LTP Research Has Done Nothing to Show Any Neural Basis for Memory Creation

In the English language "lost in the woods" is a phrase meaning "to be confused, bewildered or helpless." Neuroscientists trying to explain how human beings create memories have always been very much lost in the woods. Such scientists have no credible tale to tell on this topic. The problem is that nothing in the brain bears the slightest resemblance to some apparatus for storing learned information. Humans create various types of devices for writing information, things such as pens, pencils, paint brushes, typewriters, laser jet printers, offset printers, and the read/write heads used by a computer hard drive. Nothing in the brain bears any resemblance to such things. 

So what do you if you are a neuroscientist trying to fool people into thinking that neuroscientists like yourself have some kind of understanding of how a human could form a memory? What such people normally merely do is to senselessly repeat the same old clueless charade that neuroscientists have been doing for about fifty years: they zap a tiny bit of brain tissue, creating some tiny change that lasts about as long as a suntan or the morning dew, and they try and pass off that little change as something like information storage, even though no information was stored. This is the witless nonsense of LTP experiments. 

What is misleadingly called “long-term potentiation” or LTP is a not-very-long-lasting effect by which certain types of high-frequency stimulation performed by scientists (such as stimulation by electrodes) produces a fleeting increase in the strength of synapses. The main part of synapses are gaps between nerve cells, gaps which neurotransmitters can jump over. The evidence that LTP even occurs when people remember things is not very strong, and in 1999 a scientist stated (after decades of research on LTP) the following:

"[Scientists] have never been able to see it and actually correlate it with learning and memory. In other words, they've never been able to train an animal, look inside the brain, and see evidence that LTP occurred."

In 2007 a scientist said on page 120 of her PhD thesis, "While LTP is assumed to be the neural correlate of learning and memory, no conclusive evidence has been produced to substantiate that when an organism learns LTP occurs in that organism’s brain or brain correlate."

So-called long-term potentiation is actually a very short-term phenomenon. Speaking of long-term potentiation (LTP), and using the term “decays to baseline levels” (which means “disappears”), a scientific paper says, "potentiation almost always decays to baseline levels within a week," while noting that even after considering LTP "we would be at a loss for a brain mechanism for the storage of a long-term memory."

Another scientific paper says something similar, although it tells us even more strongly that so-called long-term potentiation (LTP) is really a very short-term affair. For it tells us that “in general LTP decays back to baseline within a few hours.” “Decays back to baseline” means the same as “vanishes.” 

Neuroscientists have long been guilty of profoundly misleading behavior in trying to persuade people that so-called so-called long-term potentiation (LTP) is a "mechanism for memory." Inducing LTP requires artificial electrode stimulation which synapses do not naturally receive.  Also, human memories can last for sixty years, but LTP is a very short-lived thing.  So why do neuroscientists keep doing LTP experiments, and why do they keep mentioning LTP as if it had something to do with memory? There are two reasons:

(1) It always sounds better if you have some sound bite or catchphrase you can mutter when someone asks how something occurs, rather than saying, "I haven't the slightest idea how it occurs." When scientists can mutter the phrase "LTP" when asked about how memories are created, it makes them sound more knowledgeable, rather than sounding like people who have no understanding of a topic. 

(2) LTP research is an easy-to-conduct "no way to fail" line of research that provides an easy way for a neuroscientist to add to his total of published papers. Scientists love these kind of "no way to fail" research opportunities. Similarly, theoretical physicists keep grinding out speculative papers about string theory or primordial cosmic inflation.  If you have learned how to write such a papers, doing another such paper is a relatively easy and safe way to get another published paper. 

In a recent article in Knowable Magazine, we have a very bad article repeating "hook, line and sinker" the groundless legend that LTP research did something to show a neural basis for memory storage. The author (Tim Vernimmen)  is a freelance science journalist who as far as I can see has little history of writing on topics of cognitive neuroscience or human memory.  The article has the extremely misleading title "It began with a rabbit: Unraveling the mystery of memory" suggesting the utterly groundless boast that scientists have done something to unravel the mystery of memory -- something that is still a hundred miles over their heads. 

