Article
Knock-in of human BACE1 cleaves murine APP and reiterates Alzheimer-like phenotypes.
The Journal of neuroscience : the official journal of the Society for Neuroscience - 6 Aug 2014
Plucińska Kaja, Crouch Barry, Koss David, Robinson Lianne, Siebrecht Michael, Riedel Gernot, Platt Bettina
Abstract excerpt
Key neuropathological hallmarks of Alzheimer's disease (AD) are elevated levels of amyloid β-peptide (Aβ) species generated via amyloid precursor protein (APP) endoproteolysis and cleavage by the rate-limiting β-site enzyme 1 (BACE1). Because rodents do not develop amyloid pathologies, we here investigated whether AD-like endophenotypes can be created in mice by expression of human bace1. To avoid pitfalls of...
Topics
- Alzheimer Disease
- Amyloid Precursor Protein Secretases
- Amyloid beta-Peptides
- Amyloid beta-Protein Precursor
- Animals
- Aspartic Acid Endopeptidases
- Circadian Rhythm
- Dark Adaptation
- Disease Models, Animal
- Food Preferences
- Gait Disorders, Neurologic
- Genotype