This technology identifies several microRNAs specific to tangle-predominant dementia and other tauopathies that enables disease modifying therapy and improved diagnosis.
The presence of abnormal neuronal and glial filamentous inclusions composed of the microtubule-associated protein tau defines a heterogeneous group of neurodegenerative disorders, termed tauopathies. Currently, there is no therapy that directly targets the underlying mechanisms of these diseases, including Alzheimer’s disease. Nor is there currently a way to clinically differentiate tangle-predominant dementia (TPD) from classical Alzheimer’s disease, a critical distinction for implementing amyloid beta targeted therapies. PET-based amyloid imaging may increase recognition of TPD but is cost-prohibitive. As such, there is a need for both a disease-modifying treatment as well as a bioassay that can differentiate between TPD and classical Alzheimer’s disease to enable improved diagnosis and selective treatment.
This technology identifies a panel of microRNAs that have been shown to target and reduce the levels of Tau expression. miRNAs have recently shown great promise in treating CNS disorders and thus this technology holds great promise as a therapeutic. Additionally, using a simple bioassay, this technology enables facile clinical distinction between TPD and classical Alzheimer’s disease. As patients with TPD typically exhibit low levels of amyloid beta protein, this technology will prevent patients with TPD from being treated with general Alzheimer’s disease therapeutics that may pose an unnecessary risk. This technology also greatly improves the ability to distinguish different subtypes of dementia and may enable drug screening for therapies specific to TPD.
This technology has been validated in post-mortem Alzheimer’s patients.
John F. Crary, M.D., Ph.D.
IR CU12162, 2957
Licensing Contact: Ron Katz