The Groundless Memory Research Boasts of the Late Susumu Tonegawa

Today's neuroscience is guilty of promoting many a groundless triumphal legend. One of those groundless socially-constructed triumphal legends is the clam that researcher Susumu Tonegawa did something to show a physical basis for memory. Tonegawa recently died, and the Transmitter magazine has a worshipful article repeating some of these groundless legends. 

The article starts out by quoting false boasts about the very low-quality 2015 paper "Engram cells retain memory under retrograde amnesia" co-authored by Tonegawa. The boasts are made by a co-author of the paper. When we look at the end of the supplemental material, and look at figure s13, we find that the experimenters were using a number of mice that was equal to only 8 in one study group, and 7 in another study group.  Such a paltry sample size does not result in any decent statistical power, and we should have no confidence in any paper using such way-too-small study groups sizes.  The paper failed to use a blinding protocol, an essential for a paper like this to be taken seriously. The paper had a thorough reliance on an utterly reliable technique for trying to judge recall in rodents: the worthless method of trying to judge "freezing behavior." All research papers relying on that method are examples of junk science, for reasons I thoroughly explain in my post here. 

Google Gemini infographic (pardon its spelling errors)

Next the Transmitter article makes this untrue claim: "In a series of papers in the 2010s, Tonegawa and his team showed that simply activating a subset of cells via optogenetics could reactivate a memory, change its valence and even create a false memory." The claim has no basis in fact. 

Let's take a look at some of the schlock work that Tonegawa and his collaborators produced on this topic, all of which is very low-quality research work utterly unworthy of praise:

• The reference in the quote above to reactivating a memory is a reference to the very low-quality 2012 paper "Optogenetic stimulation of a hippocampal engram activates fear memory recall." Figure 2 tells us that in one of the groups of mice there were only 5 mice, and that in another group there were only 3 mice. Figure 3 tells us that in two other groups of mice there were only 12 mice. Figure 4 tells us that in some other group there was only 5 mice. Such  paltry sample sizes does not result in any decent statistical power, and the results are no good evidence of anything, because the study group sizes are way-too-small for any reliable result to be claimed.  The paper has a very big reliance on the use of "freezing behavior" judgments, not a reliable method for measuring fear or recall in rodents. No convincing evidence has been provided of artificially activating a fear memory by the use of optogenetics.
• The reference in the quote above to creating a false memory is a reference to the very low-quality science 2013 paper "Creating a False Memory in the Hippocampus" co-authored by Tonegawa, which you can read here. When we look at Figure 2 and Figure 3, we see that the sample sizes used were paltry: the different groups of mice had only about 8 or 9 mice per group. Such a way-too-small sample size does not result in any decent statistical power, so the results have no weight, because the study group size is way too small for any reliable result to be honestly claimed.  The paper had a thorough reliance on an utterly reliable technique for trying to judge recall in rodents: the worthless method of trying to judge "freezing behavior." The paper makes no use of a blinding protocol, an essential for a paper like this to provide serious evidence of an effect. No convincing evidence has been provided of creating a false memory.
• The claim in the quote above about switching a valence is a reference to the 2015 low-quality science study "Bidirectional switch of the valence associated with a hippocampal contextual memory engram" co-authored by Tonegawa.  We see in that paper 5 or 6 results reported with a borderline statistical significance of only "< 0.05," so this paper is  guilty of p-hacking. No detailed description is given of how an effective blinding protocol was achieved, and only the skimpiest mention is made of blinding, so this paper fails to convince us effective blinding was achieve.  The study used only "freezing behavior" to try to measure fear or recall, without corroborating such a thing by measuring heart rates.  So the paper has done nothing to reliably measure fear or recall in the mice it studies.  The study involved stimulating certain cells in the brains of mice, with something called optogenetic stimulation. The authors have assumed that when mice "freeze" after stimulation, that this is a sign that they are recalling some fear memory stored in the part of the brain being stimulated. What the authors neglect to tell us is that stimulation of quite a few regions of a rodent brain will produce freezing behavior. So there is actually no reason for assuming that a fear memory is being recalled when the stimulation occurs. Some of the study group sizes are good, but others are too-small. Because of all of these problems, no reliable evidence has been produced of a brain storage of memory in mice. 
• Tonegawa co-authored the 2016 paper "Memory retrieval by activating engram cells in mouse models of early Alzheimer’s disease."  This very low-quality paper states that “No statistical methods were used to predetermine sample size.” That means the authors did not do what they should have done to make sure their sample size was large enough. When we look at page 8 of the paper, we find that the sample sizes used were merely 8 mice in one group and 9 mice in another group. On page 2 we hear about a group with only 4 mice per group, and on page 4 we hear about a group with only 4 mice per group. Such a paltry sample size does not result in any decent statistical power, and we should have no confidence in any paper using such way-too-small study groups sizes. The paper had a thorough reliance on an utterly reliable technique for trying to judge recall in rodents: the worthless method of trying to judge "freezing behavior." The study therefore provides no convincing evidence for any of its main claims. 

