Browsing Institute of Molecular Medicine and Genetics: Faculty Research and Presentations by Subjects
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Ganglioside metabolism in a transgenic mouse model of Alzheimer's disease: expression of Chol-1a antigens in the brainThe accumulation of Ab (amyloid b-protein) is one of the major pathological hallmarks in AD (Alzheimer’s disease). Gangliosides, sialic acid-containing glycosphingolipids enriched in the nervous system and frequently used as biomarkers associated with the biochemical pathology of neurological disorders, have been suggested to be involved in the initial aggregation of Ab. In the present study, we have examined ganglioside metabolism in the brain of a double- Tg (transgenic) mouse model of AD that co-expresses mouse/ human chimaeric APP (amyloid precursor protein) with the Swedish mutation and human presenilin-1 with a deletion of exon 9. Although accumulation of Ab was confirmed in the double-Tg mouse brains and sera, no statistically significant change was detected in the concentration and composition of major ganglio-N-tetraosyl-series gangliosides in the double-Tg brain. Most interestingly, Chol-1a antigens (cholinergic neuron-specific gangliosides), such as GT1aa and GQ1ba, which are minor species in the brain, were found to be increased in the double-Tg mouse brain. We interpret that the occurrence of these gangliosides may represent evidence for generation of cholinergic neurons in the AD brain, as a result of compensatory neurogenesis activated by the presence of Ab.
Role of Rac1 GTPase in NADPH Oxidase Activation and Cognitive Impairment Following Cerebral Ischemia in the RatBackground: Recent work by our laboratory and others has implicated NADPH oxidase as having an important role in reactive oxygen species (ROS) generation and neuronal damage following cerebral ischemia, although the mechanisms controlling NADPH oxidase in the brain remain poorly understood. The purpose of the current study was to examine the regulatory and functional role of the Rho GTPase, Rac1 in NADPH oxidase activation, ROS generation and neuronal cell death/cognitive dysfunction following global cerebral ischemia in the male rat.