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    • #20056
      Anonymous
      Inactive

      “Researchers identify a cellular defect common to familial and sporadic forms of ALS”

      A recent NIH-funded study may point to a possible therapeutic target for the disease.

      Read the announcement here:

      https://www.nih.gov/news-events/news-releases/researchers-identify-cellular-defect-common-familial-sporadic-forms-als

      What do you think of this breakthrough? Does it hold promise for ALS patients? Especially when it identifies a cell defect that is shown to be common in both sporadic and familial ALS.

    • #20077
      Anonymous
      Inactive

      This is where it gets interesting;

       

      ” If an antisense oligonucleotide drug, which stops cells from manufacturing specific proteins, was used to decrease the amount of CHMP7 within the ALS neurons, the pore never degraded. “

    • #20097
      Richard
      Participant

      If past history of so-called ALS treatment breakthroughs are any indication of any possible future ALS treatments, then this too will fizzy out into obscurity.

       

      Richard

       

      • #20109

        Dr. Rothstein works in ALS research since a long time (~20 years?). But what is presented here is not very impressive. Working with iPSC-derived is something that could be done at little cost now, and (fortunately) many teams are working on ways to mitigate TDP-43 aggregates.
        And it only pushes the goal post further away: What makes CHMP7 aggregate in the nucleus?

        I guess this work has two objectives:
        1. Participating in the run to patent TDP-43 therapies.
        2. Showing to funding parties that the lab is doing something with their money.

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