Early onset amyloid lesions lead to severe neuritic abnormalities and local, but not global neuron loss in APPPS1 transgenic mice.
APPPS1 transgenic mice develop amyloid-β 42 (Aβ42)-driven early-onset cerebral β-amyloidosis. Stereological analysis of neocortical neuron number in groups of 2-, 10-, and 17-month-old APPPS1 mice did not reveal any changes compared with wild-type control animals despite massive amyloid-β (Aβ) load and disrupted cytoarchitecture. However, in subregions with high neuron density such as the granule cell layer of the dentate gyrus, modest but significant neuron loss was found, reminiscent of findings in previously published mouse models with late onset cerebral β-amyloidosis and predominant amyloid-β 40 (Aβ40) expression.
Department of Cellular Neurology, Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany.
Niels J
NJ
Rupp
Bettina M
BM
Wegenast-Braun
Rebecca
R
Radde
Michael E
ME
Calhoun
Mathias
M
Jucker
D000367:Age Factors; D016564:Amyloid beta-Protein Precursor / Q000235:genetics*; D000818:Animals; D006801:Humans; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009410:Nerve Degeneration / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D016501:Neurites / Q000378:metabolism / Q000473:pathology*; D009474:Neurons / Q000378:metabolism / Q000473:pathology*; D058225:Plaque, Amyloid / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D053764:Presenilin-1 / Q000235:genetics*; D011897:Random Allocation; D012720:Severity of Illness Index
D016564:Amyloid beta-Protein Precursor; C508853:PSEN1 protein, human; D053764:Presenilin-1