Alzheimer’s disease is characterized by the presence of beta-amyloid plaques and neurofibrillary tangles composed of abnormal, aggregated tau protein. The earliest stage of Alzheimer’s disease is characterized by accumulation of abnormal tau protein in the entorhinal cortex. Later stages show accumulation of abnormal tau in the hippocampus and neocortex. To help test whether tau pathology originating in the entorhinal cortex (1) spreads through the brain along synaptically connected circuits, or (2) develops independently in these different brain areas, the authors generated a transgenic mouse tau model. They expressed pathological human tau protein in the mouse entorhinal cortex and then examined the distribution of tau pathology at different time points.

Their results show propagation of tau pathology from the entorhinal cortex and support a trans-synaptic mechanism of spread along anatomically connected networks of neurons. Their data do not support the hypothesis that tau pathology originates independently in these different brain areas. In general, their tau mouse model replicates the spatial and temporal aspects of early stage tau protein pathology in Alzheimer’s disease.

Liu L, Drouet V, Wu JW, Witter MP, Small SA, Clelland C, Duff K: Trans-Synaptic Spread of Tau Pathology In Vivo. PLoS ONE 7(2): e31302. doi:10.1371/journal.pone.0031302     Published Online Feb. 1, 2012.

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0031302