Targeted proteomics upon Tofersen identifies candidate response markers for SOD1-linked amyotrophic lateral sclerosis

Author:

Steffke ChristinaORCID,Baskar Karthik,Wiesenfarth Maximilian,Dorst Johannes,Schuster Joachim,Schöberl Florian,Reilich Peter,Regensburger MartinORCID,German Alexander,Günther René,Vidovic Maximilian,Petri Susanne,Weishaupt Jochen H.,Meyer Thomas,Hagenacker Tim,Grosskreutz Julian,Weyen Ute,Weydt PatrickORCID,Haarmeier Thomas,Lingor PaulORCID,Wolf Joachim,Hermann AndreasORCID,Prudlo Johannes,Günther Kornelia,Knehr Antje,Elmas Zeynep,Parlak Özlem,Uzelac Zeljko,Witzel Simon,Ruf Wolfgang Philipp,Tumani HayrettinORCID,Ludolph Albert C.,Freischmidt Axel,Oeckl PatrickORCID,Ho RitchieORCID,Brenner David,Catanese AlbertoORCID

Abstract

AbstractTofersen is the first effective and approved therapy for familial ALS caused by pathogenic variants in theSOD1gene. Following treatment with tofersen, neurofilaments in patients CSF and serum display a faster response than clinical parameters, underlining their importance as a biomarker for treatment response in clinical trials. This evidence led us to hypothesize that this novel treatment might represent an opportunity to identify additional therapy-responsive biomarkers for ALS. We chose the commercial NUcleic acid Linked Immuno-Sandwich Assay (NULISA™), to investigate a predefined panel of 120 neural, glial and inflammatory markers in CSF and serum samples longitudinally collected from SOD1-ALS patients at baseline and three months after tofersen treatment. We identified a set of proteins (beyond pNfH and NfL) whose levels differed between SOD1-ALS and the matched control group and that were responsive to treatment with tofersen, including Aβ42, NPY and UCHL1. Even though our results warrant validation in larger cohorts and longer follow-up time, they may pave the way for a panel of responsive proteins solidifying biomarker endpoints in clinical trials.

Publisher

Cold Spring Harbor Laboratory

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