Wim Robberecht

Developments in treatments for amyotrophic lateral sclerosis via intracerebroventricular or intrathecal delivery.

Prevention of intestinal obstruction reveals progressive neurodegeneration in mutant TDP-43 (A315T) mice.

The role of oligodendroglial dysfunction in amyotrophic lateral sclerosis.

Cochlear supporting cell transdifferentiation and integration into hair cell layers by inhibition of ephrin-B2 signalling.

Modifiers of C9orf72 dipeptide repeat toxicity connect nucleocytoplasmic transport defects to FTD/ALS.

Drosophila screen connects nuclear transport genes to DPR pathology in c9ALS/FTD.

Prospective Validation of 18F-FDG Brain PET Discriminant Analysis Methods in the Diagnosis of Amyotrophic Lateral Sclerosis.

Association of a Locus in the CAMTA1 Gene With Survival in Patients With Sporadic Amyotrophic Lateral Sclerosis.

Genetic ablation of IP3 receptor 2 increases cytokines and decreases survival of SOD1G93A mice.

Genome-wide association analyses identify new risk variants and the genetic architecture of amyotrophic lateral sclerosis.

C9orf72 expansion differentially affects males with spinal onset amyotrophic lateral sclerosis.

ATXN2 trinucleotide repeat length correlates with risk of ALS.

Phase Separation of C9orf72 Dipeptide Repeats Perturbs Stress Granule Dynamics.

Progranulin functions as a cathepsin D chaperone to stimulate axonal outgrowth in vivo.

Identification and characterization of Nanobodies targeting the EphA4 receptor.

Prognostic value of clinical and electrodiagnostic parameters at time of diagnosis in patients with amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis.

Inhibition of histone deacetylase 6 (HDAC6) protects against vincristine-induced peripheral neuropathies and inhibits tumor growth.

Reconsidering the causality of TIA1 mutations in ALS.

A zebrafish model for C9orf72 ALS reveals RNA toxicity as a pathogenic mechanism.

Elongator subunit 3 (ELP3) modifies ALS through tRNA modification.

HDAC6 is a therapeutic target in mutant GARS-induced Charcot-Marie-Tooth disease.

Genome-wide Analyses Identify KIF5A as a Novel ALS Gene.

Conditional deletion of Id2 or Notch1 in oligodendrocyte progenitor cells does not ameliorate disease outcome in SOD1 mice.