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P3‐286: Subcortical ischemic vascular dementia: A search for APP gene mutations
Author(s) -
Geracitano Silvana,
Bernardi Livia,
Maletta Raffaele,
Tomaino Carmine,
Gallo Maura,
Anfossi Maria,
Vasso Franca,
Colao Rosanna,
Puccio Gianfranco,
Frangipane Francesca,
Mirabelli Maria,
Smirne Nicoletta,
Muraca Maria Gabriella,
De Vito Ornella,
Dattilo Teresa,
Menniti Michele,
Bruni Amalia Cecilia
Publication year - 2008
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2008.05.1854
Subject(s) - cerebral amyloid angiopathy , senile plaques , dementia , exon , angiopathy , neuropathology , medicine , mutation , pathology , amyloid precursor protein , alzheimer's disease , amyloidosis , disease , vascular dementia , pathological , amyloid (mycology) , gene , genetics , biology , endocrinology , diabetes mellitus
Prism 7000 Sequence Detection System. TaqMan SNP genotyping products and assays. Multinomial regression models were used to determine the risk of AD and MCI-AT. Results: The T and C alleles were not independent risk factors for AD and MCI-AT ( OR 1.22; CI95%, 0.35-4.21, OR 1.04; CI95%, 0.29-3.76, respectively). This was also the case for the TT, TC and CC genotypes. Neither UBQLN1 alleles nor genotypes were independent risk factors for AD or MCI-AT. Once adjusted for sex and the presence of apolipoprotein E4 (APOE4), our results did not reveal an association between UBQLN1 polymorphism and either AMCI-AT or AD. Conclusions: This is the first Spanish’s study which evaluates the role of UBQLN1 polymorphism in cognitive impairment. UBQLN1 polymorphism is not an independent risk factor for AD or MCI-AT.