Apolipoprotein E genotyping in patients with neurodegenerative diseases

Ballering, Leo; Steffens-Nakken, Helga; Esselink, Rianne A.J.; Vos, Rob A. I. de; Steur, Ernst N.H. Jansen; Vermes, I.

doi:10.1016/s0009-9120(97)00003-9

Cited by 5 publications

(1 citation statement)

References 26 publications

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“…A process unrelated to apoE actions in neuronal repair and remodeling may also hold the clue for understanding its involvement in PD. 19,20 The present study demonstrates that the existing literature as a whole [21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39] (see figures 2, 3, and table E-2 on the Neurology Web site for references) supports a positive association between an APOE polymorphism and sporadic PD disease. 18 In the past, almost every reported association of gene polymorphism and PD has been contradicted by other studies.…”

Section: Discussionsupporting

confidence: 65%

APOE-ε2 allele associated with higher prevalence of sporadic Parkinson disease

Huang

Chen²,

Poole³

2004

Neurology

145

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Section: Discussionsupporting

confidence: 65%

APOE-ε2 allele associated with higher prevalence of sporadic Parkinson disease

Huang

Chen²,

Poole³

2004

Neurology

145

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The relevance of apolipoprotein E polymorphism to Alzheimer's disease

Narayanan

1999

Indian J Clin Biochem

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The apo E gene located on chromosome 19 in humans is polymorphic. The three apo E isoforms E2, E3, and E4 are coded by three common alleles of the gene. The amyloid plaques in brains of Alzheimer disease (AD) patients are known to contain apo E. There is an increased prevalence of E4 allele in AD patients, apo E exhibits increased binding to a peptide AI3 deriving from amylold precursor protein, apo E, the risk factor for late AD d~sease is unable to prevent formation of paired helical filaments which in turn destabilizes neuronal microtubules.A variety of molecular techniques are available for apo E genotyping using DNA amplified by the polymerase chain reaction (PCR). The high guanine to cytosine content of apo E is problematic to the extent that the yield of PCR product and hybridization stringency can be compromised. The specificity of diagnosis of late-onset AD can be improved when results of apo E genotyping are evaluated together with clinical criteria.

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