Abundant filamentous deposits made of hyperphosphorylated, insoluble and filamentous tau inclusions are the main pathological characteristic of many neurodegenerative diseases referred to as tauopathies. In Alzheimer’s disease, and some other tauopathies filamentous tau appears to spread in a stereotypic manner as the disease progresses. The propagation of tau pathology during the clinical course of tauopathies points to the existence of intercellular tau aggregate transfer mechanisms. Tau isoform composition, lesions shape, and morphology of filaments can differ between tauopathies, suggesting the existence of distinct tau strains. We have shown that the intracerebral injection of tau aggregates in mice induced filamentous tau inclusions and the spread of pathology to anatomically connected brain regions. In addition, we were able to recapitulate the original tau lesions in mouse brain after inoculation of homogenates prepared from cerebral tissue of patients who died from tauopathies. In conjunction with other findings, this is consistent with the intercellular transfer of tau aggregates and the fact that distinct tau strains may cause distinct tauopathies, based on the involvement of specific brain regions and cell types. Many different approaches to treating tauopathies are currently being explored, with a few compounds already in clinical development. The inhibition of cell-to-cell transmission of pathological aggregates may constitute an effective mechanism-based therapeutic strategy for most human neurodegenerative diseases.