CoRE: Long Covid, Lyme and related conditions clinic at Mt Sinai hospital

Jonathan Edwards · Oct 31, 2024

'Improving signs of T cell exhaustion' sounds an awful lot like a wing and a prayer to me.

forestglip · Oct 31, 2024

Oh, and then the separate Simmaron trial gives a different reason:

Our publication on elevated ATG13 showed that a significant number of ME/CFS patients display serological evidence of autophagy disruption. We have shown that this deficit in autophagy is due to the chronic activation of mTOR. Without properly functioning autophagy, there is significant cellular stress, immune activation, and not enough energy for the cell to do well.

Rapamycin is an mTOR inhibitor. It is an FDA approved drug that was initially developed to protect patients during a kidney transplant. It has a well understood safety profile. This study will track autophagy markers and ME/CFS symptoms in patients who are treated with low-dose rapamycin by participating clinicians.
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SNT Gatchaman · Oct 31, 2024

https://en.wikipedia.org/wiki/MTOR_inhibitors

(It's pretty complicated).

I also note the following in An Isolated Complex V Inefficiency and Dysregulated Mitochondrial Function in Immortalized Lymphocytes from ME/CFS Patients (2020, International Journal of Molecular Sciences) —

One of the key upstream regulators of mitochondrial protein expression is TOR Complex I (TORC1 whose catalytic subunit is mTOR, the mechanistic Target Of Rapamycin). We found that TORC1 activity is elevated in ME/CFS lymphoblasts. The expression of mitochondrial enzymes involved in electron transport is known to be upregulated by TORC1 via selective activation of translation via inhibitory phosphorylation of the TORC1 target 4E-BP1 [20]. In addition to its actions on the translation of nuclear-encoded mitochondrial proteins, TORC1 upregulates the expression of transcription factors PGC-1α (transcriptionally via Yin Yang 1) and TFAM (translationally), which respectively induce the transcription of nuclear and mitochondrial genes encoding mitochondrial proteins [19]. Most notable amongst the mitochondrial proteins whose translation is upregulated by TORC1 are nuclear-encoded subunits of Complexes I and V [20], the two respiratory complexes whose expression we found to be the most evidently elevated in the whole cell proteomes of ME/CFS lymphoblasts.
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duncan · Oct 31, 2024

I cannot navigate their website. I'm curious as to the credentials of the researchers and clinicians involved in all three diseases, but particularly Lyme. This is in New York. Who are their ME/CFS experts? They're are plenty of good names in that area. Lyme experts? LC? I would think the names of all those involved (beyond just Putrino) would be spotlighted - maybe they are and I just can't find them.

Calling late stage Lyme "long Lyme" is a bit jarring, almost cutesy, and may put off purists like me.

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CoRE: Long Covid, Lyme and related conditions clinic at Mt Sinai hospital

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CoRE: Long Covid, Lyme and related conditions clinic at Mt Sinai hospital

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