Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the two most common neurodegenerative disorders. Neuropathologically, AD is characterized by the presence of extracellular amyloid-β (Aβ) plaques and intracellular tau-associated neurofibrillary tangles whereas PD involves deposition of α-synuclein containing Lewy bodies.1 Though AD and PD are considered distinct neurodegenerative entities, there is evidence for Lewy body pathology in AD 2 and Alzheimer’s-type pathology in PD 3 suggesting overlap between these two disorders. Importantly, although tau-associated pathology is considered a hallmark of AD, genome-wide association studies (GWAS) in PD have identified several polymorphisms in and around the tau encoding microtubule-associated protein gene (MAPT) 4,5 indicating that similar biochemical perturbations may contribute to both AD and PD. 6 Furthermore, prior reports investigating the genetic relationship between MAPT and AD risk have been conflicting, with some studies finding a positive association 7–8 and other studies showing no association 8–9, indicating that the role of the MAPT gene in influencing Alzheimer’s neurodegeneration is still largely unknown.
