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Neurons & Immune Cells

watersprite

lost
V.I.P Member
Adding non-neuronal brain cells called microglia to cortical organoids speeds up the rate at which their neurons mature, increases the synchronization of their firing and appears to reduce cell stress, according to a new study. “

The brains of children with autism do not prune unneeded connections between neurons as they age, leaving them with too many of these neuronal links, according to a study published 21 August in Neuron1.
Article here.
 
I remember when the initial discovery of more neuron dendrites in autistics came out in 2014. Already they were speculating on how to reduce the number.

mad.jpg


But I find this line of research a bit scary and would never let anyone prune my organoids. Lets say you took 'Serum X' and after a while you started feeling more relaxed, less anxious, positively chill. How do you know it will stop? What if it keeps on going till you have the brain activity of....

plant.jpeg


A beautiful Ficus. Perfect for the foyer or patio window.

;)
 
Seems interesting.

@Gerald Wilgus, @Neonatal RRT - I would love to hear your thoughts/opinions on this article.

So, what if all those unpruned connections are what makes a lot of AS people really good at their special interests? Are we going to lose specialist autistics in the drive to make sure everyone is good at socializing?
 
Seems interesting.

@Gerald Wilgus, @Neonatal RRT - I would love to hear your thoughts/opinions on this article.

So, what if all those unpruned connections are what makes a lot of AS people really good at their special interests? Are we going to lose specialist autistics in the drive to make sure everyone is good at socializing?
While in vitro this may suggest the role of the microglia in modulating functions of innate immunity in associated cells, extrapolating to the functional brain environment is far too premature. Too many times I've seen the disconnect between model systems in vitro and in vivo, whole animal, results. I had at one time only modest success in that correlation when looking at differences in vitro between undifferentiated and differentiated mammary gland epithelial cells when their behavior in the animal was strikingly different.
 
I’m wondering if, for those of us with ASsD & relsted neurological issues that are hidden by coping strategies, does the stress and fatigue of that result in burnout, or if not, could they end up with an autoimmune disease.
I’ve read excerpts from studies noting patients with autoimmune illness have sub-normal amounts of vitamin D in their systems, but if that is a cause or a result, the study authors did not speculate.

It makes me wonder too, if the developing brain’s lack of immune cells was a cause of autism or if there could be other factors causing a barrier of sorts, keeping those immune cells away from the work they’d normally do in the growing brain.
 
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I’m wondering if, for those of us with ASsD & relsted neurological issues that are hidden by coping strategies, does the stress and fatigue of that result in burnout, or if not, could they end up wirh an autoimmune disease.
I’ve read excerpts from studies noting patients with autoimmune illness have sub-normal amounts of vitamin D in their systems, but if that is a cause or a result, the study authors did not speculate.

It makes me wonder too, if the develiping brain’s lack of immune cells was a cause of autism or if there could be other factors causing a barrier of sorts, keeping those immune cells away from the work they’d normally do in the brain.
I refuse to speculate since correlation is not causation. The evidence required between an observation and proof of specific effect is very significant, far more than the authors present. There is the observation that genes responsible for viral immune response are suppressed, but they offer no measurement of innate immune function, especially the interleukin system. "could" seems to be doing a lot of heavy lifting in this arfticle. and there appears to be a lot of gaps between observation and measurement of actual effect.
 
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While in vitro this may suggest the role of the microglia in modulating functions of innate immunity in associated cells, extrapolating to the functional brain environment is far too premature. Too many times I've seen the disconnect between model systems in vitro and in vivo, whole animal, results. I had at one time only modest success in that correlation when looking at differences in vitro between undifferentiated and differentiated mammary gland epithelial cells when their behavior in the animal was strikingly different.
So the results noted here are good in that they suggest further work. Shine a torch so to speak, toward more experiments, to ask more questions about the in vitro neurons, not to jump the gun & start extrapolating.
 
I refuse to speculate since correlation is not causation. The evidence required between an observation and proof of specific effect is very significant, far more than the authors present.
Thank you. I get reminders about that from my son (who works for the NIH here in MT) every time I start doing that.
:)
I still like thinking about stuff so I hope it’s not too irksome to keep reminding me.
 
Seems interesting.

@Gerald Wilgus, @Neonatal RRT - I would love to hear your thoughts/opinions on this article.

So, what if all those unpruned connections are what makes a lot of AS people really good at their special interests? Are we going to lose specialist autistics in the drive to make sure everyone is good at socializing?

I would need to chew on this topic and pull up some more information. The context presented is speaking of "the developing brain", so I would have to keep my comments within this realm.

Studies that I have read on autistic immune function within the brain (adults and children) suggest an excess of immune cells and an overabundance of oxidative reactions. I would have to re-read these to remind myself of whether or not the immune cells are due to an immune response,...or it's the excess of immune cells that are causing the inflammation and pro-oxidant/anti-oxidant imbalances.

Furthermore, it is well-known within the autism research community that all autistic brains (adults and children) are not the same, and depending upon the specific areas of brain that are focused upon in the experiments, may find areas of an excess of synaptic connections and other areas with insufficient synaptic connections. The autistic brain is often quite heterogeneous with regards to this. In other words, we cannot say that autistic brains, as a whole, are lacking in or have excesses of anything,...it's not a homogeneous organ.
 
@Neonatal RRT, @Gerald Wilgus - Thank you! :)

Seems like from multiple facets, it's way to early to draw any conclusions from the findings in the article.
Brain science is so fascinating to me. I wish I could download the medical knowledge you two have to my brain. lol
 
Studies that I have read on autistic immune function within the brain (adults and children) suggest an excess of immune cells and an overabundance of oxidative reactions. I would have to re-read these to remind myself of whether or not the immune cells are due to an immune response,...or it's the excess of immune cells that are causing the inflammation and pro-oxidant/anti-oxidant imbalances.
Exactly. Without assays or indirect measures of cytokines as well as innate systems like Interleukins, one can fall into the trap of a post hoc ergo propter hoc fallacy.

While my immunology is quite dated, I have enjoyed following how SARS-CoV-2 creates dysfunction of the innate and adaptive immune systems. Particularly interesting is a superantigenic region of the spike protein, separate from the active site, that induces toxic shock like effects similar to some bacterial superantigens. An insertion unique to SARS-CoV-2 exhibits superantigenic character strengthened by recent mutations.
 
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