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S3‐03‐06: tau pathology in Young people and its progression Before Abeta Deposition
Author(s) -
Thal Dietmar,
Upadhaya Ajeet Rijal,
Fändrich Marcus,
Del Tredici Kelly,
Braak Heiko
Publication year - 2011
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2011.05.2373
Subject(s) - pathology , tauopathy , senile plaques , neurofibrillary tangle , immunohistochemistry , neocortex , dementia , alzheimer's disease , cerebral amyloid angiopathy , locus coeruleus , tau protein , medicine , biology , neuroscience , disease , neurodegeneration , central nervous system
forms of frontotemporal dementia, establishing that tau protein dysfunction is sufficient to cause neurodegeneration and dementia. Thus, transgenic mice expressing mutant (e.g. P301S) human tau in nerve cells exhibit the essential features of tauopathies, including neurodegeneration and abundant filaments made of hyperphosphorylated tau protein. In contrast, mouse lines expressing single isoforms of wild-type human tau do not produce tau filaments or display neurodegeneration. Methods: Here we have used tau-expressing lines to investigate whether experimental tauopathy can be transmitted. Results: We show that the injection of brain extract from mutant P301S tau-expressing mice into the brain of transgenic wild-type tau-expressing animals induces the assembly of wild-type human tau into filaments and the spreading of pathology from the site of injection to neighbouring brain regions. The study will be complemented by the intracerebral injection of human tissues from various tauopathies into the brain of both transgenic wild-type tau-expressing mice and wild-type B6 mice.