Will Form 2220 Dependents
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Will Form 2220 Dependents

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Hello and welcome to the webinar today entitled Auto Fuji and Yoda generation my name is Ray Chan I'm a product manager about technique and I'll be your moderator for today's event like we thank everyone for attending today and I'm happy to welcome our featured speaker professor David Rubenstein this webinar supported by Bauer technique power technique brings together two prestigious life science research brands warranty systems Novus biologicals chakras bioscience putting simple and about cell Diagnostics to pra scientific research community with a comprehensive and world-class portfolio of antibodies proteins small molecules assays and instruments Novus is an industry leader in the development of esophageal research tools before we begin I would like to briefly highlight the range of tofurkey research tools available from Bauer techne bow technique provides a wide range of antibodies proteins and enzymes small molecule auto AG inhibitors and activators and esophageal inducing peptides you can explore more with our interactive pathway for Tov G research in the online Novus pathway resource pages click on the key targets an interactive pathway to discover available products Novus Bart caused knock out validated LC freebie antibody and b100 2,220 is a gold standard to monitor a phagosome formation and at ofuji induction where over 770 citations has been recognized by site AB as the most cited antibody for esophageal research and it has been extensively validated by leading etaf the G research groups around the world bow techne antibodies have been extensively validated with different validation pillars including genetic biological orthoan independent antibody strategies Novus has released three new highly specific and sensitive rabbit recombinant monoclonal antibodies these have been validated by both CRISPR knockout and biological validation strategies and across a wide range of applications in the upper right hand corner of the screen you will see a tab called resources in that tab you'll find extra content that relates to today's webinar Netaji handbook is available from Novus that gives an overview of the key molecular players and regulatory mechanisms as well as a helpful protocols and assays to measure a tough OG this white paper from Novus provides an overview of Vltava G in neurodegenerative diseases focusing on dysfunctional Auto Fujii and the key molecular factors that link tattoo in this highly cited and detailed review Menzies and colleagues discuss the importance of Vltava G function for brain health outlining connections between Auto fatigue dysfunction and neurodegenerative disorders the potential photo for G as a very predict strategy is discussed before handing over control to our speaker I have just a few housekeeping items to address throughout the webinar we invite you to submit any questions you have for David using the ask a question box just below the presentation screen these questions will be asked to david directly following the presentation now I like to introduce our speaker for today professor David Rubenstein David is a UK dementia Research Institute professor professor molecular neurogenetics at the University of Cambridge deputy director of the Cambridge Institute for medical research an academic lead of the Alzheimer's research Cambridge drug discovery Institute he has been a leader in the field of tough OG particularly in the context of neurodegenerative diseases his laboratory has pioneered the strategy of Tophet of regulation as a possible therapeutic approach in various Nino to general diseases and he has identified drugs and neural pathways that may be exploited he has made key contributions to eliminating the relevance of esophageal defects as a disease mechanism and to basic cell biology his laboratory has also identified drug war pathways independent of Topher G that may be relevant to diseases caused by aggregate prone proteins these insights open offer avenues for developing potential therapies david has been elected as a fellow of the Royal Society the Academy of Medical Sciences and as an ember member he has won numerous awards was contributions most recently the water to Spielberg spry 20-18 recognizing his work on Netaji and neurodegeneration and with that i like to hand over control to david thanks ray this afternoon I'm going to tell you about the autocracy lies on pathway neurodegenerative diseases this slide shows the brain of somebody who's died of Huntington's disease compared to an h-back normal brain you can seen the Huntington's brain there's extensive loss of the Straits and giving rise to these large ventricles as well as market loss of the cortex compared to the normal brain these pathological changes give rise to the hallmark features of Huntington's disease abnormal movements cognitive deterioration and psychiatric suits of ecology one of the dreadful features of this autosomal dominant disease is that it has an immediate age of onset around 40 and that's one has the situation where many people find out they've got the diagnosis of Huntington's disease after they've had children and this is indeed what you see in this slide this lady has Huntington's disease and this is a daughter her daughter unfortunately carries the mutants Huntington chromosome however at the moment she's entirely normal she's a cambridge graduates and olympic athletes so she's actually a bit more than normal one of our key objectives is to see how we can find ways to by this young lady as many years of normal disease-free life as possible so can we find ways of delaying the onset of the disease in addition we keen to develop strategies that might ameliorate the condition in a mother we work on Huntington's disease not only because it's a terrible condition in its own right but because it shares key features with most neurodegenerative diseases that afflict people and that is the formation of inclusions we the neurons comprising the aggregate prone protein particularly to that disease so here you see these inclusions or aggregates within neurons and Huntington's disease you see this with tau in Alzheimer's disease you see it with prions in crown diseases you see it with alpha synuclein Parkinson's disease various proteins.

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