There exist several dozen lines of transgenic mice that
express human amyloid - β protein precursor (AβPP) with Alzheimer's disease (AD)- linked mutations.
Specifically, rodents genetically modified to
express human amyloid precursor protein (hAPP), which can lead to the debilitating plaques that form in the brains of Alzheimer's patients, seem to struggle to find the hidden platform relative to their healthy peers.
Not exact matches
Importantly, intraperitoneal inoculation of pancreatic homogenates containing IAPP aggregates into transgenic mice
expressing human IAPP dramatically accelerates IAPP
amyloid deposition, which was accompanied by clinical abnormalities typical of T2D, including hyperglycemia, impaired glucose tolerance, and a substantial reduction on β cell number and mass.
C. elegans
expressing a modified form of
human amyloid - β survived three or four more days following infection in the gut with Candida albicans, compared to wild - type worms that did not
express the peptide.
Young mice that
expressed high levels of
human amyloid - β (but did not have pathological plaques) infected in the brain with Salmonella typhimurium were more likely to survive the infection compared to wild - type mice that did not
express the peptide, Tanzi, Moir, and their colleagues found.