A close look at the memory research work of Susumu Tonegawa  will fail to find any studies that provide any good evidence for the grander boasts made in the titles of the papers. Although he apparently did some good work in another field (immunology), Susumu Tonegawa was a crappy experimenter in the field of cognitive neuroscience.  The praising quotes about him in the Transmitter article are mostly from scientists often guilty of the same type of bungling and poor experimental design that Tonegawa was so often guilty of. 

The Transmitter article also links to these very low-quality papers co-authored by Tonegawa:

• A Tonegawa study claimed to have “identified engram cells” in the prefrontal cortex. It was a study entitled “Engrams and circuits crucial for systems consolidation of a memory.”  In Figure 1 (containing multiple graphs), we learn that the number of animals used in different study groups or experimental activities were 10, 10, 8, 10, 10, 12, 8, and 8, for an average of 9.5. In Figure 3 (also containing multiple subgraphs), we have even smaller numbers. The numbers of animals mentioned in that figure are 4, 4, 5, 5, 5, 10, 8, 5, 6, 5 and 5. None of these numbers are anything like what would be needed for a moderately convincing result, which would be a minimum of 15 or 20 animals per study group. No detailed description is given of an effective blinding protocol.  The study relies on judgments of freezing behavior of rodents, which is not a reliable way of measuring fear or recall in rodents. 
• Tonegawa co-authored a study "Brain-wide mapping reveals that engrams for a single memory are distributed across multiple brain regions." It is a very low-quality piece of work using way-too-small sizes such as only 7 mice and only 9 mice. The study relies on judgments of freezing behavior of rodents, which is not a reliable way of measuring fear or recall in rodents. 

Tonegawa got a Nobel Prize not for any memory research, but for work in an entirely different area: immunology. 

Tonegawa founded a memory research lab at MIT. Every time I study the rodent memory research results of that lab I find research as low-quality as Tonegawa's memory research papers. For a look at some bogus boasts and very bad experimental methods employed by researchers at that lab, see my post here. 

I might try to put myself in the shoes of the person writing the gushing Transmitter article, and ask: what is going through the mind of such a person when you get that person falling "hook, line and sinker" for such junk science studies? Trying to imagine the person's train of thought, I can imagine the person thinking something like this:

The studies were published in major journals such as Nature and Cell. And the researchers worked at big prestigious universities such as MIT. And the papers were peer-reviewed. So the claims of the studies were probably true. If the authors had made untrue claims, the peer reviewers would have prevented publication. 

But the actual situation is this:

• The church-like neuroscientist belief community (in which professors serve like priests) is a community that has long been addicted to very low quality methods of neuroscience research, largely so that it can maintain the illusion that its cherished but easily debunked belief dogmas are true.  
• Junk cognitive neuroscience research is more the rule than the exception these days, even at laboratories of major universities such as Harvard and MIT. 
• Leading journals such as Nature and Cell are routinely publishing very low-quality research in cognitive neuroscience. Such journals do not have published research standards guaranteeing high-quality research work in neuroscience. 
• Peer-reviewers of submitted papers in cognitive neuroscience tend to be other researchers following research practices as bad as the methods of papers they are asked to review. Such peer-reviewers don't like to reject papers for being guilty of the same research methodology sins that the peer reviewers themselves are guilty of. So peer review does very little to prevent the publication of junk low-quality studies making false claims in their titles and abstracts. 

I can give an analogy for the type of memory research Tonegawa typically did. Imagine that you are testing whether people can get more "heads" flips than "tails" flips when flipping coins, if the people try to use psychokinetic "mind over matter" power to cause a "heads" flip. Imagine if you tested several small groups, each consisting of only 8 or 9 people.  There would be a good chance that one of the groups would report a better-than-50% number of "heads" flips. But that would be mere chance at work, and the effect would disappear if you used larger test groups such as 40 subjects per group. Imagine you also did not verify what each coin flip was, but relied on self-reports by the coin flippers of whether a coin on the ground viewed 10 meters away had landed "heads" or "tails." That would not be a reliable way of observing what the coin flips were, because some of the coin flippers might lie, or might be more prone to say that some not-very-clearly-seen coin had landed "heads."  Such an experiment would be  similar to a typical Tonegawa experiment. He typically used way-too-small study groups much smaller than 15, and reported claimed effects that chance could very easily have produced, effects that would disappear if a larger study group (such as 30 subjects) had been used. And the "freezing behavior" method he typically used to try measure fear or recall in rodents was as unreliable as self-reports from coin flippers viewing a coin from ten meters away. 

