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COVID can infect dopamine neurons, causing neuron senescence, and potentially brain fog and depression. But 3 drugs can rescue these infected neurons

Hip

Senior Member
Messages
17,979
A 2024 study found that SARS-CoV-2 is able to infect dopaminergic neurons, triggering an inflammatory and cellular senescence response. Such an infection in the brain's dopamine neurons may potentially explain long COVID symptoms such as brain fog and depression, an article about the study states.

The study then demonstrated that three FDA-approved drugs can reverse the senescence in these COVID infected dopamine neurons. These three drugs are:
  • Metformin (treats diabetes)
  • Riluzole (treats amyotrophic lateral sclerosis, a motor neuron disease)
  • Imatinib (treats cancer)
Metformin has hit the COVID news previously: when taken during a COVID infection, metformin was shown in a study to reduce the risk of developing long COVID by 42%. The study used the following metformin dosing during the 14 days of the COVID infection:
The metformin dose was titrated over 6 days: 500 mg on day 1, 500 mg twice daily on days 2–5, then 500 mg in the morning and 1000 mg in the evening up to day 14.

Metformin is generally well-tolerated, but quite a few ME/CFS patients have reported a major worsening of symptoms and a major crash after just one or two tablets of metformin. So clearly some ME/CFS patients react badly to metformin, and thus anyone thinking of trying this drug might want to start with very low test doses.
 

Hip

Senior Member
Messages
17,979
Do we know if the dopamine neurons being infected is common in EV infection too? D68, 71, b4, etc.

For coxsackievirus B, I seen studies showing these can chronically infect neural progenitor cells, and astrocytes in the brain.

There are also studies finding a connection between coxsackievirus B and Parkinson's, a disease involving destruction of dopamine neurons.
 
Messages
15
What dose is it safe to start with? Is it ok to divide the tablet? Where I live it costs 2 USD in the pharmacy and I am pretty sure I can buy it without a prescription.
 

Gondwanaland

Senior Member
Messages
5,100
Metformin is generally well-tolerated, but quite a few ME/CFS patients have reported a major worsening of symptoms and a major crash after just one or two tablets of metformin. So clearly some ME/CFS patients react badly to metformin, and thus anyone thinking of trying this drug might want to start with very low test doses.
Could this be the reason?

https://bmcbiol.biomedcentral.com/articles/10.1186/s12915-014-0082-4

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6304344/

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Abstract
Metformin is the most widely prescribed drug to treat patients with type II diabetes, for whom retrospective studies suggest that metformin may have anticancer properties. However, in experiments performed with isolated cells, authors have reported both pro- and anti-apoptotic effects of metformin. The exact molecular mechanism of action of metformin remains partly unknown despite its use for over 60 years and more than 17,000 articles in PubMed. Among the various widely recognized or recently proposed targets, it has been reported consistently that metformin is capable of inhibiting mitochondrial respiratory chain Complex I. Since most of the effects of metformin have been replicated by other inhibitors of Complex I, it has been suggested that the mechanism of action of metformin involved the inhibition of Complex I. However, compared to conventional Complex I inhibitors, the metformin-induced inhibition of Complex I has unique characteristics. Among these, the most original one is that the concentrations of metformin required to inhibit Complex I are lower in intact cells than in isolated mitochondria. Experiments with isolated mitochondria or Complex I were generally performed using millimolar concentrations of metformin, while plasma levels remain in the micromolar range in both human and animal studies, highlighting that metformin concentration is an important issue. In order to explain the effects in animals based on observations in cells and mitochondria, some authors proposed a direct effect of the drug on Complex I involving an accumulation of metformin inside the mitochondria while others proposed an indirect effect (the drug no longer having to diffuse into the mitochondria). This brief review attempts to: gather arguments for and against each hypothesis concerning the mechanism by which metformin inhibits Complex I and to highlight remaining questions about the toxicity mechanism of metformin for certain cancer cells.
 
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