#synaptic pruning

[jadefarringtonlaunceston]

This probably won't come as news to most people following me, but research confirms that autistic people have unique brain wiring.

Some people consider autism to be a set of difficulties, characterised only by a list of behaviours in the Diagnostic and Statistical Manual of Mental Disorders (DSM) and similar.

Being autistic isn't a disorder or condition. The way autistic people's brains are wired exists independently of any decision to reduce it to a list of distressed behaviours and supposed 'deficits' and put these in a manual. It's a naturally occurring neurotype and autistic people have different social and communication styles and sensory experiences.

People are born autistic and that cannot be changed or cured. Nor do most autistic people want it to be. No one can become autistic at a later stage - though many autistics are only identified in adulthood or not at all.

Trauma Geek - Trauma and Neurodiversity Education has written about how being autistic or ADHD results in differences in the way synaptic pruning occurs. These differences in wiring have been found to show up in scans.

Autism research is still heavily biased towards searching for causes and cures, despite the fact that surveys of autistic people show their priority for research is mental health and wellbeing. This latest research highlights the need to stop wasting huge amounts of time and money on the former and shift to what autistic people actually want. It could also have big implications for diagnostic procedures.

Read more:

Autism research finds autistic brains are wired differently

What is a neurotype?

Trauma Geek on synaptic pruning differences in autistics and ADHDers

The research paper, TW for disorder language

Do autistic researchers focus on the things autistic people want them to?

Why I choose not to use the terms ASD or ASC

[aeontimaeuscrux]

Cognitive Pruning

Definition: Cognitive pruning is a cognitive phenomenon in which the human brain selectively eliminates or weakens less relevant or less frequently accessed memories and information to make room for the retention and consolidation of more important or frequently used knowledge and experiences. It is an adaptive process that helps optimize memory resources and prioritize information based on its significance and utility.

Cognitive Pruning aligns with the concept of “Epistemic Relevance” in epistemology, the branch of philosophy concerned with knowledge and belief. Epistemic relevance explores how individuals determine which information is relevant to their beliefs and understanding of the world. Cognitive pruning can be seen as a practical manifestation of this philosophical concept, as it reflects the brain’s innate ability to discern and prioritize information deemed relevant to one’s cognitive processes.

“In the labyrinthine meadows of memory, the mind becomes an efficient gardener, trimming away the overgrown vines of trivial recollections to nurture the blooming roses of knowledge. Cognitive pruning, the brain’s art of forgetting, is the sculptor of our mental landscape, ensuring that the most meaningful and useful memories take root and flourish.”

-Me. Today. Just Now

[raffaellopalandri]

From Knowledge to Wisdom: The Art of Refinement, Integration, and Application

When I discuss them with people, I see that knowledge and wisdom are often used interchangeably, yet they are distinct in essence and function. Photo by Janko Ferlic on Pexels.com Knowledge consists of facts, experiences, and learned information, while wisdom arises from the synthesis, discernment, and application of knowledge in a meaningful and ethical way. In an age where vast amounts of…

[helenwhiteart-blog]

Thinking differently: life without an inner voice

I picked up a book “The Untethered Soul” By Michael A Singer as recommended in one of my podcasts the other day…however, I didn’t get very far before I was stopped in my tracks, forced to digest something described in the very first pages. Of course, I’m aware that so many self-help books refer to people having an inner voice, often an inner critic, that needs to be retrained in order to make…

[in-tua-deep]

do yall think constructs like. age? idk if a secunit has uhhh survived long enough to maybe truly answer that question but maybe a comfortunit has

does the cubicle/repair process like. replace organic tissue with young tissue? match or clone the tissue around it? i’m assuming that there’s some organic tissue, like neuro tissue, they have that is vital to function and not able to be replaced without straight up killing them

[hakethishere]

Why Lena doesn’t figure out Kara is Supergirl - psychoanalysis

A psychological reason for which Lena doesn’t realize Kara is Supergirl is that when faced with two similar objects the human mind likes to categorize and therefore looks for differences over similarities, especially when similarities are obvious.

