Category specific dysnomia after thalamic infarction: a case-control study.

Category specific naming impairment was described mainly after cortical lesions. It is thought to result from a lesion in a specific network, reflecting the organization of our semantic knowledge. The deficit usually involves multiple semantic categories whose profile of naming deficit generally obeys the animate/inanimate dichotomy. Thalamic lesions cause general semantic naming deficit, and only rarely a category specific semantic deficit for very limited and highly specific categories. We performed a case-control study on a 56-year-old right-handed man who presented with language impairment following a left anterior thalamic infarction. His naming ability and semantic knowledge were evaluated in the visual, tactile and auditory modalities for stimuli from 11 different categories, and compared to that of five controls. In naming to visual stimuli the patient performed poorly (error rate>50%) in four categories: vegetables, toys, animals and body parts (average 70.31+/-15%). In each category there was a different dominating error type. He performed better in the other seven categories (tools, clothes, transportation, fruits, electric, furniture, kitchen utensils), averaging 14.28+/-9% errors. Further analysis revealed a dichotomy between naming in animate and inanimate categories in the visual and tactile modalities but not in response to auditory stimuli. Thus, a unique category specific profile of response and naming errors to visual and tactile, but not auditory stimuli was found after a left anterior thalamic infarction. This might reflect the role of the thalamus not only as a relay station but further as a central integrator of different stages of perceptual and semantic processing.

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.

Lack of association of interleukin-1beta polymorphism with Alzheimer's disease in the Jewish population.

A growing body of evidence suggests that Alzheimer's disease (AD) is associated with local inflammation processes, including the activation of inflammatory cytokines. We performed a case-control association study between sporadic AD patients and the exon 5 position +3953 polymorphism in the potent pro-inflammatory cytokine, interleukin-1beta (IL-1B). Recent association studies of this locus with AD revealed conflicting results, suggesting that the association - if it exists - is not universal but rather population specific. In our study no association was detected with AD: neither as a risk factor nor as a modifier gene affecting the age at onset and disease progression. These findings show no evidence for an association between the IL-1B +3953 polymorphism and AD in the Jewish population.

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.

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.

An autonomic nervous system biofeedback modality for the treatment of attention deficit hyperactivity disorder--an open pilot study.

OBJECTIVE: To study the effect of a new non-invasive technique of non-cognitive biofeedback called Autonomic Nervous System Biofeedback Modality on the behavioral and attention parameters of a sample of children with attention deficit hyperactivity disorder. METHOD: 19 subjects attending regular schools, who met DSM-IV criteria for attention deficit hyperactivity disorder, received four sessions of Autonomic Nervous System Biofeedback Modality treatment. The heart rate variability was measured before and after the treatment, as were measures of efficacy including Conners' Teacher Questionnaires (28 items), the Child Behavior Check List for parents and teachers and Continuous Performance Test. RESULTS: Positive treatment effect was observed in all the subjects. The parent's Child Behavior Check List and Conners' Teacher Questionnaires of the whole group showed statistically significant differences. The teacher's Child Behavior Check List showed positive change not reaching statistical significance. A positive correlation between heart rate variability changes and improvement of symptoms of attention deficit hyperactivity disorder was found. CONCLUSION: These are preliminary findings of apparent efficacy of Autonomic Nervous System Biofeedback Modality treatment for attention deficit hyperactivity disorder in children. Future controlled trials are warranted.

An estimate of the prevalence of dementia among community-dwelling elderly in Israel.

The study goal was to identify the prevalence of dementia among elderly people aged 65 and over living in the community in Israel. The target population included 47,834 community-dwelling elderly aged 65 and over in Jerusalem. Of this population, 1,624 elderly were randomly sampled according to ten strata of sex and age groups. The study included initial screening for 'suspected' dementia cases followed by in-depth clinical evaluation to determine whether an individual indeed suffered from dementia. One fifth (19.2%) of the elderly aged 65 and over, living in the community in Jerusalem, were found to have dementia at varying levels of severity. When the specific rates of elderly with dementia in the community in Jerusalem by gender and age groups were applied to data on the total elderly population in the community in Israel at the end of 2002, the prevalence of dementia was an estimated 16.7%. The percentage of elderly with dementia in Israel is in the upper range of rates quoted in other studies. The health and social service systems in Israel will have to make provisions to care for a much larger number of dementia sufferers than has been previously estimated.

The Fas promoter polymorphism at position -670 is not associated with late-onset sporadic Alzheimer's disease.

The Fas antigen is a cell surface receptor-mediating cell apoptosis. Recent studies have demonstrated that Fas-associated apoptosis is involved in the pathogenesis of Alzheimer's disease (AD). Moreover, the Fas gene is located on chromosome 10q24.1, a region of linkage to late-onset AD (LOAD). These two criteria, pathobiological and positional, make the Fas antigen an interesting candidate for an association with AD. We performed a case-control association study between the common A/G polymorphism at position -670 in the Fas gene (TNFSRF6) promoter and sporadic AD in Jews, investigating whether this locus acts as a risk factor or whether it has a modifying effect. An association has recently been detected by Feuk et al. in the Scottish population between this locus and the risk of early-onset AD (EOAD), but not of LOAD. In agreement with Feuk et al., we found no association between this locus and the risk of LOAD (n = 86). However, in our small sample of patients with EOAD (n = 19), no association was found either. No interactive effect was found between the Fas promoter polymorphism at position -670 and the known risk factor of LOAD, apolipoprotein E epsilon4, and no association was detected with disease progression. These findings show no evidence for an association between the Fas promoter polymorphism at position -670 and AD in our population.

An association study of a polymorphism in the heparan sulfate proteoglycan gene (perlecan, HSPG2) and Alzheimer's disease.

Accumulating evidence indicates that the heparan-sulfate-proteoglycan (perlecan, HSPG2), as well as other specific proteoglycans, are involved in amyloidogenesis and tau aggregation in Alzheimer's disease (AD). Moreover, the HSPG2 is located on chromosome 1p36, a region of linkage to late-onset AD (LOAD). These two criteria, pathological and positional, make the HSPG2 an interesting candidate for an association with AD. We performed a case-control association study between the common intron 6 BamHI polymorphism at a region of putative heparan-sulfate (HS) attachment sites in the HSPG2 gene and sporadic AD in Jews. No association was detected with AD, neither as a risk factor nor as a modifier gene affecting the age at disease onset and disease progression. In addition, no interactive effect was found with the known risk factor for AD, the apolipoprotein E (APOE) epsilon4. These findings show no evidence for association between HSPG2 intron 6 BamHI polymorphism and AD in our population.