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Search: L773:0959 4965 > Örebro University

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1.
  • Löf-Ohlin, Zarah M., et al. (author)
  • Relative telomere length in patients with late-onset Alzheimer's dementia or vascular dementia
  • 2008
  • In: NeuroReport. - London : Lippincott Williams and Wilkins. - 0959-4965 .- 1473-558X. ; 19:12, s. 1199-1202
  • Journal article (peer-reviewed)abstract
    • Telomeres generally shorten with age. An accelerated shortening of the telomeres has been linked to several age-related disorders. We hypothesized that the relative length of telomeres could discriminate between patients with late-onset Alzheimer's disease (AD) and vascular dementia (VaD). A quantitative real-time PCR method was used to calculate the relative telomere length in 76 age-matched and sex-matched, newly diagnosed late-onset AD or VaD patients recruited from our Memory Unit. No significant difference was found in the relative telomere length between AD and VaD cases neither in men (P=0.315) nor women (P=0.12). Thus, we could not confirm that the length of telomeres would predict which form of dementia, late-onset AD or VaD that develops.
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2.
  • Okonkwo, David O., et al. (author)
  • Cyclosporin A limits calcium-induced axonal damage following traumatic brain injury
  • 1999
  • In: NeuroReport. - : Lippincott Williams & Wilkins. - 0959-4965 .- 1473-558X. ; 10:2, s. 353-358
  • Journal article (peer-reviewed)abstract
    • In traumatic axonal injury, Ca2+ influx across a focally damaged axolemma precipitates local mitochondrial failure, degradation of the subaxolemmal spectrin network and compaction of neurofilaments, which collectively contribute to axonal failure. In previous studies, cyclosporin A pretreatment preserved mitochondrial integrity and attenuated axonal failure following trauma. Here we investigate whether this CsA-linked protection was related to the concomitant blunting of intra-axonal, Ca2+-induced cytoskeletal changes in traumatic axonal injury, assessed with antibodies targeting spectrin proteolysis and neurofilament compaction. CsA pretreatment dramatically reduced Ca2+-induced cytoskeletal damage following injury; CsA-treated rats, compared with vehicle-treated rats, displayed a 70% decrease in immunoreactive/damaged profiles. We suggest that CsA-mediated preservation of mitochondrial integrity enables the restoration of ionic and metabolic homeostasis thereby short-circuiting Ca2+-induced proteolysis in injured axons. 
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