LBP-1c/CP2/LSF gene polymorphism and risk of sporadic Alzheimer's disease.

The e4 allele of apolipoprotein E (ApoE) accounts for an estimated 45–60% of the genetic risk for late onset sporadic Alzheimer’s disease, suggesting that it may be possible to identify other genetic loci that could account for the remaining risk associated with this disease. Recently, a biallelic polymorphism (G/A) in the 3′ untranslated region (UTR) of the transcription factor LBP-1c/CP2/LSF (for brevity, CP2) has been implicated in Alzheimer’s disease susceptibility, with the 3′-UTR A allele being associated with a reduction in the risk of sporadic Alzheimer’s disease.1–3 The CP2 gene is a plausible candidate for influencing Alzheimer’s disease risk: it is located near the LDL receptor related protein gene within the Alzheimer’s disease linkage region on chromosome 12; it controls the expression of several genes (α2 macroglobulin, glycogen synthase kinase-3β); and it interacts with different proteins (serum amyloid A3, interleukin 1α, tumour necrosis factor α, and Fe65 protein) and viruses (herpes simplex virus type I or human immunodeficiency virus) that are probably linked to Alzheimer’s disease pathogenesis.14 In the present study, we investigated the potential association of the CP2 polymorphism in a sample of sporadic early onset and late onset cases along with age and sex matched control subjects from southern Italy. The Alzheimer’s disease group consisted of 166 patients (62 men and 104 women) from the Apulia region with a mean (SD) actual age of 69.4 (10.3) years, including 95 patients with sporadic late onset disease (age at onset ⩾70 years; mean age 78.1 (4.9) years; 64 women and 31 men), and 71 patients with sporadic early onset disease (age at onset <70 years; mean age 63.7 (4.3) years; 50 women and 21 men). A clinical diagnosis of probable Alzheimer’s disease was made according to the NINCDS/ADRDA criteria.5 The age at onset of Alzheimer’s …