We read about a 1973 paper by Bliss and Lomo in which some rabbits had their brains artificially zapped after "stimulating electrodes were constructed from electrolytically sharpened tungsten wire insulated with several coats of varnish." We have a claim that the paper is "now considered a turning point in the study of learning and memory." No, it was only the opening of a dead end that has led nowhere.  Very many similar papers have been done, but LTP research has done nothing to show any credible neural basis by which memories could be formed. Vernimmen then makes this false claim: " Bliss and Lømo had discovered something momentous: a phenomenon called long-term potentiation, or LTP, which researchers now know is fundamental to the brain’s ability to learn and remember." No, researchers do not know any such thing, and LTP research has done nothing to show any neural basis for learning or memory. 

Vernimmen then makes this untrue claim: "By the early 1970s, neuroscientist Eric Kandel had demonstrated that some simple forms of learning can be explained by chemical changes in synapses — at least in a species of sea slug." No, Kandel did not show any such thing. Vernimmen is repeating one of the many groundless legends of neuroscience. We hear this myth sometimes stated as a claim that Kandel won a Nobel Prize for showing that sea slugs can learn by changes in synapses.  The official page listing the year 2000 Nobel Prize for physiology states only the following: "The Nobel Prize in Physiology or Medicine 2000 was awarded jointly to Arvid Carlsson, Paul Greengard and Eric R. Kandel 'for their discoveries concerning signal transduction in the nervous system.' " The Nobel committee did not make any claim that synapses had been discovered as the basis of memory. 

The paper in question can be read here. The paper fails to mention a testing of more than a single animal, thereby strongly violating rules of robust experimental research on animals (under which an effect should not be claimed unless at least 15 subjects were tested).  We have no reliable evidence about memory storage from this paper. If the paper somehow led to its authors getting a Nobel Prize, that may have been a careless accolade.  The Nobel Prize committee is pretty good about awarding prizes only to the well-deserved, but it may occasionally fall under the gravitational influence of scientists boasting about some "breakthrough" that was not really any such thing.  In some cases the Nobel Prize committee awards science Nobel Prizes it should not have awarded. A notable case (the case of Christian Anfinsen) is discussed in my post here, which notes misstatements in one year's press release for a Nobel Prize. 

Vernimmen then spends several paragraphs discussing techniques of Bliss and Lomo, and then makes the following laughable statement:

"After a few brief periods of high-frequency stimulation, the oscillations would become more pronounced for up to 10 hours, indicating that neurons in the rabbit’s hippocampus responded more strongly — an enduring change that would later become known as long-term potentiation. This looked a lot like the kind of activity many scientists suspected to be at the root of learning and memory."

There are three things very laughable about this statement: 

(1) The attempt to claim that some utterly artificial technique involving zapping a rabbit with electrodes might be "the kind of activity many scientists suspected to be at the root of learning and memory." People are not zapped with electrodes when they learn. 

(2) The misleading use of the word "enduring" to describe a very short-term effect lasting only "up to ten hours."

(3) The attempt to insinuate that this very short-lived effect had some relevance to explaining memories, which in humans can last for 60 years. 

Vernimmen then makes another incorrect statement, saying, "Neuroscientist Richard Morris showed that giving rats a drug that blocks the NMDA receptor impairs their ability to learn how to navigate a maze that untreated rats can easily figure out." No, he did not show that. A 2014 study was entitled "Hippocampal NMDA receptors are important for behavioural inhibition but not for encoding associative spatial memories." And a 2011 study found this:

"We found that inducible knockout mice, lacking NMDA receptor in either forebrain or hippocampus CA1 region at the time of memory retrieval, exhibited normal recall of associative spatial reference memory regardless of whether retrievals took place under full-cue or partial-cue conditions. Moreover, systemic antagonism of NMDA receptor during retention tests also had no effect on full-cue or partial-cue recall of spatial water maze memories. Thus, both genetic and pharmacological experiments collectively demonstrate that pattern completion during spatial associative memory recall does not require the NMDA receptor in the hippocampus or forebrain."

Vernimmen then goes into a discussion of chemical events occurring in synapses. He fails to provide any reason for claiming that any of the chemistry he discusses has anything to do with memory. Vernimmen gives us an extremely misleading visual showing four steps of synaptic transmission, the process by which chemicals pass over a synaptic gap.