Theory

Consider this thought exercise, imagine two groups of similar looking people but with completely different biology. It would probably make sense that as an observer you would try to find the smallest differences between these two groups in order to be able to tell them apart. It happens often in the world, it is part of the human developmental psychology. It helps infants be able to tell apart similar faces, and it perfects in time based on expertise through synaptic pruning.

In other words it is what makes bird enthusiasts able to figure out which birds are female or male in the same species. Or how car enthusiasts are able to tell apart similar cars. If you’re interested look up the FFA (fusiform face area) and it’s role as visual the expertise module, there are many neuro scientific studies on it.

This categorization becomes increasingly clear when the sense of me vs them in social psychology comes into play.

Lena’s Case

Now applying the same theory to Supergirl TV. Oftentimes we hear Lex’s emphasis on how kryptonians look like humans and how they are actually different from them. Us vs Them. Would it be plausible to believe that Lena growing up in the Luthor household, bearing a scientific mind would be rather inclined to look for dissimilarities rather than similarities between supergirl and other humans? Please consider her first invention in National City, the alien detector device. A little device designed to highlight these dissimilarities, coded by Lena herself. She is a scientist her expertise lies (also) in telling humans apart from aliens, biologically, not visually.

Taking it a step further. Would it be plausible that when faced with Kara and Supergirl, two people similar in so many ways (driven, ethical, stubborn, blonde, blue eyes) that she would overlook the similarities and try to find the slightest of differences in order to latch on to some small sense of security by categorizing Supergirl as “the other”.

(I could also expand on how Kara explains that Supergirl is what she can do and not who she is, further emphasizing my point on obvious emphasis on biological “otherness” over appearance) yada yada but i won’t :))

It does all boil down to cognitive dissonance and Lena’s will to overlook the similarities if we were to simplify it all. But I just thought it would do the story some justice if I could explain how neuropsychology supports that these simple disguises are more effective than one might think.

Im such a nerd, pls forgive my rant. I have a link to the study i’m referencing :) I am nothing if not thorough :)

https://www.sciencedirect.com/topics/neuroscience/fusiform-face-area#:~:text=Several%20functional%20neuroimaging%20studies%20have,configurations%20(Kanwisher%2C%202000).

[covid-safer-hotties]

Also preserved on our archive

By Jasmin Fox-Skelly

Microglia are the brain's resident immune cells. Their job is to patrol the brain's blood vessels looking for invading pathogens to gobble up. But what happens when they go rogue?

Historically they've been overlooked – seen as simple foot soldiers of the immune system. Yet increasingly, scientists believe that microglia may have a more directorial role, controlling phenomenon from addiction to pain. Some believe they may even play a key role in conditions such as Alzheimer's disease, depression, anxiety, long Covid, and myalgic encephalomyelitis (ME), also known as chronic fatigue syndrome.

But what exactly are microglia?

There are two types of cells that make up the brain. Neurons, also known as nerve cells, are the brain's messengers, sending information all over the body via electrical impulses. The other type – glia – make up the rest. Microglia are the smallest member of the glia family and account for about 10% of all brain cells. The small cells have a central oval-shaped "body" from which slender tendril-like arms emerge.

"They have a lot of branches that they are continually moving around to survey their environment," says Paolo d'Errico, a neuroscientist at the University of Freiburg, Germany. "In normal conditions they extend and retract these processes in order to sense what is happening around them."

When performing well, microglia are essential to healthy brain function. During our early years, they control how our brain develops by pruning unnecessary synaptic connections between neurons. They influence which cells turn into neurons, and repair and maintain myelin – a protective layer of insulation encasing neurons, without which transmission of electrical impulses would be impossible.

Their role doesn't stop there. Throughout our lifetimes, microglia protect our brains from infection by seeking out and destroying bacteria and viruses. They clean up debris that accumulates between nerve cells, and root out and destroy toxic misshapen proteins such as amyloid plaques – the clumps of proteins thought to play a role in the progression of Alzheimer's disease.

Yet in certain circumstances they can go rogue.

"There's two sides to microglia – a good side and a bad side," says Linda Watkins, a neuroscientist at the University of Colorado Boulder.

"They survey for problems, looking for unusual neural activity and damage. They're on the watch for any kind of problems within the brain, but when they get super excited, they turn from being the vigilant good guys to the pathological bad ones."

