Journal
NEURON
Volume 47, Issue 2, Pages 191-199Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2005.06.030
Keywords
-
Categories
Funding
- NCI NIH HHS [CA88325, R24 CA088325] Funding Source: Medline
- NIA NIH HHS [R01 AG022595, R01 AG022595-01, R01 AG022595-02] Funding Source: Medline
Ask authors/readers for more resources
Considerable circumstantial evidence suggests that A beta 42 is the initiating molecule in Alzheimer's disease (AD) pathogenesis. However, the absolute requirement for A beta 42 for amyloid deposition has never been demonstrated in vivo. We have addressed this by developing transgenic models that express A beta 1-40 or A beta 1-42 in the absence of human amylold 0 protein precursor (APP) overexpression. Mice expressing high levels of A beta 1-40 do not develop overt amyloid pathology. In contrast, mice expressing lower levels of A beta 1-42 accumulate insoluble A beta 1-42 and develop compact amyloid plaques, congophilic amyloid angiopathy (CAA), and diffuse A beta deposits. When mice expressing A beta 1-42 are crossed with mutant APP (Tg2576) mice, there is also a massive increase in amyloid deposition. These data establish that A beta 1-42 is essential for amyloid deposition in the parenchyma and also in vessels.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available