His four-part visual is showing the same thing as depicted below:

Synaptic transmission

Misleadingly, Vernimmen's  visual is labeled "How memories form: the steps of LTP." Synaptic transmission is not memory formation. All of the chemicals involved in synaptic transmission are extremely short-lived chemicals that do not even last a day, and have average lifetimes of less than an hour. 

Vernimmen seems to have got very badly confused here. The groundless hand-waving claim made by neuroscientists about memory and synapses is that a memory can form by a strengthening of synapses, something requiring at least hours.  But the strengthening of a synapse is not synaptic transmission, the passing of chemicals over a synaptic gap, which occurs instantly. Also, synaptic transmission is a natural event occurring throughout the brain, while the LTP produced by electrode stimulation (as in the experiment of Bliss and Lomo) is an artificial event produced by inserting manufactured electrodes into a brain.  So for Vernimmen to have a visual describing natural synaptic transmission and to label that as "How memories form: the steps of LTP" is a very bad example of bunk and baloney. Natural synaptic transmission is neither LTP nor memory formation. Neuroscientists do not claim that synaptic transmission (the passing of chemicals across synaptic gaps) explains memory formation.  Vernimmen's diagram has a bungling caption in which a synaptic gap (the gap between two synaptic clefts) is labeled as an example of a "strong connection." When neuroscientists are talking about a strengthening of connections in brains, they mean more synapses between neurons and stronger synapses, not anything in a gap between synapses. 

Vernimmen then makes the claim that LTP causes dendritic spines to grow. The claim is irrelevant to explaining how memories form, both because dendritic spines are too-shorted lived to explain memories lasting for decades, and also because LTP produced by electrode stimulation (as in the experiment of Bliss and Lomo) is an artificial event produced by inserting manufactured electrodes into a brain, not a natural occurrence.  See my post "Imaging of Dendritic Spines Hint That Brains Are Too Unstable to Store Memories for Decades" for the evidence about the short lifetimes of dendritic spines. 

Vernimmen then gives us this passage:

" Bear and his team at MIT, for example, were the first to show that LTP is involved in the formation of fearful memories in mice. In a 2006 experiment, they trained mice to avoid a dark area where they’d previously received an electric shock to the feet. Meanwhile, they used an electrode to record how neurons in the hippocampus responded. 'Sure enough, there was LTP,'  says Bear:"

The reference is to the low-quality paper here, which does not qualify as robust research, because it used a study group size of only seven mice. And you don't show that something explains memory by showing that it exists when a memory is formed. There are endless thousands of things going on in the brain and body while a memory is formed. 

Vernimmen ends with a groundless self-serving quote by Bliss that "The weight of evidence suggests that LTP is central to the physiology of memory storage."  No neuroscientists do not have any understanding of any such thing as a "physiology of memory storage." Nothing in Vernimmen's article has substantiated the claim that LTP has anything to do with human memory.  From the standpoint of actually doing something to credibly explain human memories that can last for 50 years, research on LTP has been the deadest of dead ends. 

It seems that whoever is in charge of quality control at Knowable Magazine isn't doing a good job. Vernimmen's article had lots of false information, and at its bottom we ironically see the sight below. First, there is a link to an article with the ludicrous title "Making the case against memories as evidence." Then there is a plea for donation to the magazine, with the claim that this will "fight misinformation." Oops, it seems that our self-described "misinformation fighters" are guilty of spreading some very bad false information of their own. And clearly these guys are really, really bad at understanding memory, as they have made the utterly goofy claim that memories should not be counted as evidence. If you followed that principle, then half of the murderers in prison would be set free, basically everyone convicted because of the testimony of a witness. 

Below are some of the very many reasons for rejecting claims that human memories are formed by any neural mechanism:

