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Human Apolipoprotein E Redistributes Fibrillar Amyloid Deposition in Tg-SwDI Mice
Human apolipoprotein E changes the pattern of amyloid plaque buildup in a mouse model
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Abstract
Both human ApoE3 and ApoE4 proteins led to a strong reduction in cerebral microvascular amyloid in transgenic mice.
- Human ApoE genotype is associated with changes in the accumulation of amyloid in the brain, specifically shifting from microvascular to parenchymal forms.
- Transgenic mice carrying human ApoE3 or ApoE4 showed extensive fibrillar parenchymal plaque amyloid alongside reduced microvascular amyloid.
- There was no significant difference in total levels of amyloid-beta peptides or in their soluble and insoluble forms between the different ApoE backgrounds.
- Strong colocalization of all ApoE proteins with fibrillar amyloid deposits was observed in the mice.
- The changes in amyloid distribution corresponded with a shift in the activation of microglia, suggesting a response to the spatial accumulation of amyloid.
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