On 23 April, US researchers from the University of California published an article reporting the development of a new mouse model demonstrating aspects of Alzheimer’s disease (AD)-like pathology. The study appears in the journal Nature Communications.
Over 170 AD mouse models have been generated, however these models mimic early-onset AD, also known as familial autosomal-dominant forms of the disease, which accounts for less than 5% of total AD cases. These existing AD mouse models contain disease-causing mutations found in familial risk human genes such as the amyloid precursor protein and presenilin 1.
In the published paper, scientists used a new approach by changing three amino acids in the mouse amyloid precursor protein. This leads to age-dependent impairments in cognition, inflammation, synaptic plasticity, brain volume and others consistent with human changes. This mouse model is what the researchers are calling a “platform model” for late-onset AD, which encompasses 95% of AD cases. “This mouse is a foundational step toward modelling late-onset AD with its hallmark features of plaques and tangles,” said Grant MacGregor, professor of developmental and cell biology and study co-author.
