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Post-acute COVID-19 cognitive impairment and decline uniquely associate with kynurenine pathway activation, 2022, Brew et al

jaybee00

Senior Member
Messages
605
https://www.medrxiv.org/content/10.1101/2022.06.07.22276020v1

Abstract
Cognitive impairment and function post-acute mild to moderate COVID-19 are poorly understood. We report findings of 128 prospectively studied SARS-CoV-2 positive patients. Cognition and olfaction were assessed at 2-, 4- and 12-months post-diagnosis. Lung function, physical and mental health were assessed at 2-month post diagnosis. Blood cytokines, neuro-biomarkers, and kynurenine pathway (KP) metabolites were measured at 2-, 4-, 8- and 12-months. Mild to moderate cognitive impairment (demographically corrected) was present in 16%, 23%, and 26%, at 2-, 4- and 12-months post diagnosis, respectively. Overall cognitive performance mildly, but significantly (p<.001) declined. Cognitive impairment was more common in those with anosmia (p=.05), but only at 2 months. KP metabolites quinolinic acid, 3-hydroxyanthranilic acid, and kynurenine were significantly (p<.001) associated with cognitive decline. The KP as a unique biomarker offers a potential therapeutic target for COVID-19-related cognitive impairment.
 

Violeta

Senior Member
Messages
3,113
I wonder how the virus causes this effect? Anyone know?

I found this, but the first sentence seems to indicate that the infection increases IDO and the third sentence seems to be saying that the problem involves a decrease in IDO.

1) The SARS-CoV-2 infection affects the KYN levels by inducing the production of the pro-inflammatory cytokine, interferon-gamma (IFN-ɣ) that stimulates the kynurenine pathway enzyme, indoleamine-2,3-dioxygenase (IDO).

2) SARS-CoV-2 infection can lead to an inflammatory response that affects the levels of some intracellular glycoproteins, such as the intercellular cell adhesion molecule-1 (ICAM-1) and the vascular cell adhesion protein-1 (VCAM-1).

3) A decrease in IDO during pathogenic infections leads to an increase in VCAM-1 in endothelial cells of vessel walls.
 
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Violeta

Senior Member
Messages
3,113
1) The SARS-CoV-2 infection affects the KYN levels by inducing the production of the pro-inflammatory cytokine, interferon-gamma (IFN-ɣ) that stimulates the kynurenine pathway enzyme, indoleamine-2,3-dioxygenase (IDO).

Kefir: A protective dietary supplementation against viral infection

Kefir can act as an anti-inflammatory agent by reducing expression of IL-6, IL-1, TNF-α, and interferon-γ.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7655491/
 

Violeta

Senior Member
Messages
3,113
Interesting...

I know I'm late to the quinolinic acid party, but better late than never.

It's something to work on. I have seen info saying that glutamate is involved in postherpetic neuralgia, which is the cause of my worst, most consistent pain.

Quinolinic acid stimulates synaptosomal glutamate release and inhibits glutamate uptake into astrocytes

https://pubmed.ncbi.nlm.nih.gov/11900857/
Quinolinic acid stimulates glutamate release by activating the NMDA receptor in the presynaptic neuron. ...in astrocytes it decreases the expression of glutamate transporters... thus increasing extracellular glutamate levels.
 
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Forummember9922

Senior Member
Messages
187
Interesting...

I know I'm late to the quinolinic acid party, but better late than never.

It's something to work on. I have seen info saying that glutamate is involved in postherpetic neuralgia, which is the cause of my worst, most consistent pain.

Quinolinic acid stimulates synaptosomal glutamate release and inhibits glutamate uptake into astrocytes

https://pubmed.ncbi.nlm.nih.gov/11900857/
Quinolinic acid stimulates glutamate release by activating the NMDA receptor in the presynaptic neuron. ...in astrocytes it decreases the expression of glutamate transporters... thus increasing extracellular glutamate levels.
Thanks for this- Doesnt appear to be easily attainable correct?
 

Violeta

Senior Member
Messages
3,113
Thanks for this- Doesnt appear to be easily attainable correct?
I'm not sure what you mean.

But let me add this from the study:

"These data provide additional evidence that neurotoxicity of QA may be also related to disturbances on the glutamatergic transport system, which could result in the neurological manifestations observed when this organic acid accumulates in the brain."

The glutamate is ending up in extracellular space and causing toxicity.

So the quinolinic acid might be what's causing glutamate issues for some people.

Parkinson's is a well studied disease, and glutamate plays a part in it. Here's a study about glutamate and Parkinson's.

https://touchneurology.com/parkinso...-the-pathophysiology-of-parkinsons-disease-2/

I haven't read the whole study yet, but here's a sentence explaining that glutamate overactivity is very damaging, no matter what causes it.

In summary, loss of nigral dopaminergic neurons and the subsequent striatal depletion of dopamine in PD leads to glutamate overactivity in the basal ganglia where high concentrations of glutamate can damage nervous tissue.
 

Violeta

Senior Member
Messages
3,113
Berberine holds anti-inflammatory activity and can treat UC effectively. The anti-inflammatory property of berberine is tightly related to the suppression of IFN-γ signaling pathway, which is crucial in immune-inflammatory responses of the colon mucosa.
 

hapl808

Senior Member
Messages
2,313
Berberine gave me very strange muscle pains.

Kefir improves my digestion, but worsens my tachycardia.
 

almost

Senior Member
Messages
163
Thanks for this- Doesnt appear to be easily attainable correct?
If you are OK bypassing the paywall, this has worked for me:
Tavares, et. al, 2002, Quinolinic Acid

Quinolinic Acid is a big interest of mine, as my NutrEval showed I had very high levels. Their guide says that it is the brain "on fire" and needs to be addressed, but has to be done so at the source, with no guide as to find what the source is. Sulforaphanes can help reduce, but aren't really a treatment. I've brought this up to a Neurologist and a Neurosurgeon and both just ignored my report. Can't bill for a treatment, it doesn't exist, I guess.

I think it is a big deal, but have no idea how to approach solving it.
 

Violeta

Senior Member
Messages
3,113
If you are OK bypassing the paywall, this has worked for me:
Tavares, et. al, 2002, Quinolinic Acid

Quinolinic Acid is a big interest of mine, as my NutrEval showed I had very high levels. Their guide says that it is the brain "on fire" and needs to be addressed, but has to be done so at the source, with no guide as to find what the source is. Sulforaphanes can help reduce, but aren't really a treatment. I've brought this up to a Neurologist and a Neurosurgeon and both just ignored my report. Can't bill for a treatment, it doesn't exist, I guess.

I think it is a big deal, but have no idea how to approach solving it.
1721086642396.png
 

almost

Senior Member
Messages
163
What is the source of the pic?

I already take lot of antioxidants, for various reasons. My point is I believe this is just having lots of bailers on a sinking ship. That's a great thing to have. I want to know why the ship is taking on water, so to speak.
 

Violeta

Senior Member
Messages
3,113
What is the source of the pic?

I already take lot of antioxidants, for various reasons. My point is I believe this is just having lots of bailers on a sinking ship. That's a great thing to have. I want to know why the ship is taking on water, so to speak.
It's from @Manuel 's recent thread.

You are right to look for the cause.
 
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