Cognitive/memory problems because of low serotonin

[dopamimetic]

So I stumbled over an article linking long COVID (which I learned comes with a bunch of unusual symptoms like cognitive dysfunction and memory problems) with low serotonin in the body. Now I was both on S/NRIs, mostly venlafaxine, from 17-34 without solid medical indication, prescription was just prolonged infinitely and until I switched to fluoxetine for tapering I couldn't quit due to intense withdrawal so I carried on taking it. Quitted 1.5 years ago and am long over PAWS but have a couple of lingering stuff, the easily measurable one is premature ejaculation but also subjectively memory impairment. I was always good at memorizing stuff but e.g. currently attempting to learn Spanish and seem to hit a wall, I keep forgetting faster than I am able to learn and developed an aversion against studying so the books lay unused next to my computer. I also had COVID, no symptoms besides a dulled sense of taste and only discovered by coincidence because I was an inpatient at that time and they wanted to try a new COVID test. But Long COVID is unlikely when I didn't get more symptoms, isn't it?

Now I wonder whether my problems might be due to low central serotonin. The mentioned article doesn't really differentiate between bodily and central serotonin but I guess those are connected?

Would it be worth the attempt to go on Auvelity (bupropion + DXM) because I have the least adverse feelings against that vs. the usual SSRI suspects but it will be difficult to convince my gf so I want to find supporting evidence before I go ahead. I know, I know, I should ask a doctor about this but they were so negligent with me in the past that I like to do my own additional research.

 

[Skorpio]

How will Auvelity be different with regard to serotonin than just a plain SNRI? The NMDA and sigma effects will differ, but it is a pretty typical snri when it comes to serotonin

 

[Neuroprotection]

it’s very difficult to prove a Direct link between individual neurotransmitter levels and complex aspects of cognition involved in things like learning a new language. antidepressants can add a further layer of complexity when used long-term because they cause changes to neurotransmitter receptors. however, the brain is remarkably resilient and things like exercise and good diet as well as adequate sleep can go along way in helping it recover. in regards to low serotonin, i’ll do some research on how that affects cognition, though I doubt peripheral serotonin levels are a good indicator of serotonin in the brain.

 

[AlsoTapered]

it’s very difficult to prove a Direct link between individual neurotransmitter levels and complex aspects of cognition involved in things like learning a new language. antidepressants can add a further layer of complexity when used long-term because they cause changes to neurotransmitter receptors. however, the brain is remarkably resilient and things like exercise and good diet as well as adequate sleep can go along way in helping it recover. in regards to low serotonin, i’ll do some research on how that affects cognition, though I doubt peripheral serotonin levels are a good indicator of serotonin in the brain.

Ah - so you now see how simplistic and basic MOST current testing is. You seem a VERY good mind.

 

[Neuroprotection]

Ah - so you now see how simplistic and basic MOST current testing is. You seem a VERY good mind.

Yes, that’s true in most cases. It’s not that good modern testing methods aren’t available, just that many researchers stick to very old outdated models, probably because they are simple and cheap. If it’s for pharmaceutical research, there is the added incentive of manipulating results for the companies own advantage. nevertheless, tests examining multiple parameters and things like promoter driven transcription which can be activated by an inert drug can produce much more accurate results in the field of gene transcription.

 

[someguyontheinternet]

Yes, that’s true in most cases. It’s not that good modern testing methods aren’t available, just that many researchers stick to very old outdated models, probably because they are simple and cheap. If it’s for pharmaceutical research, there is the added incentive of manipulating results for the companies own advantage. nevertheless, tests examining multiple parameters and things like promoter driven transcription which can be activated by an inert drug can produce much more accurate results in the field of gene transcription.

Which researchers are sticking to outdated methods?

 

[negrogesic]

Which researchers are sticking to outdated methods?

Very old methods like the forced swim test are still widely used to test the efficacy of antidepressants despite these tests being questionable.

Animal testing is still valuable when it comes to say analgesics (and perhaps anxiolytic drugs to a degree), but seems less useful when it comes to antidepressants (especially as there is a move away from serotonergic antidepressants).

 

[someguyontheinternet]

Very old methods like the forced swim test are still widely used to test the efficacy of antidepressants despite these tests being questionable.

Animal testing is still valuable when it comes to say analgesics (and perhaps anxiolytic drugs to a degree), but seems less useful when it comes to antidepressants (especially as there is a move away from serotonergic antidepressants).

Which assays would you suggest?

 

[negrogesic]

Which assays would you suggest?

I don't know enough about the field to answer that question frankly.

 

[AlsoTapered]

The truth is that since the route cause of depression is still under debate, it's difficult to know what IS a valid animal model of depression.

It's worth noting how many antidepressants actually obtain a market licence and are then withdrawn since doctors who treat depressed patients quickly discover that a new drug doesn't work.

 

[Neuroprotection]

Very old methods like the forced swim test are still widely used to test the efficacy of antidepressants despite these tests being questionable.

Animal testing is still valuable when it comes to say analgesics (and perhaps anxiolytic drugs to a degree), but seems less useful when it comes to antidepressants (especially as there is a move away from serotonergic antidepressants).

Thanks for that. What a wonderful example. another example of an old outdated and potentially seriously inaccurate model is the locomotor hyperactivity model of psychosis. many drugs can increase locomotor activity without causing psychosis in humans, even the psychostimulants, which are thought to be psychotomimetic generally only do so with prolonged and very high dose use in healthy humans. meanwhile, the Kappa opioid agonists, which decrease locomotor activity in both animals and humans, are very powerful psychotomimetic agents.

 

[Neuroprotection]

Which assays would you suggest?

I’m no scientist, but from what I read regarding antidepressant testing One can start with an old method like the forced swim test despite its inaccuracy. Additional tests like the sucrose preference test and social defeat stress procedure can be utilised to more accurately measure depressive like behaviours and antidepressant efficacy in animals.