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Oded Abramsky

Publications and source records attributed to Oded Abramsky.

26 records · Page 2Linked 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↗
PubMed2003

Transplanted multipotential neural precursor cells migrate into the inflamed white matter in response to experimental autoimmune encephalomyelitis.

Transplanted neural precursor cells remyelinate efficiently acutely demyelinated focal lesions. However, the clinical value of cell transplantation in a chronic, multifocal disease like multiple sclerosis will depend on the ability of transplanted cells to migrate to the multiple disease foci in the brain. Here, we expanded newborn rat neural precursor cells in spheres and transplanted them intracerebroventricularly or intrathecally in rats. The cells were labeled by the nuclear fluorescent dye Hoechst or by incubation with BrdU to enable their identification at 2 days and 2 weeks after transplantation, respectively. Spheres consisted of PSA-NCAM(+), nestin(+), NG2(-) undifferentiated precursor cells that differentiated in vitro into astrocytes, oligodendrocytes, and neurons. Spheres that were transplanted into intact rats remained mostly in the ventricles or in the spinal subarachnoid space. Following transplantation at peak of experimental autoimmune encephalomyelitis, cells migrated into the brain or spinal cord parenchyma, exclusively into inflamed white matter but not into adjacent gray matter regions. After 2 weeks, many transplanted cells had migrated into distant white matter tracts and acquired specific markers of the astroglial and oligodendroglial lineages. Thus, the inflammatory process may attract targeted migration of transplanted precursor cells into the brain parenchyma.

Acute Disease↗
PubMed2003

Frontotemporal dementia and parkinsonism with the P301S tau gene mutation in a Jewish family.

BACKGROUND: Frontotemporal dementia with parkinsonism linked to chromosome 17q21-22 (FTDP-17) is an autosomal dominant tauopathy manifested by a variable combination of personality changes, cognitive decline and hypokinetic-rigid movement disorder. Significant clinical and pathological heterogeneity of FTDP-17 is related in part to more than 20 different pathogenic mutations identified in the tau gene. Among others, the P301S mutation has been previously reported in three families of European and one of Japanese origin presenting with different clinical phenotypes. OBJECTIVES: To report a three-generation family of Jewish-Algerian origin with FTDP-17 due to the P301S tau mutation. METHODS: Clinical, neuropsychological and neuroimaging evaluation of 3 patients, tau genotyping, and pathological study of the proband. RESULTS: The 3 affected family members had a fairly stereotyped clinical course with early personality changes from their late 30s followed within a period of 1-2 years by a progressive cognitive and motor deterioration eventually leading to a state of akinetic mutism or death 3-5 years after the initial symptoms. The main clinical manifestations included severe dementia and hypokinetic-rigid movement disorder associated with supranuclear gaze impairment, pyramidal signs and frontal release signs. Brain imaging disclosed a variable degree of frontotemporal atrophy, ventriculomegaly and regional cerebral hypoperfusion or glucose hypometabolism. Frontal lobe biopsy in the proband revealed weak tau immunoreactivity in a few cortical neurons, in rare neurites and in some glial cells with no neurofibrillary tangles. Molecular DNA analysis identified a P301S mutation in exon 10 of the tau gene. CONCLUSIONS: The observed clinical features further expand the reported P301S phenotype and confirm a more aggressive course of the disease than in the other known tau mutations.

Adult↗
PubMed2003

Intraventricular transplantation of neural precursor cell spheres attenuates acute experimental allergic encephalomyelitis.

Brain transplantation of neural precursor cells (NPCs) has been proposed to enhance CNS regeneration. As the pathogenesis of most acute CNS diseases involves an inflammatory component, we studied whether NPC transplantation affects brain inflammation. Newborn rat multipotential NPCs were transplanted intraventriculary into acute experimental allergic encephalomyelitis (EAE) rats, a model for disseminated brain inflammation. Cells migrated into inflamed white matter and differentiated into glial cells. NPC transplantation attenuated the clinical severity of EAE and the brain inflammation, indicated by reduction in perivascular infiltrates and decreased expression of ICAM-1 and LFA-1. NPCs inhibited basal proliferation and proliferative responses to Concavalin-A and to MOG peptide of EAE rat-derived lymphocytes in vitro. Purified astrocytes inhibited lymphocyte proliferation in vitro, but did not migrate into EAE brains in vivo, and did not reduce EAE severity or brain inflammation. Thus, transplanted NPCs attenuate acute EAE via an anti-inflammatory mechanism which depends on cell ability to migrate into inflamed brain tissue.

Acute Disease↗
PubMed2003

Tryptase activates peripheral blood mononuclear cells causing the synthesis and release of TNF-alpha, IL-6 and IL-1 beta: possible relevance to multiple sclerosis.

Presence of mast cells and an increase in the concentration of their products has been reported in multiple sclerosis (MS) plaques. The most abundant secretory mediator of the human mast cell is the tetrameric protease tryptase. We demonstrate that tryptase can activate peripheral mononuclear cells (PBMCs), isolated from healthy donors as well as MS patients for the release of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6 and IL-1beta. Cytokine secretion was significantly higher in secondary progressive (SP) MS patients and healthy control (HC) individuals than in relapsing-remitting (RR) patients. Our findings suggest that tryptase is, most probably, an important mediator of inflammation in MS.

Adult↗
PubMedDate not supplied

The frequency of multiple sclerosis in jewish and arab populations in greater jerusalem.

A comparison of the incidence rate (IR) and the prevalence rate (PR) of multiple sclerosis (MS) in subgroups of the same ethnic origin, but born and living in different geographical areas, may delineate the relationship between environmental and genetic risk factors for MS. Previous epidemiological studies of MS in Israel did not include the Arab population and used diagnostic criteria that did not include MRI findings. Therefore, we studied the age-adjusted IR and PR of MS in a more recent sample in different population groups, including Arabs, of Greater Jerusalem. We found that the PR of MS in Israeli Jews is higher than previously described. Furthermore, the PR was significantly lower among immigrant Jews from Asia/Africa (A/A) than among native-born Jews of Asian/African origin (I-A/A). Since these groups have similar genetic susceptibilities to MS, the higher PR in the latter is probably due to environmental factors. Our study does not support the effect of latitude on the risk of developing MS since no difference in the PR was found between immigrant Jews from Europe/America (E/A) and native-born Jews of European/American origin (I-E/A). Among Arabs, the PR was similar to that among A/A. Therefore, we hypothesized similarity in environmental etiologic factors for MS between the countries of origin of A/A immigrants and of Arabs communities in Greater Jerusalem. The IR of I-E/A was higher than that of I-A/A and Arabs, although this difference did not reach statistical significance.

Adolescent↗