• Although it is claimed that memories are stored in the brain (specifically in synapses), there is no place in the brain that is a plausible storage site for human memories that can last for 50 years or longer. The proteins that make up both synapses and dendritic spines are quite short-lived, being subject to very high molecular turnover which gives them an average lifetime of only a few weeks or less. Both synapses and dendritic spines are a “shifting sands” substrate absolutely unsuitable for storing memories that last reliably for decades.
• It is claimed that memories are stored in brains, but humans are able to instantly recall accurately very obscure items of knowledge and memories learned or experienced decades ago; and the brain seems to have none of the characteristics that would allow such a thing. The recall of an obscure memory from a brain would require some ability to access the exact location in the brain where such a memory was stored (such as the neurons near neuron# 8,124,412,242). But given the lack of any neuron coordinate system or any neuron position notation system or anything like an indexing system or addressing system in the brain, it would seem impossible for a brain to perform anything like such an instantaneous lookup of stored information from some exact spot in the brain.
• If humans were storing their memories in brains, there would have to be a fantastically complex translation system (almost infinitely more complicated than the ASCII code or the genetic code) by which mental concepts, words and images are translated into neural states. But no trace of any such system has ever been found, no one has given a credible detailed theory of how it could work, and if it existed it would be a “miracle of design” that would be naturally inexplicable.
• If human brains actually stored conceptual and experiential memories, the human brain would have to have both a write mechanism by which exact information can be precisely written, and a read mechanism by which exact information can be precisely read. The brain seems to have neither of these things. There is nothing in the brain similar to the “read-write” heads found in computers.
• We know from our experience with computers the type of things that an information storage and retrieval system uses and requires. The human brain seems to have nothing like any of these things. 
• As discussed here, humans can form new memories instantly, at a speed much faster than would be possible if we were using our brains to store such memories. It is typically claimed that memories are stored by “synapse strengthening” and protein synthesis, but such things do not work fast enough to explain the formation of memories that can occur instantly.
• Contrary to the idea that human memories are stored in synapses, the density of synapses sharply decreases between childhood and early adulthood. We see no neural effect matching the growth of learned memories in human.
• There are many humans with either exceptional memory abilities (such as those with hyperthymesia who can recall every day of their adulthood) or exceptional thinking abilities (such as savants with incredible calculation abilities). But such cases do not involve larger brains, very often involve completely ordinary brains, and quite often involve damaged brains, quite to the contrary of what we would expect from the “brains make minds” assumption.

• For decades microscopes have been powerful enough to detect memories in brains, if memories existed in brains. Very much brain tissue has been studied by the most powerful microscopes: both brain tissue extracting from living patients, and brain tissue extracted from someone very soon after he died. Very many thousands of brains have been examined soon after death.  Microscopes now allow us to see very clearly what is in the tiniest brain structures such as dendritic spines and synapse heads. But microscopic examination of brain tissue has failed to reveal any trace whatsoever of learned information in a brain.  No one has found a single letter of the alphabet stored in a brain; no has found a single number stored in a brain; and no one has ever found even a single pixel of something someone saw a day or more before.  If memories were stored in human brains, microscopes would have revealed decisive evidence of such a thing decades ago.  But no such evidence has appeared. 
• There is nothing in the brain that looks like learned information stored according to some systematic format that humans understand or do not understand. Even when scientists cannot figure out a code used to store information, they often can detect hallmarks of encoded information. For example, long before Europeans were able to decipher how hieroglyphics worked, they were able to see a repetition of symbolic tokens that persuaded them that some type of coding system was being used. Nothing like that can be seen in the brain. We see zero signs that synapses or dendritic spines are any such things as encoded information. 
• Many humans can remember with perfect accuracy very long bodies of text, but synapses in the brain do not reliably transmit information. An individual chemical synapse transmits an action potential with a reliability of only 50% or less, as little as 10%. A recall of long bodies of text would require a traversal of very many chemical synapses. A scientific paper says, "In the cortex, individual synapses seem to be extremely unreliable: the probability of transmitter release in response to a single action potential can be as low as 0.1 or lower."

Postscript: The visual below helps clarify the fallacy that occurred when research into LTP began. Scientists were using artificial fiddling to zap the brains of mice with electricity, and then wrongly claiming that this shed light on what naturally occurs in the brain. The claims were fallacious, because when people learn and recall, they do not have electrodes or wires attached to their heads. 

Brain Imaging Shows No Appreciable Neural Correlates of Memory Activity

There have been many brain scanning studies of how a brain looks when particular activities such as thinking or recall occur. Such studies will typically attempt to find some region of the brain that shows greater activity when some mental activity occurs. No matter how slight the evidence is that some particular region is being activated more strongly, that evidence will be reported and reported as a “neural correlate” of some activity.  But a question we should be asking is: do any such studies actually show appreciable evidence of any neural correlate of the activity under examination?

