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One of the most active areas of research into Alzheimer’s disease centres on the tau protein that forms the classic neurofibrillary tangles. Aberrant intracellular inclusions composed of hyperphosphorylated filamentous tau are not only a neuropathological hallmark of Alzheimer’s disease, but are also the key pathological species in progressive supranuclear palsy and other sporadic neurodegenerative disorders, which have been collectively termed tauopathies. The discovery that pathogenic mutations in the tau gene microtubule associated protein tau (MAPT) can cause a familial neurodegenerative tauopathy has provided compelling evidence that tau dysfunction is sufficient to cause neurodegeneration. Many recent in vivo studies have shown that tau aggregates have ‘prion-like’ properties which not only allow them to transmit or seed further tau aggregation, but also spread to neighbouring cells or functionally connected brain regions. This process is referred to as ‘tau propagation’ and might explain the stereotypic progression of tau pathology in the brains of Alzheimer’s disease patients. Study of the development and spread of tau pathology in animal models requires large numbers, is time consuming and expensive. Often, the mechanisms and/or potential drug targets that are identified do not translate into humans.

3Rs benefits Thousands of transgenic mice are used per year in large pharmaceutical companies with additional breeding animals to obtain the required genotype. There are specific challenges associated with tau transgenics: • Phenotypic variability. Mice often undergo chronic treatment with a candidate drug to test for disease modifying actions. Large numbers of animals are required per treatment arm to ensure clear results.