Today's cognitive neuroscience research landscape is a swampland of junk research, groundless legends, sleazy shortcuts, poor study design, bad methods and irreproducible results. When people who did frequently bungling memory-related research as bad as Tonegawa's are lionized as "giants," it helps show how deceptive a hall-of-mirrors echo chamber legend machine the world of today's neuroscience literature is. Bogus boasts and unjustified lionization are the enemies of the quest to establish scientific truth. Science goes astray when people put on pedestals scientists who made false boasts of doing things they did not do. 

Appendix: A Short Look at the Folly of "Freezing Behavior" Estimations

When "freezing behavior" estimations go on, things typically work like this. A rodent will be trained to fear some thing such as a shock plate that gives the rodent a shock when the rodent steps on it. Then later the rodent will be placed in a cage that includes the fear stimulus such as the shock plate. The researchers will attempt to record what percentage of some time (say, a minute or 3 minutes) that the rodent was immobile when placed in such a case. This will be called a "freezing percentage," and will be claimed as a measure of how well the rodent remembered the fear stimulus. 

The technique makes no sense. In the real world, rodents don't usually freeze and become immobile when they are afraid. They are much more likely to flee. I know that from years of observing how mice act in the presence of shrieking humans, in an apartment where mice would occasionally appear. So trying to judge recall of a fearful stimulus by judging how much time a rodent was immobile in a cage makes no sense as a way of measuring fear or recall. The thing that utterly destroys the credibility of all "freezing behavior" graphs is that they can be produced in any of more than a dozen ways. A researcher can put a rodent in the cage for three minutes and graph the whole three minutes. Or he can graph only the first 30 seconds, or only the first minute, or only the first two minutes. In each ten seconds of such a three minutes, the researcher can count it as "moving" if the rodent moves one second during that period; or the researcher can count two seconds of movement as being mobility; or the researcher can use three seconds, or four seconds, or five seconds. 

There are no prevailing standards for how "freezing behavior" is judged. With there being a dozen different possibilities of how "freezing behavior" can be judged and graphed, with each having a possibility of success of about 50% (and with pre-registration -- a commitment to an exact methodology before gathering data -- being rare in neuroscience, as a neuroscientist recently confessed), it will be almost certain that the researcher will be able to choose some analysis method that will show the desired difference in "freezing behavior," even if the memory intervention being tested had no real effect. This is a large part of the reason why "freezing behavior" judgments are worthless as evidence for an increase or decrease in memory in rodents. 

A rodent may sometimes "freeze" or become immobile when seeing some fearful stimulus. But there was never any sound basis for assuming that you could reliably measure how well a rodent recalled something by measuring (over a timespan such as a minute) how immobile a rodent was in a cage that contained a fearful stimulus. No one ever did a study with a large sample size establishing the truth of such an assumption. 

Below is a depiction of a reliable method for measuring recall in rodents. 

Using this technique, a mouse is trained to avoid a fear stimulus -- the red shock plate shown in the center of the diagram. At some later date the mouse (in a hungry state) is put into the cage. If the mouse does not remember that the shock plate will cause pain, the mouse will take the direct route to the cheese, which requires crossing over the shock plate. If the mouse does remember that the shock plate will cause pain, the mouse will take an indirect and harder route, requiring it to jump up and down a set of stairs.  This is an easy and foolproof method of testing memory recall in rodents. Here we have a nice binary result -- either the mouse touches the shock plate, or it doesn't. There's no subjective element at all. 

You could use this fear stimulus avoidance technique with a setup even simpler than the one above, a setup with no stairs. You simply put a hungry mouse in a special cage with only one route to the cheese, a route that requires walking over the shock plate. If the mouse avoids the cheese, and fails to touch the shock plate, that would count as remembering that the shock plate will shock; but any touching of the shock plate would count as forgetting that the shock plate will shock. 

Instead of using good reliable objective methods such as the ones above,  today's cognitive neuroscience researchers tend to use the utterly unreliable and subjective method of trying to judge recall by trying to judge how immobile a mouse was in a cage during some arbitrary time interval such as one minute or three minutes.  This method is preferred because it is a "see whatever you want to see" method that maximizes the chance that some researcher will be able to claim some desired effect supposedly involving an increase or decrease in recall.  If peer reviewers were doing their job well, they would reject all papers using the worthless "freezing behavior" method of trying to judge recall. 