We should not be starting out by asking, "Which region of the brain changes most when a mental activity occurs?" The first and most fundamental thing to consider is: does there exist appreciable evidence of any correlation between brain states and higher mental activity? Similarly, it is a mistake to start asking, "Which person's face appears most commonly in the clouds?" It is much better to start with a simpler question such as "Is there appreciable evidence of any person's face appearing in the clouds?"

There are several types of memory activity that can be identified: 

(1) The acquisition of a new episodic memory through experience.

(2) The learning of a new physical skill by physical practice.

(3) The learning of new conceptual knowledge by school learning.

(4) Rote memorization, such as attempting to learn lists of words or names.

(5) The learning of a narrative by watching a play, TV show, or movie, or listening to a story being told.

(6) The recall of episodic memories a person has experienced.

(7) The recall of conceptual knowledge by someone answering a question or being asked to explain something. 

(8) Visual recognition, in which someone identifies some building, place or person. 

Although psychologists and neuroscientists often talk about "encoding," there is no understanding of any brain process by which knowledge is translated into synapse states or neural states. So when neuroscientists talk about "encoding" they are really just using a jargon word meaning "memory acquisition" or "learning." 

Let us look at whether there is any appreciable evidence of neural correlates for any of the eight activities listed above. 

Conceptual Learning or Memorization

• The study "Sustained Mnemonic Response in the Human Middle Frontal Gyrus during On-Line Storage of Spatial Memoranda" found no difference of more than about 1 part in 200 between different brain areas during a memorization task. 
• The study "Neural correlates of visual short-term memory for objects with material categories" found no difference of more than about 1 part in 200 between different brain areas during a memorization task. 
• The study "Neural correlates of encoding emotional memories: a review of functional neuroimaging evidence"  found no difference of more than about 1 part in 200 between different brain areas during a memorization task. 
• The study "Whole-brain functional correlates of memory formation in mesial temporal lobe epilepsy" found no difference of more than about 1 part in 200 between different brain areas during memory formation.
• The study "State-related and item-related neural correlates of successful memory encoding" found no difference of more than about 1 part in 200 between different brain areas during memory formation.
• The study "The neural correlates of recognition memory for complex visual stimuli in the Medial Temporal Lobe" found no difference of more than about 1 part in 250 between different brain areas during "memory encoding activity for faces and scenes," and about 1 part in 1000 for "memory retrieval activity for faces and scenes." 
• The paper "Neural correlates of multisensory perceptual learning" found no difference of more than about 1 part in 1000  between different brain areas

Memory Retrieval (Also Called Recollection)

• This brain scan study was entitled “Working Memory Retrieval: Contributions of the Left Prefrontal Cortex, the Left Posterior Parietal Cortex, and the Hippocampus.” Figure 4 and Figure 5 of the study shows that none of the memory retrievals produced more than a .3 percent signal change, so they all involved signal changes of merely about 1 part in 333 or smaller .
• In this study, brain scans were done during recognition activities, looking for signs of increased brain activity in the hippocampus, a region of the brain often described as some center of brain memory involvement. But the percent signal change is never more than .2 percent, that is, never more than 1 part in 500.
• The paper here is entitled, “Functional-anatomic correlates of remembering and knowing.” It shows a graph showing a percent signal change in the brain during memory retrieval that is no greater than .3 percent, less than 1 part in 300.
• The paper here is entitled “The neural correlates of specific versus general autobiographical memory construction and elaboration.” It shows various graphs showing a percent signal change in the brain during memory retrieval that is no greater than .07 percent, less than 1 part in 1000.
• The paper here is entitled “Neural correlates of true memory, false memory, and deception." It shows various graphs showing a percent signal change during memory retrieval that is no greater than .4 percent, 1 part in 250.
• This paper did a review of 12 other brain scanning studies pertaining to the neural correlates of recollection. Figure 3 of the paper shows an average signal change for different parts of the brain of only about .4 percent, 1 part in 250.
• This paper was entitled “Neural correlates of emotional memories: a review of evidence from brain imaging studies.” We learn from Figure 2 that none of the percent signal changes were greater than .4 percent,  1 part in 250.
• This study was entitled “Sex Differences in the Neural Correlates of Specific and General Autobiographical Memory.” Figure 2 shows that none of the differences in brain activity (for men or women) involved a percent signal change of more than .3 percent or 1 part in 333.
• A 2012 review study on "neural correlates of emotional memories" is one that we might expect to have a higher chance of showing a notable correlation, given the possibility of the emotions showing up as signal changes in the brain images. But the story reports no signal changes of greater than about 1 part in 1000 anywhere in the brain. 
• A brain scan study looked for neural correlates of "episodic retrieval success" during memory recall. The paper reports percent signal changes no greater than about 1 part in 500. 
• The study "Encoding Processes During Retrieval Tasks" found no difference of more than about 1 part in 300 between different brain states during episodic memory retrieval.
• The study "Neural activity associated with episodic memory for emotional context" found no difference of more than about 1 part in 200 between different brain states  during episodic memory retrieval.
• The paper "Parietal lobe contributions to episodic memory retrieval" found found no difference of more than about 1 part in 200 between different brain states during memory retrieval.
• The paper "Common and Unique Neural Activations in Autobiographical, Episodic, and Semantic Retrieval" found no difference of more than about 1 part in 200 between different brain states during memory retrieval.
• The paper "Functional-anatomic correlates of remembering and knowing" found no difference of more than about 1 part in 300 between different brain areas during memory retrieval.
• The paper "The role of the right prefrontal cortex in the retrieval of weak representations" found no difference of more than about 1 part in 500 between different brain areas during memory retrieval.

