Showing papers by "Damon Wischik published in 2017"
TL;DR: The results are consistent with earlier studies in supporting the hypothesis that LMTM might be effective as monotherapy and that 4 mg twice a day may serve as well as higher doses.
Abstract: The supplementary material is available in the electronic version of this article: http://dx.doi.org/10.3233/JAD-170560. The study was sponsored by TauRx Therapeutics (Singapore). We thank Lon Schneider and Howard Feldman for their contribution to the Scientific Advisory Board. We gratefully acknowledge study investigators and the generosity of study participants. Authors’ disclosures available online (http://j-alz.com/manuscript disclosures/17-0560r3).
134 citations
TL;DR: It is found that the PHF-core tau fragment is inherently capable of auto-catalytic self-propagation in vitro, or “prion-like processing”, that has now been demonstrated for several neurodegenerative disorders.
Abstract: Following our discovery of a fragment from the repeat domain of tau protein as a structural constituent of the PHF-core in Alzheimer's disease (AD), we developed an assay that captured several key features of the aggregation process. Tau-tau binding through the core tau fragment could be blocked by the same diaminophenothiazines found to dissolve proteolytically stable PHFs isolated from AD brain. We found that the PHF-core tau fragment is inherently capable of auto-catalytic self-propagation in vitro, or "prion-like processing", that has now been demonstrated for several neurodegenerative disorders. Here we review the findings that led to the first clinical trials to test tau aggregation inhibitor therapy in AD as a way to block this cascade. Although further trials are still needed, the results to date suggest that a treatment targeting the prion-like processing of tau protein may have a role in both prevention and treatment of AD.
36 citations
Patent•
25 Aug 2017
TL;DR: In this article, improved treatments for Frontotemporal dementia based on the use of a methylthioninium compound in combination with a compound which directly modifies synaptic neurotransmission in the brain, such as a symptomatic Alzheimer's disease treatment (e.g. acetylcholinesterase and/or memantine).
Abstract: The invention describes improved treatments for Frontotemporal dementia based on the use of a methylthioninium compound in combination with a compound which directly modifies synaptic neurotransmission in the brain, such as a symptomatic Alzheimer's disease treatment (e.g. acetylcholinesterase and/or memantine).
5 citations
Patent•
25 Jul 2017
TL;DR: In this paper, the authors provide novel regimens for the treatment of neurodegenerative disorders using methylthioninium (MT)-containing compounds, based on novel findings in relation to the dosage of MT compounds, and their interaction with symptomatic treatments based on modulation of acetylcholinesterase levels.
Abstract: The invention provides novel regimens for treatment of neurodegenerative disorders utilising methylthioninium (MT)-containing compounds. The regimens are based on novel findings in relation to the dosage of MT compounds, and their interaction with symptomatic treatments based on modulation of acetylcholinesterase levels.
5 citations