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SUMMARY:How to discover prodromal Parkinson's disease and why - Wolfgang O
 ertel\, Philips University of Marburg
DTSTART:20211117T103000Z
DTEND:20211117T113000Z
UID:TALK165814@talks.cam.ac.uk
CONTACT:Alyssa Miller
DESCRIPTION:After the discovery of the Lewy Body in 1912\, the depigmentat
 ion of the substantia nigra in 1919  and the dopamine deficit  in 1960 in 
 post mortem brain tissue of PD patients the subsequent i.v. administration
  of L-Dopa in PD patient in 1961 resulted in a dramatic symptomatic improv
 ement of the cardinal motor signs of PD patients. This therapeutic breakth
 rough initiated a 40 year long research on how to improve the symptomatic 
 dopamine replacement pharmacotherapy  (agonist\, MAO-B-inhibitor\, COMT-in
 hibitor) in PD. In 1996/7 three discoveries dramatically changed the PD re
 search field: 1) an autosomal-dominant mutation of the alpha-synuclein gen
 e (SNCA) was found to be responsible for a (rare) familiar form of PD. 2) 
 alpha-synuclein aggregates were demonstrated (in Cambridge\, UK) in the Le
 wy bodies and  subsequently PD - and its variant dementia with Lewy bodies
  (DLB) - were classified as alpha-synucleinopathies\, 3) the parasomnia RE
 M-sleep behaviour disorder (RBD) was reported to be a candidate for a prod
 romal stage of PD. In 2003 Braak and coworkers published – entirely base
 d on the neuropathological distribution of Lewy bodies in incidental Lewy 
 body brains and PD brain  the Braak PD staging. These authors  proposed th
 at PD may originate in the periphery (gastrointestinal tract\, olfactory s
 ystem). This hypothesis was challenged and recently the Body first PD vers
 us Brain first PD subtype concept was proposed by Horsager et al 2020.\n \
 n25 years after the discovery that alpha-synuclein likely plays a major ro
 le in the etiopathogenesis of  the majority of PD patiens\, therapies whic
 h target alpha-synuclein overproduction\, aggregation or try to enhance al
 pha-synuclein degradation have entered the clinical trial phase with the h
 ope\, that some of them may provide a modification of the progression of m
 anifest PD.  A recent survey on clinical trials in PD identified 65 studie
 s testing potentially disease modifying therapies in early (mostly de novo
 ) PD patients. In case one or more of these therapeutic candidates will be
  demonstrated to slow down or stop  the progression of PD\, it will be dis
 cussed to administer these compounds in the prodromal stages of PD. This l
 ater approach would test whether the compound in question allowed to delay
  or prevent the manifestation of motor signs and syBD\, mptoms of PD.\nThu
 s it will be essential to identify prodromal stages of PD with reliable bi
 omarkers and even to find progression markers of the prodromal progression
  of alpha-synucleinopathies. The talk will present recent data on how to d
 iagnose prodromal PD with the focus on REM sleep behaviour disorder (RBD).
  RBD is now considered as a common\, highly specific prodromal stage of PD
  and DLB. Based on multimodal phenotyping and long term follow-up studies 
 in RBD\, modalities like video-assisted polysomnography\, screening questi
 onnaires for RBD\, tests for olfactory function and speech parameters\, im
 aging for peripheral and central indicators (MIBG scan\, DAT SPECT\, FDG-P
 ET)\, biotissue and biofluid parameters will be discussed.\n \nDoppler et 
 al 2017\, Postuma et al 2019\, Jiang et al 2020\, Horsager et al 2020\, Do
 ppler et al 2021\, Kogan et al 2021\, Miglis et al 2021\, Perkins et al 20
 21\, Rusz et al 2021
LOCATION:https://zoom.us/j/92675147881
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