A Bullet to Their Brains Caused Little Mind Damage

 One of the very great investigation failures of today's psychologists and neuroscientists is their tendency to only search scientific papers when writing scientific papers. The fact is that there are huge additional sources of information providing very important cases of medical case histories. Those include newspapers and magazines. It is not hard to search for medical case histories documented in newspapers. For example, the free Chronicling America site allows you to search through more than 100 years of American newspapers. You can use the site by using the link below:

https://www.loc.gov/collections/chronicling-america/about-this-collection/

 Below are some of the very interesting cases I get on that site when using the search phrase "brain gone." An account you can read here is entitled "Part of Brain Gone, But Galloway Lives."  We read of a man who tried to kill himself, by shooting himself in the head. We hear that he seemed to recover well, and "talks rationally" despite the fact that he destroyed part of his brain. We read nothing mentioning any mental damage. 

Another account similar to the one above is the account below, which you can read here. We read of a man who lost four ounces of his brain (about 8 percent) after shooting himself in the head. Despite the bad brain damage, after shooting himself the man learned how to play checkers (which he had not learned before), and also apparently played checkers very well. Soon after the shooting he died. 

A similar account is below. We read of a young boy who is of an "unusually bright mind" even though he was accidentally shot through the head.

A similar account is below, from 1910. We read of a boy who "carries on an intelligent conversation" even though he has lost "five square inches" of his brain. We may presume the "five square inches" means "five cubic inches," which is about 7% of a boy's brain. 

A similar account is below. In the 1908 account we read of a man who was shot through the head, losing about 4 ounces of brain, about 6% of the brain. But after this bad brain damage, he is "appparently...in possession of all his mental faculties."

The article below appeared in the New York Times. We read of a person who was left with half a brain after he shot himself in the head, with the wound being treated by surgeons removing additional brain tissue. The patient is described as "rational." We are told "it was believed a few days ago that he would recover completely." No one would have said such a thing unless the subject had relatively little damage to mind and memory. 

The 1912 article below (which you can read here) discusses the case of a soldier who was left with about half a brain, after he was accidentally shot by another soldier, and after surgeons operated on him. We are told that after five weeks the man was "about again as usual." We hear of damage to his ability to read and write, which was restored after five months of training. Other than that, we read no mention of any damage to his memory or intellect.  The claim that he was "about again as usual" five weeks after losing half of his brain suggests there was no very great damage to his mind or memory or speaking ability. Damage to reading and writing skills could be caused by damage to perceptual and muscle ability, and does not necessarily involve any memory loss. 

Wayback Machine Archive Snapshots of This Blog's Content

Should it ever happen years in the future that you attempt to access this blog but find it is not available, you will always be able to read previous snapshots of this blog's contents using the Wayback Machine facility at www.archive.org. 

The way this Wayback Machine works is that you must type the full URL of some site whose content you want to view by examining previous captures of the site.  Follow this procedure to access previous snapshots of this blog's contents:

1. Go to www.archive.org.

2. In the search box at the top, type in the following:

3. You will see an interface allowing you to choose any of various snapshots of this blog's contents taken over the years. Choose the latest one. After doing that, you will be able to navigate this site's pages. 

The only reason I can imagine that someone would do this would be if there were some reason why the regular site (the site you are now at) was not available.  That could conceivably happen if this site were to be hacked by malicious actors, or conceivably it might happen long after my death. 

The Wayback Machine has many snapshots of the previous contents of my three blogs. You can access them by typing these URLs into the search bar of the Wayback Machine, shown above. 

https://orbpro.blogspot.com/

https://headtruth.blogspot.com/

https://futureandcosmos.blogspot.com/ 

No, Near-Death Experiences Are Not Dreams

 We have a new paper trying to explain near-death experiences, one entitled "The dying-moment dream hypothesis: heaven and hell as the brain’s final dream." The explanation is one that makes no sense: that near-death experiences are a dream. Anyone who has carefully studied near-death experiences may well realize the main reason why the hypothesis makes no sense. That reason is that dreams are kind of shadowy experiences much weaker and fainter than ordinary waking reality, but near-death experiences are routinely reported as very vivid experiences that are reported as being realer than normal life. 

The paper has two of the main tendencies of almost all papers trying to explain away near-death experiences: (1) a citation of irrelevant papers, while repeating untrue claims about such papers; (2) a failure to pay any attention to the most important fact about brain performance during cardiac arrest, which is that brains very quickly flatline within 10 to 30 seconds after the heart stops. 