  Recognition Memory

• The year 2000 study "Dissociating State and Item Components
  of Recognition Memory Using fMRI" found no difference in brain signals of more than 1 part in 100, with almost all of the charted differences being only about 1 part in 500. 
• The study "Remembrance of Odors Past: Human Olfactory Cortex in Cross-Modal Recognition Memory" found no difference in brain signals of more than 1 part in 200.
• The study "Neural correlates of auditory recognition under full and divided attention in younger and older adults" found no difference in brain signals of more than 1 part in 500.
• The study "Neural Correlates of True Memory, False Memory, and Deception" asked people to make a judgment of whether they recognized words, some of which they had been asked to study. The study found no difference in brain signals of more than about 1 part in 300.
• The study "The Neural Correlates of Recollection: Hippocampal Activation Declines as Episodic Memory Fades" was one in which "participants performed a recognition task at both a short (10-min) and long (1-week) study-test delay." The study found no difference in brain signals of more than about 1 part in 300.
• The study "The neural correlates of everyday recognition memory" found no difference in brain signals of more than about 1 part in 500.
• The study "Neural correlates of audio‐visual object recognition: Effects of implicit spatial congruency" was one in which participants attempted a recognition task. The study found no difference in brain signals of more than about 1 part in 200.

We can summarize such results as follows: brains do not look any different and do not seem to act any different when a person is forming a new memory or recalling something previously learned or recognizing something previously encountered. Differences of  merely 1 part in 200 can be best explained as random fluctuations, the type of tiny blips that occur all the time in bodily things such as heart rate and breathing rate.  Such data is consistent with the idea that your brain is not the storage place of your memories, and that the formation and retrieval of memories is not a brain process. Also consistent with such an idea is the fact that no one has ever discovered a memory by examining brain tissue. No one has ever learned anything about a person's knowledge by examining the brain of a dead person. There is also no robust evidence for the storage of memories in animal brains. Claims to have detected memory storage spots in animal brains are junk science claims that do not hold up to critical scrutiny.  Typically an examination of the study group sizes used in any such study will show a failure to use study group sizes adequate to produce robust evidence. Neuroscientists lack any credible theory of how human episodic and conceptual knowledge could be translated into brain states or synapse states. What we know about synapses and the dendritic spines they are attached to (such as the less-than-monthly lifetimes of the proteins in such things, and their constant random remodeling) conflicts dramatically with claims that synapses could be a storage place of memories that can last for decades. 