"Out-of-control microglia are now thought to be behind a variety of modern diseases and conditions."

What makes them go rogue? When microglia sense that there is something wrong in the brain, such as an infection, or a large presence of amyloid plaques, they switch into a super-reactive state.

"They become much larger, almost like big balloons, and they pull in their appendages and start moving around, munching up damage like little Pac-Mans," says Watkins.

Activated microglia also release substances known as inflammatory cytokines, which serve as a beacon, calling other immune cells and microglia to action. Such a response is necessary to help the body fight off invaders and threats. Usually after a certain amount of time, microglia revert back to their "good" status.

However, it appears sometimes microglia can stay in this super-excited state long after the infectious agent has disappeared. These out-of-control microglia are now thought to be behind a variety of modern diseases and conditions.

Take addiction. This condition has historically been viewed as a disorder of the dopamine neurotransmitter system, with imbalances of dopamine being to blame for sufferers' increasingly drug-focused behaviour.

But Watkins has a different theory. In a recent academic article, Watkins and scientists from the Chinese Academy of Sciences argue that when a person takes a drug, their microglia see the substance as a foreign "invader".

"What we found out through our own research, was that a variety of opiates activate microglial cells, and they do so at least in part through what's called the 'toll like receptor' (TLR)," says Watkins.

"Toll like receptors are very ancient receptors designed to recognise foreign objects. They're supposed to be there to detect fungi, bacteria and viruses. They're the 'not me, not right, not okay' receptors."

When microglia detect drugs such as opiates, cocaine or methamphetamine they release cytokines, which causes the neurons that are active at the time of drug-taking to become more excitable. Crucially, this leads to new and stronger connections between the neurons being formed, and more dopamine being released – strengthening the desire and craving for drugs. The microglia change the very architecture of the brain's neurons, leading to drug-taking habits that can last a lifetime.

The evidence to support this theory is compelling. For one, drug abusers have raised inflammation and inflammatory cytokines in the brain. Reducing inflammation in animals also reduces drug-seeking behaviour. Watkin's team has also shown that you can stop mice from continually seeking out drugs like cocaine by blocking the TLR receptor and preventing microglial activation.

With ageing, glial cells become more and more primed and ready to over respond as the years go by – Linda Watkins Microglia could play an important role in chronic pain too, defined as pain that lasts longer than 12 weeks. Watkins' laboratory has shown that after an injury, microglia in the spinal cord become activated, releasing inflammatory cytokines that sensitise pain neurons.

"If you block the activation of the microglia or their pro-inflammatory products, then you block the pain," says Watkins.

According to Watkins, microglia could even explain another phenomenon; why elderly people experience a sharp decline in their cognitive abilities following a surgery or infection. The surgery or infection serves as a first hit which "primes" microglia, making them more likely to adopt their bad guy status. Following surgery, patients are often given opioids as pain relief, which unfortunately activates microglia again, causing an inflammation storm that eventually causes the destruction of neurons.

The field of research is in its infancy, so these early findings should be treated cautiously, but studies have shown that you can prevent post-surgery memory decline in mice by blocking their microglia.

"If I walk up to you and, without any forewarning whatsoever, slap you across the face, I get away with it the first time. But you don't let me get away with it the second time because you're primed, you're ready, you're on guard," says Watkins.

"Glial cells are the same way. With ageing, glial cells become more and more primed and ready to over respond as the years go by. And so now that they're in this prime state, a second challenge like surgery makes them explode into action so much stronger than before. Then you get opioids, which are a third hit."

This "priming" of microglia could even be behind Alzheimer's disease (AD). The main risk factor for AD is age, and if microglia become more ready to respond as we get older, it could be a factor. At the same time, one of the main hallmarks of AD is the build-up of clumps of amyloid protein in the brain. This process begins decades before symptoms of confusion and memory loss become detectable. One of microglia's jobs is to hunt down and remove theses plaques, so it's possible that over time, repeated activation causes microglia to permanently switch into rogue mode.

"The accumulation in the brain of amyloid induce microglia to became more reactive," says D'Errico.