Below are some of the irrelevant papers cited by "the dying-moment dream hypothesis" paper:

Irrelevant Papers Cited by Those Trying to Give Brain Explanations for Near-Death Experiences, Most Having Misleading Titles
"Surge of neurophysiological coherence and connectivity in the dying brain"	This 2013 paper co-authored by Borjigin had a misleading title. Rats were given a chemical causing their heart to stop. The paper failed to show any such "coherence" or "connectivity," but merely showed a very quick flatlining of the brain waves of the rats, occurring within a few seconds after their hearts stopped. In this context it is not honest to describe a momentary blip as a "surge." A 2017 paper was "Electroencephalographic Recordings During Withdrawal of Life-Sustaining Therapy Until 30 Minutes After Declaration of Death." That 2017 paper studied the brain waves of four humans who died in Ontario, Canada after their hearts stopped. These were patients different from the four Michigan, USA patients whose deaths were documented in the 2023 Borjigin paper described below.  Referring to the 2013 paper co-authored by Borjigin, the 2017 paper stated, "We also did not observe any well-defined EEG states following the early cardiac arrest period as previously reported in rats." Of course -- brain electrical activity stops when the heart stops, or only a few seconds later. The paper points out that "one must be careful about false positive EEG signals from muscular and/or cardiac sources."  Motion and muscle activity shows up on EEG readouts, producing what are called motion artifacts. An involuntary muscle twitch (or a movement by a medical person of part of an unconscious body) a few seconds after death may show up as a blip on an EEG reading. A year 2025 scientific paper ("Near-death experience during cardiac arrest and consciousness beyond the brain: a narrative review") states this: "In the context of circulatory arrest, cortical electrical waves in the alpha (8-13Hz) and beta (13-30Hz) bands disappear after an average of 6.5 seconds, while at the same time, the background activity of EEG is replaced by slow waves at delta frequency (<4Hz), which progressively attenuate and lead to a flat EEG recording with no measurable electrical wave pattern around 10-30 seconds—a neural process called isoelectricity or electrocerebral silence (Clute & Levy, 1990; de Vries et  al., 1998; Singer et  al., 1991; Smith et  al., 1990; van Lommel, 2023, p. 28; Visser et  al., 2001; Vriens et  al., 1996). Furthermore, in monkeys and cats, the EEG becomes isoelectric within 20 seconds of the cessation of cerebral blood flow (Hossmann & Kleihues, 1973). The EEG results suggest that cortical electrical activity critical for consciousness, namely alpha and beta activity reflecting top-down connectivity, is eliminated within an average of 6.5 seconds following CA [cardiac arrest]."
"Surge of neurophysiological coupling and connectivity of gamma oscillations in the dying human brain."	Here we have another misleading use of the word "surge" in a 2023 science paper title, a paper co-authored by Borjigin. The paper merely describes a little brain activity in two people after a respirator was turned off, with no evidence of brain activity continuing for more than a few seconds after the heart has stopped. The lines on brain waves charts go up and down, and there are seven or so channels of brain waves (including a gamma channel); so at any second you can usually find some little line going up and call that a "surge," although at the same time other lines (representing other brain wave channels) will probably be going down. Using the term "surge" in the title of the paper was misleading, rather like  tracking the price of Microsoft, seeing it go up 2% at 2:00, and calling that a surge. Almost any random ten seconds of brain wave activity can be statistically analyzed to show a little "surge" somewhere, if you're willing to dredge up secondary statistical measures.  In this context it is not honest to describe a momentary blip as a "surge. Shamefully, the journal Science has an article on this paper with the misleading headline "Burst of brain activity during dying could explain life passing before your eyes"; and the Smithsonian site has an equally misleading click-bait headline of "Surging Brain Activity in Dying People May Be a Sign of Near-Death Experiences." There is no evidence that either of these two people had an experience of "life passing before their eyes" or anything like near-death experiences. The subjects were unconscious when the respirator was turned off, and there is no evidence of any consciousness. Unconscious people have gamma wave activity (the activity reported), and you have plenty of gamma activity while you are sleeping. No "neural correlates of the NDE" were reported by the paper. As two MDs point out in a commentary on this paper, "The researchers reported no evidence whatsoever that these brain activities were correlated with conscious experiences in those two patients—and no reason to compare these results with prospective NDE studies in patients who have survived a cardiac arrest." For a discussion of the misleading statements made by Borjigin and others writing about this study, see my post here.
"Asphyxia-activated corticocardiac signaling accelerates onset of cardiac arrest,"	A 2015 paper co-authored by Borjigin, and sometimes cited as evidence that there is a "surge of chemicals" in dying brains, something relevant to explaining near-death experiences. The main reason that the study is not reliable experimental science is that it uses a way-too-small study group size of only 7 rodents. To be robust evidence, experimental studies attempting to show the effects of interventions in rodents require a sample size of at least 15 or 20 rodents per study group, and almost always a much larger number of rodents. When such experimental studies use only much smaller study group sizes such as 7 rodents per study group, they in general deserve only scorn, particularly when they are guilty of two failures this paper was guilty of: a failure to follow a blinding protocol, and a failure to report a sample size calculation (which typically occurs when experimenters know the study group sizes are way too small).  Another reason why this paper is not reliable evidence for any surge of chemicals in dying rodents is that it was attempting to do something that could not reliably be done in 2015: to track changes in levels of brain chemicals existing in only the tiniest trace amounts, over a time period of a few minutes. There did not exist in 2015 any technology capable of reliably tracking such chemicals over so short a time span. The relevant graph in the paper is Figure 4. There we see a graph purporting to track some brain chemicals existing at levels of only about 20 nanomoles. That's an incredibly tiny amount. In 2015 there did not exist any technology capable of reliably tracking changes in brain chemicals existing in such tiny amounts, over the span of a few minutes.  The authors state, "To probe the neurochemical basis of the heightened cortical activities, we performed minute-by-minute microdialysis in the frontal and occipital lobes of unanesthetized rats (n = 7) before and during asphyxiation and analyzed cortical dialysates using liquid chromatography-mass spectrometry (LC-MS)." In 2015 that was not a reliable technology for tracking changes in minute traces of neurotransmitters in rodents over a period of a few minutes, particularly when using a way-too-small study group size such as only 7 rodents.  None of the supposedly increasing chemicals listed in this 2015 paper are hallucinogens, so it makes no sense for the press to be claiming the paper has a relevance to explaining near-death experiences.  The 2015 paper mentioned above entitled "Asphyxia-activated corticocardiac signaling accelerates onset of cardiac arrest" claimed to use a technology called liquid chromatography-mass spectrometry (LC-MS). In 2015 there did not exist any technology for reliably tracking changes over a few minutes in neurotransmitters such as serotonin existing in only the tiniest trace amounts such as a  few nanomoles.  The pitfalls of this LC-MS technology are discussed in the 2012 paper here ("Pitfalls Associated with the Use of Liquid Chromatography–Tandem Mass Spectrometry in the Clinical Laboratory"), which states this: "However, application of this technology is not automatically or necessarily translated into accurate results. Its pitfalls have to be recognized and must be addressed systematically. In particular interferences from in-source transformation of metabolites, differential matrix effects of analyte and internal standard and isobaric transitions can lead to inaccurate results of LC-MS/MS analyses." The "Asphyxia-activated corticocardiac signaling accelerates onset of cardiac arrest" reports increases in dopamine and serotonin at death. But even if such things occur, they cannot explain near-death experiences.  The paper "Effects of dopamine in man" describes an experiment in which authorities gave 13 subjects a 1% infusion of dopamine, which is enough to cause levels of dopamine to increase by very many times. The paper makes no mention of any hallucinations produced, nor does it mention any mental effects. The paper here involved experiments that increased by very many times (between 100 times and 1000 times, in other words 10000% to 100000%)  the serotonin levels in human volunteers, by infusions of serotonin. No hallucinations were reported.
"Enhanced Interplay of Neuronal Coherence and Coupling in the Dying Human Brain"	This paper with a misleading title reported on some EEG readings of a silent dying patient.  The press tried to make the paper sound as if it had some relevance to near-death experiences, which was ridiculous, because the silent dying patient reported no experience at all. The paper had a misleading title, because no actual "coherence" was observed in the dying patient.  The paper here casts cold water on the "Enhanced Interplay of Neuronal Coherence and Coupling in the Dying Human Brain" paper discussed above, implying that whatever it observed may have been an artifact of muscle movement, which produces confounding signals in EEG readings.

