Main points – These “conditions” represent a significantly different memory mechanic representing the world than “normal”. “HfA” (I need to come up with a better word than “autism”, I’m so done with it) types have an “objectless” memory paradigm and imagine things as collections of properties rather than objects to bind things to. Asperger’s represents the opposite, everything is an object bound to a master object.
Both of these provide pretty significant advantages in memory flexibility compared to normal, however because they do not function “as expected” they return different than expected behavioral output compared to social expectation. These phenotypes are searching for ways to force their unique memory constructions to behave more like social training expects, classic round hole, square peg kind of thing.
Age effects, “masking”, “virtual machine” on “autistic” phenotypes are the result of gathering enough data to emulate expected social response and allows for the social flexibility of HfA phenotypes and leadership/”Reality Distortion Field” mechanics of high functioning Asperger’s phenotypes.
HfA unusual “self awareness” is the result HfA construction of self being a collection properties. Asperger lack of “self awareness” is the result of not binding external properties to their construction of self. For an HfA, “I could be anything”, for Asperger – “I am this.”
Introduce term: “Valence Smashing” – Down-select process returns too many options which match criteria resulting in error state. Brains can “artificially” “valence smash” a “decision” to re-weight returned data and allow valence/salience binding and ultimately behavior. Usually we are trained to do this with the amygdala complex (“Valence up”), often it’s done with the habenula complex, etc. We should be able to train to use any/all of the valence centers to “overweight” valence to re-weight decision data.
Edit: HfA and Asperger’s are almost certainly completely different etiologically. HfA sensory memory mapping/dorsal property extraction is probably a unique, phenotypically stable property. Asperger’s appears to be “extreme normal” memory mechanics.
Lol, I bet nearly the entire gender irrelevance crowd is some degree of HfA construction (note: this has nothing to do with “sexuality”). Ugh, honestly wading into this type of shit makes me anxious just thinking about it and I want no part of it so I’ll stop here but leave that only because it should be a testable mechanic.
Edit 2: Okay, another note, “HfA” and “Asperger’s” (Maybe “Synths and Certains”, can I get away with this?) are not opposites, and there’s no reason both can’t exist at the time on different streams. Generally, “Certains” (and most people) are ventral dominant, and “Synths” are always dorsal dominant. Since the mechanic largely seem to rely significantly on stream weighting, someone could have an equally overstrength relative to function stream on both sides of the hippocampus. E.g. For external processes, they could strongly weight things dorsally, but for internal processes strongly weight things ventrally. Wow, what’s the presentation matrix on this, something like 36 depending on how valence center calculations work?
Which brings another interesting point – while the hippocampus is the stream deconstruction/construction point, the actual stream dominance is determined by valence center calculations. Someone can be extremely ventrally dominant in the NAcc for instance, while being extremely dorsal dominant in the amygdala complex. These are consistent mechanics for everyone, and these stream weights across valence centers are literally “personality”.
Could we one day define “excited” as “High amygdala complex dorsal weight with Low ventral habenula complex” weight? What would the “science of cognition” look like if we stopped assuming “feelings” and “personality” were made out of magic?
It was always interesting to me how extreme people can re-weight their existing memories based on existing context, the idiom “It’s a thin line between love and hate” comes to mind. The idea of it has always completely shocked and befuddled me, but if “feelings” are valence weights… this makes sense.
Extending this a bit further, isn’t this exactly what most stimulation/drug “treatments” are attempting to do, juice a preferred valence center (particularly those that target the dlPFC attempting to juice dorsal weights…)
Another thought, we might be able to tie these constructions to specific genetics. We can almost certainly tie these traits to constructions genetics. Synths would exhibit extreme BDNF mechanics. Need to find data on constructions which “overexpress” BDNF and check this. Actually, maybe not BDNF but GDNF. GDNF, might be a better target although my brain is telling me there’s a ton more BDNF material to work with.
Maybe we could even describe synths as a stable phenotype with both “over developed” dorsal valence center weights/hippocampal dorsal stream weight and this “BDNF/GDNF overexpression”? We should also see obvious differences in rhinal cortex activation as well.
The “autism” part comes specifically from the hypothalamus/mammillary bodies/supramammillary nucleus -> Hippocampal CA2 circuit either over or under weighting “innate” behavioral data. Is it “stuck”, “overstrength”, or “understrength”?
We should definitely see differences in rhinal cortex activations, the “map” for synths is so much more complex than certains. No, this isn’t correct – map complexity is more an artifact of pontine/olivary signal performance (ugh… g for an absolutely inappropriate and stupid comparison). We should still see a difference in activation because synths are dumping the full sensory data to long term memory instead of stripping it into objects first.
