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SUMMARY:Special LMNN SEMINAR // “Biomarkers in Parkinson’s disease”
DTSTART:20170126T090000
DTEND:20170126T100000
DTSTAMP:20260916T052754Z
UID:77136d46682bd091e7ace8bb1e760e56842511ddb0930121e5bb4541
CATEGORIES:Conferences - Seminars
DESCRIPTION:Brit Mollenhauer\, Paracelsus-Elena-Klinik Kassel\, Kassel\, G
 ermany\nMany fundamental decisions in medicine rely on biomarker\, to sign
 al the risk of developing a disease (marker of trait)\, to indicate manife
 station of the disease (marker of state)\, to monitor the speed of its pro
 gression and response to therapy (marker of rate)\, and to predict its cou
 rse (marker of fate). The modality of a biomarker ranges from e.g. a clini
 cal measure or a functional test\, to biological fluid markers and imaging
  markers.\nParkinson's disease (PD) is the second most common neurodegener
 ative disorder affecting more than 5 million people worldwide. PD is a hig
 hly complex multifactorial disease characterized by a heterogeneous clinic
 al manifestation and variable progression. The diagnosis of PD is largely 
 clinically based with low sensitivity and specificity\, especially in the 
 first five years of clinical diagnosis. A major challenge in the field is 
 the lack of insight into the exact underlying biologic mechanisms\; thus o
 nly symptomatic treatments are available and a neuroprotective approach is
  lacking. The prevalence of PD is expected to increase dramatically over t
 he next years as the population ages.[1] The field of PD research will gre
 atly benefit from the knowledge of relevant\, disease-specific biomarkers 
 in including accepted\, easily practiced and validated assays for the quan
 tification as diagnostic and progression biomarker as well as markers to i
 dentify subjects at risk to develop PD.\nDue to the heterogeneity at the n
 europathological level\, even when diagnosed as a ‘typical parkinsonian 
 syndrome’ in the clinic by a movement disorder expert a single biomarker
  is unlikely to correctly identify all forms of parkinsonism. Furthermore\
 , a single laboratory value is unlikely to function as a specific and sens
 itive indicator trait\, state\, rate and fate. Optimally different marker 
 modalities (biofluids and structural/functional imaging as in AD research)
  need to be combined.\nAs a first step we have shown that intracellular α
 -synuclein (aSyn)\, a key protein in PD pathogenesis\, is released to the 
 extracellular space and quantification of total aSyn can be useful as diag
 nostic biomarker in extracellular cerebrospinal fluid (CSF) for PD\, shown
  in different independent cohorts. The clinical diagnostic utility of tota
 l aSyn has been limited for a number of reasons\, including the finding th
 at changes in the level of total aSyn in PD patients vs. healthy controls 
 are modest\, as shown in the multicenter Parkinson Progression Marker Init
 iative [2].  Therefore there is a need to explore and validate new marker
  candidates for PD. We have therefore established a new cohort (DeNoPa coh
 ort) of 159 at enrollment recently diagnosed and still drug naïve PD pati
 ents and 110 healthy controls and established an algorithm for the improve
 d diagnosis for PD [3]. Following this cohort biannually we explored multi
 modal progression markers [4]. CSF aSyn is longitudinally in the first two
  years after the clinical diagnosis relatively stable [4] [5] and to explo
 re the possibly more active phase of the disease before the onset of motor
  symptoms we extended the DeNoPa cohort to premotor subjects with idiopath
 ic REM sleep behavior disorder (RBD).\nOur investigations include clinical
  investigations\, imaging and biochemically in biological fluids untargete
 d proteome analysis\, targeted proteome in search of posttranslational for
 ms of aSyn\, metabolome\, microbiome and genome analyses.\n
LOCATION:SV 1717 https://plan.epfl.ch/?room==SV%201717
STATUS:CONFIRMED
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