Our data clearly show that ApoB is sufficient to induce motor disability and motor neuron degeneration, and its removal from sALS CSF via filtration or immunodepletion attenuates neurotoxicity, establishing a novel sALS-specific therapeutic target and proof-of-concept to support targeted reduction of ApoB via CSF pheresis35–37 as a therapeutic strategy for sALS patients. Here, APOB is linked to Motor neuron atrophy.