Reports summarize apoptosis cell biology research from University of Paris, Department of Pathology
2007 AUG 21 -- Data detailed in "Apoptosis in cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy" have been presented. In this recent report, researchers in Paris, France conducted a study "To test the hypothesis that an apoptotic process plays a role in the pathogenesis of cerebral lesions in cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), we examined samples from frontal, temporal, insular, and occipital regions, basal ganglia, and cerebellum from 4 patients with CADASIL, 2 with Binswanger disease, and 3 controls. Apoptotic cells were identified using in situ end labeling and activated caspase 3 immunostaining." "Immunolabeling for Notch3, the beta-amyloid protein precursor, and phosphorylated neurofilament protein was performed on successive sections. Apoptosis of vascular cells was markedly increased in status cribrosus in CADASIL, both in basal ganglia and subcortical white matter, suggesting that concomitantly with Notch3 deposition it may play a causative role in the dilatation of Virchow-Robin spaces. Neuronal apoptosis was found in CADASIL, mostly in cortical layers 3 and 5. Its severity correlated semiquantitatively with the extent of ischemic lesions and axonal damage in the underlying white matter. It was more severe in demented patients. Only occasional apoptotic neurons were found in the Binswanger cases and none in the controls," wrote F. Gray and colleagues, University of Paris, Department of Pathology. The researchers concluded: "This supports the view that neuronal apoptosis may contribute to cortical atrophy and cognitive impairment in patients with CADASIL and that it may, at least partly, result from axonal damage in the underlying white matter." Gray and colleagues published their study in the Journal of Neuropathology and Experimental Neurology (Apoptosis in cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy. Journal of Neuropathology and Experimental Neurology, 2007;66(7):597-607). For additional information, contact F. Gray, Universite Paris VII, Dept. of Pathology, APHP Hopital Lariboisiere, 2 rue Ambroise Pare, 75475 Paris, France. Publisher contact information for the Journal of Neuropathology and Experimental Neurology is: American Assn Neuropathologists Inc., 1041 New Hampshire St., Lawrence, KS 66044, USA. Keywords: France, Paris, Apoptosis Cell Biology, Apoptosis, Cell Biology, Experimental Neurology, Neuropathology. This article was prepared by Life Science Weekly editors from staff and other reports. Copyright 2007, Life Science Weekly via NewsRx.com.
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