We found that microglia are able to internalise the amyloid protein, and then move to another region before releasing it again – Paolo d'Errico "They start to release all these inflammatory signals, but the point is that since these amyloid plaques continue to be produced, there is constant chronic inflammation that never stops. This is really toxic for neurons."

Chronically activated microglia can engulf and kill neurons directly, release toxic reactive species that damage them, or start "over-pruning" synapses, destroying the connection between nerve cells. All these processes could ultimately lead to the confusion, loss of memory, and loss of cognitive function that characterises the disease.

In a 2021 study, d'Errico even found that microglia can contribute to the spread of Alzheimer's disease by transporting the toxic amyloid plaques around the brain.

"In the early stages of Alzheimer's there are particular regions in the brain that seem to accumulate plaques, such as the cortex, the hippocampus, and the olfactory bulb," says d'Errico.

"In the later stages of the disease there are many more regions that are affected. We found that microglia are able to internalise the amyloid protein, and then move to another region before releasing it again."

Some of the symptoms of Alzheimer's, such as forgetfulness and loss of cognitive function, are similar to those suffering from long Covid, and it's possible that errant microglia could be behind "brain fog" too. For example, one of the main factors that cause microglia to turn rogue is the presence of a viral infection.

"Abnormally activated microglia may start over pruning of synapses in the brain, and this may lead to cognitive decline, memory loss, and all those symptoms related to the brain fog syndrome," says Claudio Alberto Serfaty, a neurobiologist at the Federal Fluminense University, in Rio de Janeiro, Brazil, who summarised the evidence for this theory in a recent review article.

The hope is that this new way of thinking will eventually lead to new treatments.

For example, clinical trials for new Alzheimer's drugs are currently underway that aim to boost microglia's capacity to destroy amyloid. However, as with all Alzheimer's drugs, such a strategy would work best in the early stages of the disease, before significant neural death has occurred.

For addiction, one idea is to swap the errant microglia that have gone wrong with the "normal" microglia that are present in the brains of non-drug takers. This concept, known as microglia replacement, involves grafting microglia into the specific brain regions by bone marrow transplantation.

However, such an approach would prove difficult. After all, active microglia are necessary to fight off infections; in fact, they're vital for brain function.

"In theory, yes it could work, but keep in mind that you don't want to disrupt microglia all over your brain, it would need to be localised," says Watkins. "Microinjecting microglia into specific brain areas would be very invasive. So, I think we need to look for something that's safe for that kind of a treatment."

--

[gianteyedcrow]

Cannot get over the fact that Tim saw Robin doing his backflips off of buildings and his brain connected the dots that boy has NO synaptic pruning happening

[stone2stars]

Convince me that sleeping late at night is bad with all your cards 🙅 I'll resist with everything I have (I really believe I should sleep earlier but I don't have a really good reason to, like something that puts me fear)

-🦐 (shrimp is out of questions atm, I need to go back to school to have some ideas to disturb your peace)

You want fear? Alright.

Chronic sleep deprivation—especially from staying up late while forcing your circadian rhythm out of sync—disrupts the glymphatic system, the brain’s literal cleaning network.

That system? It clears out metabolic waste like Beta-amyloid plaques aka the stuff linked to Alzheimer’s.

So every time you skip sleep or delay it past when your internal clock expects rest, you’re lowering your brain’s ability to scrub out neurological trash. Over time, that gunk builds up and slows cognition, memory, and executive function.

You know that foggy, irritable, “what was I doing again?” feeling after a late night? That’s your prefrontal cortex lagging behind because its fuel reserves are torched and its synaptic pruning is off schedule.

Your immune system gets sluggish. Your hormones misfire. You’re more likely to develop insulin resistance. Your risk of heart disease spikes.

And worst of all?

Your brain adapts.

You stop noticing how impaired you are. You think you’re functioning normally, but the lights are flickering upstairs and nobody’s doing maintenance.

The body can handle the occasional late night. But make it a habit? You’re not rebelling. You’re slowly corrupting your own code.

You asked for fear. There it is.

[ben-marco]

The way some people act about child parts is alarming to say the least. The amount of misinformation around these parts is ridiculous. I've seen folks say that when a child part fronts, your brain "regresses" to become a child's brain.

