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BEGIN:VEVENT
DTSTAMP:20260613T010131Z
DTSTART;VALUE=DATE-TIME:20180703T123000
DTEND;VALUE=DATE-TIME:20180703T133000
SUMMARY:Seminar: Perturbed TDP-43 autoregulation in novel mouse and human
  knock-in models of ALS-FTD\, Dr Jemeen Sreedharan\, Post Doctoral Fello
 w in Neurodegeneration Research and Honorary Consultant Neurologist\, Ki
 ng’s College Hospital
TZID:Europe/London
UID:20180703-8a17841a63d087630163f300c1773cf1@warwick.ac.uk
CREATED:20180612T081039Z
DESCRIPTION:Abstract: Amyotrophic lateral sclerosis–frontotemporal dement
 ia (ALS-FTD) constitutes a devastating disease spectrum characterized by
  43-kDa TAR DNA-binding protein (TDP-43) pathology. Understanding how TD
 P-43 contributes to neurodegeneration will help direct therapeutic effor
 ts. We created a TDP-43 knock-in mouse with a human-equivalent mutation 
 in the endogenous mouse Tardbp gene. TDP-43Q331K mice demonstrate cognit
 ive dysfunction and a paucity of parvalbumin interneurons. Critically\, 
 TDP-43 autoregulation is perturbed\, leading to a gain of TDP-43 functio
 n and altered splicing of Mapt\, another pivotal dementia-associated gen
 e. Furthermore\, a new approach to stratify transcriptomic data by pheno
 type in differentially affected mutant mice revealed 471 changes linked 
 with improved behavior. These changes included downregulation of two kno
 wn modifiers of neurodegeneration\, Atxn2 and Arid4a\, and upregulation 
 of myelination and translation genes. Finally\, human cells with the TDP
 -43Q331K mutation demonstrate TDP-43 misregulation (unpublished). With o
 ne base change in Tardbp/TARDBP\, these studies identify TDP-43 misregul
 ation as a pathogenic mechanism that may underpin ALS- FTD and exploit p
 henotypic heterogeneity to yield candidate suppressors of neurodegenerat
 ive disease.
LOCATION:MBU (A151)\, Medical School Building\, Gibbet Hill
CATEGORIES:BiomedicalSciences,BMS_CDB
LAST-MODIFIED:20180612T081039Z
ORGANIZER;CN=Jas Bains:
END:VEVENT
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