Brain Oligomeric β-Amyloid but Not Total Amyloid Plaque Burden Correlates With Neuronal Loss and Astrocyte Inflammatory Response in Amyloid Precursor Protein/Tau Transgenic Mice
Entorhinal cortex
Amyloid (mycology)
P3 peptide
DOI:
10.1097/nen.0b013e318217a118
Publication Date:
2011-04-12T06:40:40Z
AUTHORS (10)
ABSTRACT
It has long been assumed that β-amyloid (Aβ) had to assemble into fibrillar amyloid plaques exert its neurotoxic effects in Alzheimer disease. An alternative hypothesis is soluble oligomers ofAβ play a much larger role neuronal damage than the insoluble component. We have tested these competing hypotheses vivo by studying clinicopathologic correlates of oligomeric Aβ species and classic brains double-transgenic APP-tau mice up 17 months age. Biochemical immunohistochemical measures brain exponentially increased with Oligomeric load correlated morphological markers deposition. In contrast total plaque burden, amount deposits labeled conformational epitope-specific antibody Nab61 closely loss numbers astrocytes entorhinal cortex CA1 hippocampal subfield. However, like other measurements, burden did not correlate well memory deficits mice. The number glial fibrillary acidic protein-positive most tightly impairment cell loss. Based on findings, we hypothesize astrocyte response, which likely triggered accumulation, adversely affects cognition might also contribute death this model.
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