General Information

Transgene: The Arctic mutation was introduced into a hAPP minigene (having Swedish and Indiana mutations) directed by the platelet-derived growth factor β-chain promoter. Two hAPP-Arc lines (Arc6 and Arc48) were established.

Mutation: Arctic (E22G), Swedish, and Indiana

Promoter: Platelet-derived growth factor βchain promoter

Origin: C57BL/6Hsd

Phenotype

Neuropathological analysis:

Compared to J20 mice (TJL #004661) the Arctic mice formed amyloid plaques faster and more extensively, even though they had lower Aβ 1-42/1-40 ratios. Relative levels of hAPP and of the β-secretase-generated C99 fragment were lower in Arc6 and higher in Arc48 than in J20 mice.

Behavioral:

Pending

Availability

Lennart Mucke, MD
Gladstone Institute of Neurological Disease
1650 Owens Street
San Francisco, CA 94158
Email: Lmucke@gladstone.ucsf.edu

Reference

Primary:

Cheng I H, Palop J J, Esposito L A, Bien-Ly N, Yan F, Mucke L. Aggressive amyloidosis in mice expressing human amyloid peptides with the Arctic mutation. Nat Med. 10(11): 1190-2, 2004. Abstract.

Associated:

Mucke L, Masliah E, Yu G-O, Mallory M, Rockenstein E M, Tatsuno G, Hu K, Kholodenko D, Johnson-Wood K, McConlogue L. High-level neuronal expression of aβ1-42 in wild-type human amyloid protein precursor transgenic mice: synaptotoxicity without plaque formation. J Neurosci 20:4050-4058, 2000. Abstract.