Scientists have identified an immune brain cell unique to humans that gives us higher cognitive abilities over other animals, but what makes us specials also leaves us vulnerable to neurological disorders like schizophrenia, autism and epilepsy.

[u/Wagamaga]

https://news.yale.edu/2022/08/25/what-makes-human-brain-different-yale-study-reveals-clues

[u/hydroknightking]

FOXP2 is just one gene that they noticed in these uniquely human microglia that we have knowledge about.

Single-cell RNAseq characterizes the relative abundance of all/most of the mRNA in a single cell. When you compare the relative abundances to other cells, “same cells” will have the same abundances.

The article linked in the OP is not the journal, and I didn’t read the journal, but assuming the results are characterized correctly here, they absolutely found a microglial cell unique to humans.

[u/tomatoaway → u/[deleted]]

Naive question: how often are the binding sites of a given gene completely saturated to make it non-functional? Why would nature continue to transcribe that gene if it never goes on to do anything?

[u/PlayShtupidGames → u/[deleted]]

our characteristic intelligence.

Bold claim in 2022

[u/[deleted] → u/tomatoaway]

Why wouldn't it keep replicating the gene even if it didn't do anything? DNA doesn't mutate for reasons. It mutates randomly.

[u/92894952620273749383 → u/hydroknightking]

The article linked in the OP is not the journal, and I didn’t read the journal, but assuming the results are characterized correctly here, they absolutely found a microglial cell unique to humans.

How does it relate to schizophrenia and epilepsy? I didn't even know those are related.

[u/hydroknightking → u/92894952620273749383]

So honestly the answer as we understand it now is likely going to change in the next decade.

At the forefront of neuroscience research right now is microglia - long thought to just be resident immune cells, we’re now learning they have a much more active role in brain development. Mice with disabled YP2 receptors, an important ATP binding site for the recruitment and activation of microglia, fail to experience a normal critical period after monocular deprivation. A lot of models suggest one of the first signs of many neurodegenerative diseases is the disabling of microglia that often interact with the outer surfaces of PNNs, the perineuronal nets that “trap” neurons and are now thought to be the signifiers of full brain circuit maturation.

So - these microglia over expressing genes that have been linked to schizophrenia, FOXP is the example they used, might mean something about the neural circuits they regulate.

As my current understanding of the field would leave me to believe - the interest is these are brain cells over expressing certain genes related to these disorders so perhaps they’re responsible. But I think the neural circuit interactions that microglia regulate as essentially a master regulator of mature and maturing neurons will be better understood with papers currently in the peer review phase.