No, sorry. A child part fronting doesn't undo decades' worth of brain development and synaptic pruning.

Did not think we'd be here in 2024 still having to remind people that all alters occupy the same physiological body and brain. But here we are, I guess.

[saphinaspeaks]

Therapist had to walk me through a thought process today and it's kinda life changing.

Ever since my diagnosis I've lived with this fear of becoming "sicker"

This was in part due to some bad experiences I had with an unmedicated family member. But also due to a study I found a few years ago.

I don't remember much about the study like author, site, source, or title. But what I think I remember is a statistic about cognitive decline in schizophrenia patients.

iirc they stated that the average schizophrenic will lose anywhere from 15-20 iq points throughout the course of their life.

I assumed this was due to erroneous processes like bad synaptic pruning, or something.

So I had this false notion that "getting sicker" is actually a physical deterioration.

So as my symptoms evolved I deemed myself as getting sicker.

My therapist today helped me understand some things. Like the missing context for this study.

An IQ test is used to quantify things based on academic ability. Like math problems, reading comprehension etc.

If you take someone who is in psychosis, and ask them to sit down and do long division, your gonna have a bad showing.

That person is so focused on survival, delusions etc. To focus on unimportant shit like math.

So OF COURSE your gonna see a significant decline.

She pointed out that schizophrenia isn't like cancer. It doesn't spread around in your body, and pull you apart and damage organs etc. There isn't varrying degrees of schizophrenia.

People can measure things like symptom impact, or function level with those symptoms.

The progression of symptoms i was experiencing is simply the result of different levels of coping with symptoms.

Not decline.

I decided to think of it as a reflection on the surface of water. Ever changing in response to stimuli. A symptom is like a ripple. It may blur the picture for a little while. But it will eventually return to a clear picture.

Idk if this makes any sense but it was Def a truth bomb for me.

[mindshelter]

the xina and miguel reunion does not stop being baffling because it is just... ridiculous on every single level. miguel put xina through the worst heartbreak of her life and a year later he walks into her apartment while she's not home. it looks like it always has. goes directly into her bedroom and picks up at the framed photo at her bedside (does she just ... look at it every night?) he does some mild nostalgia-induced property damage and joins her on the balcony. she looks like she always has. they sip on some soda. dead, he says, when asked how his sorry excuse of a father is.

they stare deeply into each other's eyes and you can see both their brains shut down. action potentials: zero. synaptic pruning but the shears are wrecking the entire hedge. she finally asks why he showed up. oh yeah, i actually want you to restore the only tether to you i have left. (she's the only thing that listens to me without judgement and i feel safe enough being completely honest with. and it's just an extension of you.)

(letting you go was like losing a limb, could you give me something to replace it, even if it's not the real thing? as long as it's from you. i don't want something new.)

they stare at each other some more. at some point miguel takes off his jacket and is sipping out of a mug like he lives there. he has not seen her in a year. after miguel's life spiralled because he was nonconsensually drugged with wine, and he accepts two drinks—one of which is unsealed—from her without question.

(everyone wants to hurt me. trust you anyway.)

(it's good to see you again.)

[birchbritches]

We Try to Truncate

what's something to truncate that won't short us out, won't flout the running-start necessary to jump a synaptic cleft repeatedly, that repetitive necessary motion won't poop out, an oopsie-daisy or intentional ending when endless sendings of well-wishes would undo finality selfishly or skew any closure into just next steps,

an aerobic effort deprived until there's a cellular shift and everything willy-nillies into working with what's left, not a tactic exactly but what's doable in the midst of dooms or what'd we'd choose to let fall and who we'd let down when we're finally willing to admit to some doing, how no doing doles no dooms, that, though we'd swallow it whole and let that be the be-all end-all of kabooms,

it doesn't go down, it subverts us like inertia to what's always ongoing, a coiling workup of what's able to be cut down and who'd survive some pruning and who wouldn't and how we'd weigh the outcomes, how even after infinite considerations we're getting it wrong and likely the outcomes didn't come to better, how bitter we'd be with having had to think, and we try to truncate

[maaarine]

What Is Synaptic Pruning? (Jacquelyn Cafasso, Healthline, Sep 18 2018)

"Synaptic pruning is a natural process that occurs in the brain between early childhood and adulthood. During synaptic pruning, the brain eliminates extra synapses.