Interesting this also implies not all synths or certains are “autistic”, but anyone actually can be “a little autistic” because it’s just a function of that SuM->CA2 circuit strength/weighting. It’s probably more common to see at the extreme ends of presentation like this because the same mechanics which are mashing the dorsal/ventral weights also mash the SuM->CA2 circuit.
Thinking we could definitely make a questionairre that would discern these traits a lot better than anything else out there. Questions which ask individual to make manipulations of their “self” concept will be “easy” for Synths, and difficult for Certains. Questions which require absolute binary responses, particularly opinion based ones, will be “easy” for Certains, but difficult for Synths. We could actually extend this out to domains which approximate the function of each particular valence center.
Which begs the question, is the dorsal/ventral dominance split the 30/70 percent we see in psychological excitory/inhibitory theory, and “autisms” are more likely to diagnosed in ventral dominant phenotypes because they are such extreme presentations of “normal”? Is the full “autistic phenotype” population of ~10-12% in western countries just end clipping? Are nearly all “anxiety” “mental health” presentations actually just dorsal dominant presentations?
Is “anxiety” even a stable enough description to use here? Anxiety is an artifact of error states, this seems like a phenomenologically dependent word doesn’t it? It’s pretty likely that there’s completely different “anxieties” which are being lumped together because we literally can’t imagine other people’s internal states.
Seems like the core mechanic is ability to correctly generate “expected” behavioral outputs, which generates warning states on stored engrammatic social data. “Behavior” is an executed memory program, and memory programs require valence and salience to transfer into long term storage.
Oh god. Of course. Fucking astrocytes. My anti-selection bias mechanisms are begging for mercy right now. I would both kill and die for an explanation more consistent than astrocytes for this stuff just to break the anxiety.
Does Stroop test illustrate dorsal dominate processing?
Edit 3: Going to reference this up – will dump those down here for now.
Information Integration and Information Storage in Retinotopic and Non-Retinotopic Sensory Memory
Attention can operate on object representations in visual sensory memory
Motor memories of object dynamics are categorically organized
The importance of ultrastructural analysis of memory
Molecular and cellular mechanisms of engram allocation and maintenance
Reciprocal activation within a kinase effector complex: A mechanism for the persistence of molecular memory – Incorrect assumptions, but a good look at mechanics.
On the novel mechanisms for social memory and the emerging role of neurogenesis – The CA2 reciprocally modifies valence centers.
Functional differentiation in the transverse plane of the hippocampus: An update on activity segregation within the DG and CA3 subfields – Dorsal stream mechanics, object discrimination
Persistent modifications of hippocampal synaptic function during remote spatial memory – Long term and short term memory have different mechanics, CA1 for sensory memory dump, EC<->CA1 dynamics.
Stable continual learning through structured multiscale plasticity manifolds – Some interesting ideas here
Cerebellar connectivity maps embody individual adaptive behavior in mice – Self construct mostly modelled in the cerebellum. This map is used to strip (and inject) egocentric context in the hippocampal transform.
A model for self-organization of sensorimotor function: the spinal monosynaptic loop – Interesting model despite Hebbianism, probably irrelevant but contextually speaks to motor learning.
Dynamics of Hippocampal Protein Expression During Long-term Spatial Memory Formation – Short term and Long term memory have different mechanics.
Target frequency modulates object-based attention – Stream construction priorities
Can faces affect object-based attention? Evidence from online experiments – Couple of interesting points, especially horizontal bias.
Extracting Object Identity: Ventral or Dorsal Visual Stream? – dissociability of information type between dorsal/ventral streams
Shape representations in the primate dorsal visual stream – difference between dorsal/ventral stream performance, motor associations
Representation of Object Weight in Human Ventral Visual Cortex – Ventral specific functions, what’s missing/reduced in synths.
Object shape and surface properties are jointly encoded in mid-level ventral visual cortex – Cont of above
Connectivity of the ventral visual cortex is necessary for object recognition in patients – Cont, reflects degree of perceptive differences
Perceptual integration rapidly activates dorsal visual pathway to guide local processing in early visual areas – Cont above
Neuronal correlates of motion-defined shape perception in primate dorsal and ventral streams – Primate behavioral interdependence between streams
Task-Relevant Representations and Cognitive Control Demands Modulate Functional Connectivity from Ventral Occipito-Temporal Cortex During Object Recognition Tasks – Specific and significant impacts on cognition