Alzheimer’s disease (AD), the most common cause of dementia, is an age dependent progressive neuro-degenerative disorder. Amyloid-beta (a metabolic product of amyloid precursor protein; APP) plays an important role in pathology of AD. APP may also be important in synaptic plasticity and learning and memory processes in the hippocampus.
The line 41 of mThy1-hAPPLond/swe mouse (hAPP751+) is a transgenic mouse model of AD expressing high level of human APP751 cDNA containing the London (V717I) and Swedish (K670M/N671L) mutations under the regulatory control of the murine (m)Thy-1 gene.
Six month old male mThy1-APPLond/Swe mice show hyperactivity, learning and memory deficit, and social interaction abnormalities.
This transgenic line shows mature amyloid-beta plaques, pathological hallmarks of AD, in the frontal cortex as early as 3-4 months of age and develop plaques in the hippocampus, thalamus, olfactory region, basolateral amygdala, and subiculum at the age of 5-7 months.