The author of the "dying-moment dream hypothesis" paper fails to inform his readers of the most essential relevant fact related to a discussion of potential brain explanations for near-death experiences: the fact that within 10 to 30 seconds, brains flatline after the heart stops. Any decent explanation of that reality would use the words "isoelectric" and "flatline" in an explanatory way, discussing facts like those discussed in the appendix of this post. But the author's only use of that word "isoelectric" is in a discussion of some hypothetical reality;  and his only use of the word "flatline" is one failing to explain how brains flatline within seconds after cardiac arrest. 

The fact that the brain shuts down electrically very quickly after the heart stops (becoming isoelectric, flatlining within 10 to 30 seconds) is a fact ruling out anything like dreams as an explanation for near-death experience.  The author of the "dying-moment dream hypothesis" paper conveniently fails to tell us this fact. His description of the performance of brains during cardiac arrest is extremely misleading. Instead he repeats the opposite-of-the-truth "surge" claims made in the papers stated above, none of which showed any such thing, with nothing other than the briefest of blips being reported. 

The author of the "dying-moment dream hypothesis" is making statements that have no basis in fact when he states things such as "When the brain is completely decoupled from external sensory constraints, it initiates a profound top-down projection of its own internal architecture—relying exclusively on memory and affective priors to generate a highly structured, closed-loop internal simulation." The author makes quite a few assertions about dreams that are not well-founded. 

Nothing that we know about the content of dreams gives any support to the idea that near-death experiences are some kind of dream. People almost never have dreams in which they are floating above their bodies viewing them from above (a common report in near-death experiences). People almost never have dreams in which they are traveling through a tunnel, seeing a Being of light (a common report in near-death experiences). People don't have dreams in which they are reviewing all of the events of their life (a common report in near-death experiences). While people commonly have dreams about deceased relatives, such dreams almost invariably involve such relatives existing here on Earth. People almost never have dreams in which they view some other realm of existence and see a deceased relative.