Synapses are brain structures that allows the neurons to transmit an electrical or chemical signal to another neuron.

Synaptic pruning is thought to be the brain’s way of removing connections in the brain that are no longer needed.

Researchers have recently learned that the brain is more “plastic” and moldable than previously thought.

Synaptic pruning is our body’s way of maintaining more efficient brain function as we get older and learn new complex information. (…)

This rapid period of synaptogenesis plays a vital role in learning, memory formation, and adaptation early in life.

At about 2 to 3 years of age, the number of synapses hits a peak level. But then shortly after this period of synaptic growth, the brain starts to remove synapses that it no longer needs.

Once the brain forms a synapse, it can either be strengthened or weakened.

This depends on how often the synapse is used. In other words, the process follows the “use it or lose it” principle: Synapses that are more active are strengthened, and synapses that are less active are weakened and ultimately pruned.

The process of removing the irrelevant synapses during this time is referred to as synaptic pruning. (…)

Unlike research into schizophrenia, which theorizes that the brain is “over-pruned,” researchers hypothesize that the brains of people with autism may be “under-pruned.”

Theoretically, then, this under-pruning leads to an oversupply of synapses in some parts of the brain.

To test this hypothesis, researchers looked at brain tissue of 13 children and adolescents with and without autism who passed away between ages 2 and 20.

The scientists found that the brains of the adolescents with autism had a lot more synapses than the brains of neurotypical adolescents.

Young children in both groups had roughly the same number of synapses.

This suggests that the condition may occur during the pruning process.

This research only shows a difference in synapses, but not whether this difference might be a cause or an effect of autism, or just an association.

This under-pruning theory may help explain some of the common symptoms of autism, like oversensitivity to noise, lights, and social experiences, as well as epileptic seizures.

If there are too many synapses firing at once, a person with autism will likely experience an overload of noise rather than a fine-tuned brain response."

[mxmollusca]

"Trying to explain the experience to a neurotypical person is almost a waste of time because they lack the functional capacity to truly empathize with the experience." Hey maybe don't talk about people like that because it's incredibly rude and dehumanizing

I can see I've struck a nerve, but what I'm describing here is an actual physiological difference between allistics and autistics, not a put-down. Autistic folks don't undergo the same process of synaptic pruning in childhood. We literally are processing more stimuli, and it can feel very overwhelming. Because the allistic brain is different, true empathy for the experience is very difficult.

Sympathy, too, apparently.

[darkmaga-returns]

Editorial by Dr. Lyons-Weiler

In the evolving terrain of neuroscience and public health policy, there are those rare voices who not only challenge orthodoxy but do so with scientific rigor, persistence, and a spirit of principled inquiry. Dr. Russell L. Blaylock is one of those rare voices. With the publication of “Autism Spectrum Disorders: Is Immunoexcitotoxicity the Link to the Vaccine Adjuvants? The Evidence,” we celebrate both a monumental contribution to our understanding of autism and a pivotal moment in the integration of immunology, neurodevelopment, and environmental toxicology. Blaylock’s pioneering concept of immunoexcitotoxicity—the pathological synergy between immune activation and excitotoxic neuronal injury—offers a coherent, mechanistically sound framework to explain how environmental agents, particularly vaccine adjuvants such as aluminum, may contribute to neurodevelopmental disorders like autism spectrum disorder (ASD). This article represents the culmination of decades of Blaylock’s thought, integrating discoveries across glial biology, cytokine signaling, glutamate receptor function, and mitochondrial vulnerability. Blaylock’s central thesis is as profound as it is unsettling: that repeated peripheral immune activation during critical windows of brain development—especially by aluminum-adjuvanted vaccines—can prime microglial cells and astrocytes to unleash neurotoxic cascades upon subsequent stimulation. This priming, he argues, leads to persistent disruptions in synaptic pruning, dendritic architecture, and axonal migration, all of which are essential to healthy neurodevelopment.