A research in mice has demonstrated how tangles of a so-called tau protein can spread within the brain.
Tangled masses of that tau protein contribute to several neurodegenerative diseases – those that destroy brain functions – including Alzheimer’s disease. The research has provided insights into how tau tangles spread that allow comparisons with the way prions, those that cause Creutzfeldt-Jakob Disease, destroy brain tissue.
Dr Michel Goedert of the Medical Research Council Laboratory of Molecular Biology in Cambridge contributed to the study alongside colleagues in Switzerland and Germany and the results are published today in the online edition of Nature Cell Biology.
Speaking about the study, Dr Goedert made it clear that it would be incorrect to suggest that Alzheimer’s could be contagious: ‘This research in mice does not show that tau pathology is contagious or that it can spread easily from mouse to mouse. What it has revealed is how tau tangles spread within brain tissues of individual mice. It suggests that tangles of proteins that build up in the brain to cause symptoms could have some contagious properties, within brain tissue but not between mice that haven’t been injected with tissue from another mouse and certainly not between people. The work describes an experimental system that will allow scientists to study the mechanisms that underlie the transmission and spread of the tangles of tau proteins connected to the symptoms of Alzheimer’s disease.’
Transgenic and wild-type mice were used in the study. Transgenic mice are genetically modified to carry specific genes. In this study the mice expressed the genes for the human versions of tau proteins.
The researchers injected brain tissue from mice modified to carry the gene for the form of human tau protein implicated in neurodegenerative disease into mice that carried the normal version of the human tau protein and therefore did not already have tangles in their brain tissue. They found that the injected material went on to create tangles of tau at the injection sites. Over time, the tau tangles then spread to neighbouring regions of the brain.
In another experiment, extract from the brains of mice with the gene for mutant-human-tau was injected into the brains of a wild-type mice. In comparison to the mice transgenic for human-tau, a smaller number of tau tangles developed where the tissue was injected and there was no evidence of the tau spreading throughout the brain.
Dr Goedert concluded: ‘In contrast to prion diseases, human tauopathies like Alzheimer’s are believed not to be infectious. The experimental model system we have devised, described in the Nature Cell Biology paper, makes it possible to examine similarities and differences between tauopathies and prion diseases.’
The study was a collaboration between researchers at LMB and scientists at the University of Basel, University Hospital and Novartis Institutes for Biomedical Research in Basel, Switzerland and the University of Tubingen in Germany.