I have been carefully recording my dreams for years. My post "I Keep Dreaming of Danger, Death, the Deceased and Life After Death" (which I have been updating almost every week, for years) is one of the most extensive records of a single person's dream experiences ever published, consisting of well over 500 dream descriptions.  While the dreams I have had very frequently involve the deceased and very frequently seem to symbolize the idea of life after death, there has been very little match between the content of my dreams and the content of near-death experiences.  Excluding dreams about subway tunnels and other earthly tunnels, I seem to have never or almost never had a dream matching the common report in near-death experiences of being propelled through a tunnel. I have never had a dream of encountering some mysterious or mystical Being of light. I have never or almost never had any dream of encountering a deceased person in some unearthly realm or heavenly realm. 

Dream content is something very different from near-death experiences. Near-death experiences have a high repetition of a small number of motifs,  motifs that very rarely appear in dream content. The content of dreams is enormously more diverse and varied than the content of near-death experiences.  And dreams are shadowy, faint experiences, unlike the "realer than life" experiences so often reported in accounts of near-death experiences. 

Appendix:  The term "isoelectric" or iso-electric in reference to brain waves means a flat-lining equivalent to no electrical activity in the brain, as measured by EEG readings. The paper here states, "Within 10 to 40 seconds after circulatory arrest the EEG becomes iso-electric." Figure 1 of the paper here says that such an isoelectric flat-lining occurred within 26 seconds after the start of ventricular fibrillation, the "V-fib" that is a common cause of sudden cardiac death, with "cortical activity absent." Also referring to a flat-lining of brain waves meaning a stopping of brain electrical activity, another scientific paper says, "several studies have shown that EEG becomes isoelectric within 15 s [seconds] after ischemia [heart stopping] without a significant decrease in ATP level (Naritomi et al., 1988; Alger et al., 1989)."  

Similarly, another paper refers to blood pressure, and tells us, "When flow is below 20 mL/100 g/min (60% below normal), EEG becomes isoelectric." meaning that brain electrical activity flat-lines. The 85-page "Cerebral Protection" document here states, "During cardiac arrest, the EEG becomes isoelectric within 20-30 sec and this persists for several minutes after resuscitation." Another scientific paper states this, again using the word "isoelectric" to refer to flatlining of brain waves: 

"Of importance, during cardiac arrest, chest compliance is not confounded by muscle activity. The EEG becomes isoelectric within 15 to 20 seconds, and the patient becomes flaccid (Clark, 1992; Bang, 2003)."

A recent scientific paper referring to EEG readings of brain waves states this: 

"The trajectory of EEG activity following cardiac arrest is both well defined and simple. It consists of an almost immediate decline in EEG power, which culminates in a state of isoelectricity [flatlining] within 20 s [seconds]." 

A year 2025 scientific paper ("Near-death experience during cardiac arrest and consciousness beyond the brain: a narrative review") states this:

"In the context of circulatory arrest, cortical electrical waves in the alpha (8-13Hz) and beta (13-30Hz) bands disappear after an average of 6.5 seconds, while at the same time, the background activity of EEG is replaced by slow waves at delta frequency (<4Hz), which progressively attenuate and lead to a flat EEG recording with no measurable electrical wave pattern around 10-30 seconds—a neural process called isoelectricity or electrocerebral silence (Clute & Levy, 1990; de Vries et  al., 1998; Singer et  al., 1991; Smith et  al., 1990; van Lommel, 2023, p. 28; Visser et  al., 2001; Vriens et  al., 1996). Furthermore, in monkeys and cats, the EEG becomes isoelectric within 20 seconds of the cessation of cerebral blood flow (Hossmann & Kleihues, 1973). The EEG results suggest that cortical electrical activity critical for consciousness, namely alpha and beta activity reflecting top-down connectivity, is eliminated within an average of 6.5 seconds following CA [cardiac arrest]."

You can find quite a few additional papers asserting that brains flat-line very quickly after cardiac arrest by doing Google or Google Scholar searches for the phrase "EEG becomes isoelectric" or "EEG becomes iso-electric." 

Oops: Grand Lab Tries to Prove Brain Storage of Learning, But Then Pulls the Plug

Neuroscience within academia suffers from a social disease. That disease is the sick culture of academia, a culture suffering from many problems. They include the following:

(1) Neuroscientists are members of a belief community clinging to unwarranted and groundless dogmas such as the dogma that the brain is the source of the human mind and that memories are stored in human brains (a place where microscopic examination has never discovered memories or any trace of anything anyone learned). 

