New! 17 M 32 Siberian Mouse
New! 17 M 32 Siberian Mouse
While no mouse has been found with an hereditary prion disease, it has recently become increasingly likely that it can occur and that it is not precluded by age or sex. In such a case, it may be that the variant responsible for the disease differs from that normally expressed in other mice, and other mutations may be needed to achieve susceptibility to clinical disease. In this context, it is worth noting the interesting observation that Kudo mice lacking the Hr gene, which normally occurs in humans and is protective against several prion diseases, are all but resistant to infection by mouse adapted prions. Since these mice are severely affected by other prion diseases, it seems likely that an additional mouse strain-specific factor is required to enable some strains of prions to form amyloids in these animals.
One of the strain-specific factors is the presence of RAG1 in the host, and this is potentially relevant to understanding why some mouse types are resistant or more susceptible to TSEs. Another factor is the distribution of the PrPsen gene in the mouse. Although the distribution of the PrP gene was not investigated by the authors, it has been shown that, within subtypes, mouse PrPsen polymorphisms can vary within and between species, and this may modify the protein sequence at the PrP locus and thus determine the susceptibility of different mouse strains to TSE. The polymorphism that was identified in the cats was also found in other animals, including a barbeled gundi, the species from which the cats were derived. Thus, changes in the mouse PrP gene are likely to be important in determining the susceptibility of different strains of mice to TSEs.
targeting amyloid has been difficult in the past, but recent work has shown that large receptors, such as anion-selective ca2+ channels, can be expressed in astrocytes, allowing efficient removal of a‐ and by immunological targeting of microglia and astrocytes in the cns (8,23, 24). more recently, several lines of evidence have shown that the formation of amyloid aggregates in the brains of ad patients is not restricted to neurons but is also present in microglia and astrocytes. furthermore, microglia and astrocytes have previously been proposed to be directly involved in the formation of senile plaques.40, 41. here, we targeted specific cns cell types to express the c-terminal ha-tagged binding domain of the a‐-selective ca2+ channel (caspr) to remove cerebral a‐ in the hippocampus and cortex of mice. intracerebral injections of the targeted cells were performed in mice at two different ages: early, at 1.5 months, and late, at 2.5 months. following injection of caspr-expressing astrocytes or microglia, a‐ levels in the hippocampal and cortical regions were significantly reduced. however, when combined with injections of brain-derived neurotrophic factor, a‐ levels were significantly reduced in the hippocampal regions at both ages (early, 42%, late, 50%). as expected, amyloid burden was higher at the 2.5 month time point (58%), and after combining caspr with brain-derived neurotrophic factor treatment, amyloid burden in the hippocampal region was reduced in the early (42%) and late (53%) phases. this work supports the rationale of targeting glial cells for the effective removal of cerebral a‐ in the treatment of ad.
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