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Behavioral and anatomical deficits in mice homozygous for a modified beta-amyloid precursor protein gene.

The beta-amyloid precursor protein (beta APP) gene of the mouse was disrupted by inserting into exon 2 a cassette containing a neomycin resistance gene and a putative transcription termination sequence. Contrary to expectation, brain and other tissues from mice homozygous for the insertion still contained beta APP-specific RNA, albeit at a level 5- to 10-fold lower than wild type and lacking the disrupted exon, which had been spliced out. The brain contained shortened beta APP-specific protein at a low level. Mutant mice were severely impaired in spatial learning and exploratory behavior and showed increased incidence of agenesis of the corpus callosum.

Pubmed ID: 8001115

Authors

  • Müller U
  • Cristina N
  • Li ZW
  • Wolfer DP
  • Lipp HP
  • Rülicke T
  • Brandner S
  • Aguzzi A
  • Weissmann C

Journal

Cell

Publication Data

December 2, 1994

Associated Grants

None

Mesh Terms

  • Amyloid beta-Protein Precursor
  • Animals
  • Base Sequence
  • Behavior, Animal
  • Brain
  • Exons
  • Exploratory Behavior
  • Female
  • Gene Expression
  • Homozygote
  • Learning
  • Male
  • Mice
  • Mice, Mutant Strains
  • Molecular Sequence Data
  • Mutagenesis, Insertional
  • RNA, Messenger
  • Spatial Behavior