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Real-world tofersen lowers neurofilaments in SOD1-ALS

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In 24 German early-access SOD1-ALS patients, tofersen slowed ALSFRS-R decline versus pre-treatment and cut serum NfL and CSF pNfH, but CSF pleocytosis was common.

Source

Effects of tofersen treatment in patients with SOD1-ALS in a "real-world" setting - a 12-month multicenter cohort study from the German early access program

Wiesenfarth M · EClinicalMedicine · 2024

doi.org/10.1016/j.eclinm.2024.102495Read the full paper ↗92 citationscc by

Study at a glance

Design
Other — Prospective observational follow-up in Germany’s tofersen early-access program across ten MND-NET centres
N
N=24 · SOD1-ALS patients treated March 2022–April 2023
Population
Adults with SOD1-ALS in a German early-access programme
Outcome
ALSFRS-R progression and serum/CSF neurofilament change on tofersen

Structured fields used in claim comparison tables when every cited study has a complete layer.

What they did

Investigators followed 24 SOD1-ALS patients treated via Germany’s tofersen early access program (March 2022–April 2023) across ten MND-NET centers. They tracked ALSFRS-R, progression rate, quality of life, serum NfL, CSF pNfH, CSF inflammatory markers, and adverse events using a uniform protocol and central CSF/blood assays.

What they found

Median ALSFRS-R decreased from 38.0 to 35.0 (progression 0.11 points/month), slower than pre-baseline progression (0.41 points/month; p = 0.04 in subset). Serum NfL and CSF pNfH each fell significantly (p = 0.02). No deaths occurred, but pleocytosis appeared in 73% and intrathecal immunoglobulin synthesis in 90%; two drug-related serious adverse events included autoimmune myeloradiculitis requiring immunotherapy.

The limits

What it doesn't show

There was no placebo control, sample size was small, follow-up was short and heterogeneous, and pre-baseline slopes relied on recall—so clinical benefit beyond biomarker change remains uncertain and placebo effects cannot be excluded.

Key terms

Tofersen
Antisense oligonucleotide given intrathecally to reduce SOD1 protein by degrading its mRNA.
SOD1-ALS
Amyotrophic lateral sclerosis caused by pathogenic variants in the superoxide dismutase 1 gene.
Neurofilament light chain (NfL)
Blood biomarker of axonal injury that fell during tofersen treatment.
pNfH
Phosphorylated neurofilament heavy chain measured in CSF as a marker of neurodegeneration.
ALSFRS-R
12-item functional rating scale for ALS disability used to compute monthly progression rate.
Pleocytosis
Elevated CSF white cells, here often asymptomatic but suggesting CNS immune activation.

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How many patients were included?

Common questions

Did neurofilament levels improve on tofersen?

Yes—median serum NfL and CSF pNfH both declined significantly over treatment (p = 0.02).

Was functional decline slower than before treatment?

Median on-treatment ALSFRS-R loss (0.11 points/month) was lower than pre-baseline progression (0.41) in the analyzable subset.

Was treatment safe in this cohort?

No deaths occurred, but CSF inflammation was common and two serious drug-related events included autoimmune myeloradiculitis.

How does this relate to the VALOR trial?

It corroborates VALOR/OLE NfL reductions and extends evidence to pNfH in CSF in a less selected real-world cohort.

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