Abstract:
:A great amount of evidence suggests that neuroinflammation may be a major pathogenetic mechanism in the pathophysiology of sporadic Alzheimer's Disease (sAD). Recently, polymorphisms in the endothelial nitric oxide synthase (NOS3) gene have been associated to late onset Alzheimer's Disease in a British population. However, other groups failed to replicate this finding in Asiatic and Caucasian populations. We conducted a case-control study including a clinically well-defined group of 149 sAD patients and 149 age and sex matched controls to test the association between NOS3 Glu298Asp polymorphism and sAD in an ethnically homogenous Italian population. All subjects were genotyped at NOS3 and apolipoprotein E. No significant difference was found in either allele or genotype frequencies between cases and controls, even after stratification for Apolipoprotein E4 carrier status. The NOS3 Glu298Asp polymorphism does not appear to influence the risk of developing sAD in an Italian population.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Monastero R,Cefalù AB,Camarda C,Buglino CM,Mannino M,Barbagallo CM,Lopez G,Camarda LK,Travali S,Camarda R,Averna MRdoi
10.1016/s0304-3940(03)00210-6keywords:
subject
Has Abstractpub_date
2003-05-08 00:00:00pages
229-32issue
3eissn
0304-3940issn
1872-7972pii
S0304394003002106journal_volume
341pub_type
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