptional activity and apoE protein levels, and risk for AD. SN - 1059-910X UR - https://www.unboundmedicine.com/medline/citation/10936877/Apolipoprotein_E_gene_promoter_polymorphisms_in_Alzheimer's_disease_ L2 - https://doi.org/10.1002/1097-0029(20000815)50:4<261::AID-JEMT2>3.0.CO;2-B DB - PRIME DP - Unbound Medicine ER -