www.lesswrong.com/posts/uYXjSHmHyjbNzuZqk/brain-structure-and-iq-how-myelin-elev...
3 corrections found
Multiple sclerosis is a disease where a patient’s immune system attacks their own myelin sheathing cells, resulting in de-myelination in both the peripheral and central nervous systems.
Multiple sclerosis is classically a central nervous system disease, affecting myelin in the brain, spinal cord, and optic nerves—not both the peripheral and central nervous systems.
Full reasoning
This sentence overstates the scope of standard multiple sclerosis pathology. Authoritative medical references describe MS as a disease of the central nervous system (CNS).
- Cleveland Clinic: “Multiple sclerosis (MS) damages the protective cover around nerves called myelin in your central nervous system” and “affects your brain and spinal cord.”
- MedlinePlus (U.S. National Library of Medicine): “Multiple sclerosis (MS) is a nervous system disease that affects your brain and spinal cord.”
Those sources contradict the article’s claim that MS results in demyelination in both the peripheral and central nervous systems. While there are rare overlapping or distinct disorders involving both CNS and PNS demyelination, that is not the standard definition of multiple sclerosis itself.
2 sources
- Multiple Sclerosis (MS): What It Is, Symptoms & Treatment
Multiple sclerosis (MS) damages the protective cover around nerves called myelin in your central nervous system... Multiple sclerosis (MS) is an autoimmune condition that affects your brain and spinal cord (central nervous system).
- Multiple Sclerosis | MS | MedlinePlus
Multiple sclerosis (MS) is a nervous system disease that affects your brain and spinal cord. It damages the myelin sheath, the material that surrounds and protects your nerve cells.
Ephaptic coupling refers to the phenomenon whereby nearby axons may trigger an action potential in each other with no synaptic connection whatsoever, purely through the changes in the ambient intercellular magnetic fields.
Ephaptic coupling is generally described as interaction via extracellular electric fields/potentials, not purely through ambient magnetic fields.
Full reasoning
The article’s definition misstates the mechanism. In the neuroscience literature, ephaptic coupling is ordinarily described as non-synaptic interaction mediated by extracellular electric fields or electrical potentials.
- A Frontiers review states that contemporary work shows that weak electric fields can produce physiological effects and describes neurons influencing one another through field effects in surrounding tissue.
- A PLOS One paper on ephaptic interaction states directly that “neurons might interact via electric fields” and calls such processes ephaptic interactions.
So the problem is not the basic idea that nearby axons can influence one another without synapses; it is the claim that this occurs purely through ambient intercellular magnetic fields. That is not the standard mechanism described by the cited research field.
2 sources
- A historical review of ephaptic field research: from early foundations through contemporary renaissance
Contemporary research has established that weak electric fields (0.1-5 V/m) can produce measurable physiological effects... action potential propagation itself is a longitudinal electromagnetic coupling phenomenon... while ephaptic interactions represent transverse electromagnetic coupling through surrounding tissue.
- Weak Sinusoidal Electric Fields Entrain Spontaneous Ca Transients in the Dendritic Tufts of CA1 Pyramidal Cells in Rat Hippocampal Slice Preparations
Neurons might interact via electric fields and this notion has been referred to as ephaptic interaction... there has been a notion that neurons might interact via electric fields, and such processes have been referred to as ephaptic interactions.
the arcuate fasciculus in humans has extensions leading into the temporal gyri which are not present in our ape relatives.
Chimpanzees do have direct arcuate fascicle connections into the middle temporal gyrus; they are weaker than in humans, not wholly absent in apes.
Full reasoning
This sentence is too strong. It says temporal-gyrus extensions of the arcuate fasciculus are not present in our ape relatives, but later high-resolution comparative work found that chimpanzees do have such a connection.
- The 2025 Nature Communications paper reports that chimpanzees have a direct AF connection into the middle temporal gyrus (MTG), although it is weaker than in humans.
- Even the 2008 Rilling abstract is more cautious than the post: it says the human temporal lobe projection is “much smaller or absent in nonhuman primates,” not categorically absent in apes.
So the accurate summary is that humans have a stronger/more expanded temporal projection of the arcuate fasciculus, but it is incorrect to say temporal-gyrus extensions are simply not present in ape relatives.
2 sources
- Long arcuate fascicle in wild and captive chimpanzees as a potential structural precursor of the language network
We demonstrate that both wild and captive chimpanzees have a direct AF connection into the MTG, albeit weaker than in humans. This finding challenges the notion of a strictly human-specific AF morphology.
- The evolution of the arcuate fasciculus revealed with comparative DTI
Here we compared cortical connectivity in humans, chimpanzees and macaques... and found a prominent temporal lobe projection of the human arcuate fasciculus that is much smaller or absent in nonhuman primates.