gMG Connect
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Consensus meta-analysis of genome-wide association studies for Alzheimer's disease and related dementias. - PubMed

Consensus meta-analysis of genome-wide association studies for Alzheimer's disease and related dementias. - PubMed

Source : https://pubmed.ncbi.nlm.nih.gov/42237039

A meta-analysis identified 91 genetic loci associated with Alzheimer's disease and related dementias risk. Sixteen are newly discovered. Further validation is required for some loci.


The study identifies 91 loci linked to Alzheimer's disease and related dementias (ADRD) risk, with 16 novel ones. Further validation is needed for 18 loci from European-ancestry studies.

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Long-term effectiveness, safety, and cost-effectiveness of intravenous immunoglobulin for generalized myasthenia gravis in an era of molecular targeted drugs: Insights from Japanese post-marketing surveillance. - PubMed

Long-term effectiveness, safety, and cost-effectiveness of intravenous immunoglobulin for generalized myasthenia gravis in an era of molecular targeted drugs: Insights from Japanese post-marketing surveillance. - PubMed

Source : https://pubmed.ncbi.nlm.nih.gov/42275909

IVIg shows long-term effectiveness and cost-effectiveness in managing generalized myasthenia gravis, with no new safety concerns reported over two years.


IVIg demonstrates long-term effectiveness and cost-effectiveness for generalized myasthenia gravis, with a median time to retreatment of 386 days and MG-ADL responder rates of 65.7% on day 14 and 46.7% on day 180, without new safety concerns.

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The ADAPT-SC phase 3 study showed SC efgartigimod was noninferior to IV administration in reducing IgG and improving outcomes in gMG. Extension data support durable tolerability and sustained disease control.

Review gMG FcRn data

  • 3w
    love having another mechanism and tool on the arsenal, looks like this will become a mainstay of treatment.
  • 3w
    Muscle weakness from an autoimmune mechanism.

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3w

Did you know? Generalized myasthenia gravis (gMG) is driven by pathogenic IgG autoantibodies—primarily anti-AChR—that impair neuromuscular transmission. FcRn inhibition accelerates IgG catabolism, rapidly reducing pathogenic autoantibody titers. This mechanism offers a novel therapeutic target distinct from acetylcholinesterase inhibitors or broad immunosuppression.

How do you currently assess disease burden and treatment response in your gMG patients?

NCCN Guidelines

How do you currently assess disease burden and treatment response in your gMG patients?

  • 3w
    One has to look at subjective QOL, functional status.
  • 2mo
    I look at a patients functional status. What activities of daily living do they have problems with. What activities are they no longer doing. And then at Show More

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3w
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In gMG, how do you account for the fluctuating, invisible nature of disease burden — the days patients appear fine but are managing significant fatigue, anxiety, and fear of exacerbation — in your overall clinical assessment?
  • 3w
    Listen carefully with uninterrupted conversation.
  • 1mo
    Unpredictable nature of gMG is warrants detailed discussion with the patient be better assess general well-being.

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