Aggregation of altered tau protein is arguably the primary cause of brain cell death in the late stages of Alzheimer’s disease. It is quite fundamental in cells, involved in maintaining the cytoskeletal structure of microtubules, but nonetheless can be removed without any great disruption of function – though the evidence is mixed on whether that means no unwanted side-effects. This approach has been tried in mice altered to generate similar pathology to that of human Alzheimer’s disease. Researchers here instead examine the outcome of removing tau in young mice and find that it actually improves the metabolism of the brain and measures of cognitive function. Mice are not humans, but perhaps it is the case that we might all be enhanced by some form of therapy that can greatly reduce levels of tau in the brain, and not just through a greater ability to resist the onset of age-related neurodegeneration.
Tau is a protein that associates with microtubules and is found prominently in the axons of neurons. Abnormal modifications of tau are involved in a number of neurodegenerative diseases, known as tauopathies, which are characterized by the formation of pathological deposits of tau. Hyperphosphorylated