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Alzheimer’s disease (AD), the most common form of dementia, is associated with two pathological hallmarks: parenchymal beta amyloid deposition and intraneuronal neurofibrillary tangles formed from hyperphosphorylated tau. However, lack of understanding of how these primary pathologies result in cognitive deficits remains a hurdle to the development of meaningful therapeutics.

To investigate a translatable model related to tau pathology, we studied changes in EEG characteristics with age in the P301L tauopathy mouse model.  P301L mice overexpress the 4R/2N isoform of human tau under control of the mouse prion promoter on a C57BL/6 background.   We correlated EEG signatures to the development of tau pathology measured by histopathological methods.  Given that neuroinflammation is implicated as the effector of synaptic dysfunction induced by primary amyloid and tau pathology in AD, we also investigated whether expression of P301L tau was associated with neuroinflammatory changes.