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3rd International Conference on Alzheimer’s Disease & Dementia

Toronto, Canada

Claude M Wischik

Claude M Wischik

University of Aberdeen, UK

Title: The place of Tau in the Pathology, treatment and prevention of Alzheimer’s disease and Frontotemporal Dementia

Biography

Biography: Claude M Wischik

Abstract

In Alzheimer’s disease (AD), the microtubule associated protein Tau, is implicated in a self-amplifying aggregation cascade which kills nerve cells and transmits the pathology to otherwise healthy neurons, spreading the disease throughout the brain in manner that is quantitatively linked to the degree of clinical dementia. A similar process occurs for Synuclein in PD. rnThe Tau Aggregation Inhbitors (TAIs) we have developed block this process in cell models and reduce Tau pathology in transgenic mouse models. The first of these (methylthioninium, MT) to be tested in a large Phase 2 clinical trial in AD reduced the rate of disease progression by 90% over 12 months on clinical and imaging endpoints. The brain concentration required for clinical efficacy is the same as that required for TAI activity in model systems. Phase 3 trials in mild and moderate AD are currently underway globally (including Canada) aiming to confirm the Phase 2 results, using an improved version of the drug (LMTX®). We are also conducting a Phase 3 trial in FTD, where either Tau or TDP-43 proteins aggregate, both blocked by LMTX®. The initial results will be available in the first half of 2016.rnIf the Phase 3 trials are successful, LMTX® could be used preventatively, since Tau aggregation affects about 50% of the over-45 population, but progresses slowly at the early stages. LMTX® also reduces pathology in a Synuclein mouse model of PD, so we aim to conduct trials with LMTX® in PD in the future. rn

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