Journal article

Ablation of tau causes an olfactory deficit in a murine model of Parkinson's disease

Leah C Beauchamp, Jacky Chan, Lin W Hung, Benjamin S Padman, Laura J Vella, Xiang M Liu, Bradley Coleman, Ashley I Bush, Michael Lazarou, Andrew F Hill, Laura Jacobson, Kevin J Barnham

ACTA NEUROPATHOLOGICA COMMUNICATIONS | BMC | Published : 2018

Abstract

Parkinson's disease is diagnosed upon the presentation of motor symptoms, resulting from substantial degeneration of dopaminergic neurons in the midbrain. Prior to diagnosis, there is a lengthy prodromal stage in which non-motor symptoms, including olfactory deficits (hyposmia), develop. There is limited information about non-motor impairments and there is a need for directed research into these early pathogenic cellular pathways that precede extensive dopaminergic death in the midbrain. The protein tau has been identified as a genetic risk factor in the development of sporadic PD. Tau knockout mice have been reported as an age-dependent model of PD, and this study has demonstrated that they..

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