There's also the other 90% of sporadic ALS patient

There's also the other 90% of sporadic ALS patients.. That's what "two years of reading" and 15 minutes on google got you. Read all you want, but if you don't understand what you're reading it's not knowledge acquisition. I could sit here and address every random paper you scrape up that you think supports your baseless conjectures, but it looks like that would simply encourage more of the same.

Quote:

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Amyotrophic lateral sclerosis disease (ALS) is a multifactor and multigenic disorder with still unknown aetiology and pathogenesis. Even if several new genes associated to ALS have been described, SOD1 gene is considered the major gene involved in ALS pathogenesis.

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Period. You might have to read some material from this decade to learn that. Or had some clinical experience with the ALS afflicted, or a background in cell bio/proteomics... two years of reading won't necessarily give you that.

"Familial" is another quasi-subjective designation... inability to screen or prove inheritance doesn't make it so. While this is a perfect example of a clinical label (ALS) describing a disease state that can have multiple underlying causes (genetic translation, expression and regulation, environmental), the vast majority are a result of malfunction with SODs, and the vast majority are intracellular... So tell me again, how YOU propose a MAB involved in immune / chemotaxis signalling has the ability to restore SOD function in these people?