(2) This belief community exists within a hierarchical structure of authority having many resemblances to the hierarchical structure of authority within the Catholic Church. 

(3) There is a "publish or perish" culture within this belief community, in which scientists are judged by how many papers they publish and how many citations such papers get. This culture incentivizes the production of low-quality "quick and dirty" papers, papers often untruthfully making important-sounding claims that may cause such papers to be cited, driving up the citation counts of the paper authors. 

(4) There is a predominance of a variety of Questionable Research Practices such as the use of way-too-small study group sizes, a lack of the use of blinding protocols, and the use of unreliable methods such as trying to judge rodent recall by "freezing behavior" judgments. 

In the paper here we read a description of the Janelia Research Campus, which tried to do neuroscience in a different way. Part of the Howard Hughes Medical Institute, this campus was a very fancy set of labs set up on the Potomac River,  55 miles upstream of Washington D.C. The paper here describes this Janelia campus as "a state-of-the-art research campus and community of more than 350 scientists, split between individual research labs, project teams and shared scientific support groups." We read that "the new research campus would have organizational and reward structures very different from those found in academia." We read that one of its goals was to create an environment "insulating Janelia from the dominant academic culture through geographical separation." Wow, I guess the dominant academic culture must be in pretty bad shape if some giant lab would feel the need to insulate itself from that culture.

Below is a short video showing the palatial surroundings of the fancy Janelia Research Campus, which has a staff of 650, a budget of 300 million dollars, and a campus of 689 acres:

In the paper we read that after pondering what goals to pursue, it was decided that the big fancy new neuroscience research campus would undertake two grand goals: " i) understanding how information is stored and processed by neuronal circuits; and ii) developing novel imaging methods and computational tools for image analysis." The first of these research goals was quixotic folly. There has never been any good reason for thinking that learned information is stored in neuronal circuits. No one has ever come up with a decent theory as to how the very many types of things that humans learn could ever be stored in "neuronal circuits."

A recent article at The Transmitter site tells us that now this fancy Janelia Research Campus has decided to "pull the plug" on quite a few of its mouse researchers trying to find "how information is stored and processed by neuronal circuits." We read of a "major course correction." We read, "As part of the change, Janelia is also shuttering two programs and plans to phase out projects that use rodent models, The Transmitter has learned." We may presume that one of these program was the big goal of "understanding how information is stored and processed by neuronal circuits." 

Apparently the Janelia Research Campus was getting nowhere trying to back up claims that memory is stored by in neuronal circuits. Now the big fancy facility is switching gears, focusing on "whole-brain imaging of a transparent fish called Danionella."

The Janelia campus is offering a very comfy transition process for the floundering mouse researchers. The mouse researchers will be given  "roughly three years to wrap up their projects and find new positions, and Janelia plans to provide each researcher with an additional $1 million in transition funding," But despite getting these ridiculously generous terms, we read below that the mouse researchers are furious, and are screaming, "Betrayal!" 

In the Transmitter article we read this: 

 "The facility added the Mechanistic Cognitive Neuroscience program in 2019 and the 4D Cellular Physiology program in 2022. Janelia initially announced that it planned to fund each program for 15 years, but it now plans to close both to make way for the Danionella work".

No one should be surprised. "Mechanistic Cognitive Neuroscience" is a dead end that has produced no robust evidence that minds or memory could arise in any mechanistic or neural way. Those trying to produce such results have produced mainly dead-end misleading results guilty of Questionable Research Practices, results that fail to be reproduced in any convincing way. So we can hardly be surprised that some big lab would "pull the plug" on so failing a project. 

But the Janelia Research Campus has not learned any humility from the failure of its earlier grand plans. Now it announces a different research plan, a plan making mistakes similar to its previous plans. We read that it now has the grand goal of "understanding how the brain generates complex behavior." The brain does not do any such thing, so this goal will fail as badly as the previous goal of "understanding how information is stored and processed by neuronal circuits." Nature never told us that brains generate behavior or that brain store learned information in neuronal circuits. 

Janelia's press release announces this: "Janelia is betting on a decade-long scientific effort to understand how the brain generates behavior, pursuing a mechanistic account that links molecules, neurons, circuits, physiology, computation, and action in a living vertebrate." The vertebrate referred to is the transparent fish. They won't be able to understand how behavior arises from studying a fish.  

You might say "Fool's Errand #1 has been replaced with Fool's Errand #2," but it would probably be more polite to say that Quixotic Quest #1 has been replaced by Quixotic Quest #2.

Postscript: A professor of neuroscience recently boasted that experimental science "has a powerful, century-old tool kit for limiting false inferences," one that includes "preregistered analyses." But the professor confesses that "preregistration remains rare in neuroscience." Oops, it looks like our neuroscientists are not doing what they need to do to avoid false inferences.