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We need something like it. Proper understanding care based upon needs rather than ides about rehab or whatever. Just supporting people to live stably the best they can and not get worse. And then ofc more assisted living like places for those who are less severely affected. I dream of a world...

That’s interesting. So maybe one reason there was none with ME/CFS is precisely because it can be triggered by so many different things? Disparate triggers converging on something downstream? Whereas with LC there is one common trigger?

Good luck @Trish I’m using an agency atm for a couple of hours a week, lovely bloke, taken time to get used to and still can be overwhelming when I’m bad (ended up just crying with him yesterday, he was great though), but he helps bring things up to me etc, not great with cooking but can do...

May not be a great fit as they talk about neuronal injury and excitotoxicity in neurodegenerative conditions, which isn’t quite what we’re looking for, but some if the ideas and mechanisms may be useful.

Also see Glutamate Transporter EAAT2: A New Target For The Treatment Of Neurodegenerative Diseases, 2012, Lin et al Abstract Glutamate is the primary excitatory amino acid neurotransmitter in the CNS. The concentration of glutamate in the synaptic cleft is tightly controlled by interplay...

Seems potentially interesting, found while looking around astrocytes and glutamine. Also see this thread on glutamate and fatigue

Riluzole elevates GLT-1 activity and levels in striatal astrocytes Carbone, Marica; Duty, Susan; Rattray, Marcus Abstract Drugs which upregulate astrocyte glutamate transport may be useful neuroprotective compounds by preventing excitotoxicity. We set up a new system to identify potential...

Bumping this old thread as it has some interesting things on glutamate and fatigue and links with MCH neurons. Found while looking things related to astrocyte glutamate transport and coming across Riluzole.

Things I have been thinking. Do we think there are changes in the neurotransmitters themselves or changes in how they are processed? A lot of things seem to point to post synaptic so I guess receptors? But are we talking changes to the receptors or to some other part of the machinery of...

Yeah. I would like to see more focus on social care from charities. There’s obviously a demand for treatments but there are none. Meanwhile we know what many of us need to live a better life. Safe managed environments to live in which avoid triggers of worsening and have our basic needs met...

Looks like an extension/continuation of the ME Trust service. My experience is this was not useful or accommodating of the needs of people with severe me/cfs.

I’ve seen some really interesting work with adversarial iteration until agreement is reached. Sounds like what you’re doing?

Plenty of those in medicine who peddle disinformation and sycophancy as we well know.

Interesting @Mij I think something like thst was mentioned on this which I was listening to recently https://www.bbc.co.uk/sounds/play/m001byym And some of thenother points raised where discussed. A good listen

Yes I meant actual research not personal stories, sorry if that wasn’t clear.. I remember people had looked at family history and me/cfs itself but wondered if anyone had looked at the data of other conditions.

Has anyone looked at family history and incidence of other neurological conditions in people with ME/CFS? Are people more likely to have family members with PD or other conditions? Would this even be useful given we’re now getting direct genetic data?

Some more discussion on daratumumab and the blood brain barrier here https://www.jnjmedicalconnect.com/products/darzalex-faspro/medical-content/darzalex-darzalex-faspro-blood-brain-barrier-and-central-nervous-system-involvement

Thanks. I wondered about that. It seems cited in lots of other papers but guess that doesn’t mean much.

And this paper talks about effects of inhibiting CD38, which I think an anti-cd38 mab would do in some circumstances? May tie in to the NAD+ stuff above? Inhibition of CD38 and supplementation of nicotinamide riboside ameliorate lipopolysaccharide‐induced microglial and astrocytic...

I have been pondering astrocytes and CD38 and apparently daratumumab (edit: may be able to) cross the blood brain barrier The Daratumumab Crosses the Blood Brain Barrier, 2018, Vercruyssen et al Vercruyssen, Marie; El Hachem, Georges; Maerevoet, Marie Abstract NK/T cell lymphoma is a rare...