Biomedical subjects

Eli Wertman

Publications and source records attributed to Eli Wertman.

3 recordsLinked to original sources

PubMed2003

An association study of the codon 72 polymorphism in the pro-apoptotic gene p53 and Alzheimer's disease.

Recent studies have demonstrated that p53-associated apoptosis is involved in the pathogenesis of Alzheimer's disease (AD). We performed a case-control association study between sporadic AD and the common proline/arginine polymorphism at codon 72 in the pro-apoptotic gene p53, in 109 sporadic AD patients and in 111 controls. This polymorphism has been intensively investigated for association with cancer, but so far not with AD and neurodegeneration. We found no association between this locus and the risk for AD. No association was detected also for the age at disease onset and for disease progression, and no interactive effect was found with apolipoprotein E e4. These findings show no evidence for an association between p53 codon 72 polymorphism and AD in our population.

Aged↗

PubMed2003

A polymorphism in the complement component C1r is not associated with sporadic Alzheimer's disease.

A growing body of evidence suggests that Alzheimer's disease (AD) is associated with local inflammation processes. Complement activation is one of the cardinal pathological features of the inflammation. Intensive AD association studies investigating polymorphisms in inflammatory-related genes have been recently performed, mainly in cytokines, but much less has been focused on AD association with polymorphisms in complement components. We performed a case-control association study between the codon 135 polymorphism in the complement component C1r gene and sporadic AD. No association was detected with AD: neither as a risk factor, and nor as a modifier gene affecting the age at disease onset and disease progression. No interactive effect was found with apolipoprotein E e4. These findings show no evidence for association between C1r codon 135 polymorphism and AD in our population.

Aged↗

PubMed2002

Reading direction and spatial neglect.

Many American and European investigators have reported that hemispatial neglect is more frequent and more severe after right than left hemisphere lesions. This hemispheric asymmetry may be due to biological asymmetries, learned behavior, or both. Readers of European languages, unlike readers of Semitic languages, scan from left to right. Learned rightward scanning may increase the unilateral neglect associated with right hemisphere lesions and reduce the severity of neglect associated with left hemisphere lesions. To learn if hemispheric asymmetries of neglect are influenced by learned scanning behavior, we used line bisection and cancellation tasks to study patients with unilateral stroke who read only a Semitic or European language before the age of fifteen. We found that independent of reading direction, unilateral neglect was more commonly associated with right than left hemisphere lesions. After right hemisphere damage right to left readers bisected lines closer to center than left to right readers, but on the cancellation test readers of European languages did not perform differently than readers of Semitic languages. These findings suggest that whereas learned scan direction may influence the severity of neglect when measured by line bisection, these learned directional scans cannot fully account for the observed hemisphere asymmetries of neglect. They also suggest that the line bisection test is more influenced by the direction of scanning than is the cancellation test.

Aged↗