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. Author manuscript; available in PMC: 2015 Nov 27.
Published in final edited form as: Nat Rev Neurosci. 2010 Nov 19;11(12):791–797. doi: 10.1038/nrn2935

Figure 2. LRRK2, α-synuclein and tau.

Figure 2

Human genetic, animal model and biochemical data support the idea that there are relationships between three gene products important in the genetic risk of familial and sporadic Parkinson’s disease, LRRK2, α-synuclein and tau. Here, I have put LRRK2 at the ‘top’ of the pathway, based on the observation that human cases with mutations in LRRK2 can have either α-synuclein or tau positive pathology and also that LRRK2 can accelerate (+ sign) α-synuclein pathology in a mouse model. Whether the same is true for LRRK2 and tau is not known, but I have made the assumption here that it could be. Finally, whether there is a truly triangular relationship in that Tau dysfunction can influence α-synuclein pathology or vice versa is unknown, and so this is indicated by a dotted line. Finally, the likely outputs of α-synuclein and tau dysfunction, namely changes in synaptic vesicle function and microtubule stability are indicated at the bottom of the diagram