Accumulation of tau protein is associated with neurodegenerative diseases including Alzheimers and Parkinsons diseases as well as other tauopathies.  Tau protein isoforms are created by alternative splicing of exons 2, 3 and 10. The regulation of tau splicing is specific to stage of development, physiology and location. Errors in tau splicing can occur in both exons and introns and, depending on the error, result in changes to protein structure or loss of function.  Aggregation of these abnormal tau proteins correlates directly with pathogenesis and disease progression. Minigenes have been used by several researchers to help understand the regulatory components responsible for mRNA splicing of the TAU gene.