Within the neuroscientist belief community that resembles a tribe or church, there is a pathological tradition under which signal variations of merely about 1 part in 200 are regarded as evidence for the brain being more actively engaged in some area. In no other field of biological study are variations so small regarded as good evidence. Let us imagine some scientist testing whether there is any truth to the common belief that your heart beats a little faster when you meet someone you are in love with. We can imagine a scientist hooking up heart rate monitors to young men, and analyzing the moments when young men met for a dinner date the female friends they were in love with. Now suppose the scientist found that the heart rate of such men only increased by 1 part in 200 at such meeting times (by an average of only about one third of a beat per minute).  How would this result be reported? It would be reported as a null result. The paper would claim that it had debunked the common idea that your heart beats faster when you meet your true love, and would say that the 1 part in 200 discovered was no significant evidence for such an effect. Only in the community of neuroscientists are 1 part in 200 signal change effects claimed as substantial evidence. In all other fields of biology, such a difference would be dismissed as negligible.

Let's imagine you are a neuroscientist who does some experimental brain scanning study looking for a neural correlate of some memory activity. You fail to find any appreciable evidence for such a thing, finding no difference of more than 1 part in 200 in brain activity. Now, you have a choice. You can either honestly write up your paper as a null result, using a title such as "Failure to find a neural correlate of recollection." But you know that in your neuroscientist community the habit of researchers is to report 1 part in 200 variations as positive results. And you know that science journals have a very big  publication bias, which is a strong tendency to prefer publishing papers reporting a positive result.  So do you do the honest thing decreasing your chance of paper publication (one that will irritate your colleagues by defying their customary behavior), or do you "go with the herd" and report your result as a "neural correlate"? Given the "publish or perish" culture in academia (in which the number of papers you publish and the number of citations they get is regarded as all-important), you may feel irrestible pressure to just follow the dysfunctional convention, and report your negligible correlation finding as a "neural correlate."  

You can get an idea of general conventions about correlation interpretation by doing a Google search for "guidlines for correlation interpretation." This will produce various papers like the one here, which give us interpretation guidelines such as this:

Size of correlation	Interpretation of correlation
.90 to 1.00	Very high correlation
.70 to .90	High correlation
.50 to .70	Moderate correlation
.30 to .50	Low correlation
.00 to .30	Negligible correlation

Clearly, following guidelines such as these, a percent signal change of only 1 part in 200 should be interpreted as a negligible correlation. Neuroscientists speak dishonestly when they try to pass off negligible results as being neural correlates of some kind of mind activity. 

The ability of neuroscientists to find correlation false alarms is illustrated in a 2021 paper entitled "Neurons in the mouse brain

correlate with cryptocurrency price: a cautionary tale."  The paper tells us this, referring to financial instruments mice cannot possibly know anything about:

"Out of ~40.000 recorded single neurons, ~70% showed a significant correlation with Bitcoin or Ethereum prices. Even when using the conservative Bonferroni correction for multiple comparisons, ~35% of neurons showed a significant correlation, which is well above the expected false positive rate of 5%."

After reading such a paper, you may realize how the "1 part in 200" signal changes typically reported in neural correlate studies are no robust evidence that brains are worker harder when someone learns or remembers anything. 

Postscript: A year 2026 paper by 9 scientists says this: "Despite many years of research, the quest to identify neural correlates of perceptual consciousness (NCC) remains unresolved."

EEG Studies Fail to Provide Robust Evidence That Brains Think or Retrieve Memories

To try to provide evidence for their claims that memories are stored in the brain and that brains produce mental phenomena such as thinking and imagination, neuroscientists look for what they call neural correlates of mental activity. A neural correlate of a mental activity would be some sign that a brain acts differently or looks differently when someone does a particular type of mental activity such as thinking or recalling. 

The most common way that a neuroscientist will look for a neural correlate of a mental activity is to image someone's brain while he is doing some mental activity, typically using an fMRI scanner.  In my post "The Brain Shows No Sign of Working Harder During Thinking or Recall," I discussed the failure of such studies to provide robust evidence that brains produce thinking or recall.  The following are tips for analyzing such studies:

(1) Search for the phrase "percent signal change" to quickly find out how much of a difference was found during some mental activity. A large fraction of all fMRI-based neural correlate studies will use such a phrase. 

(2) Find out the sample size used, and whether a sample size calculation was used to determine whether the sample size was adequate. The vast majority of fMRI-based neural correlate studies fail to provide a sample size calculation, and the vast majority of such studies use way-too-small study group sizes, so small that they are not reliable evidence for anything. 

What you will typically find is that such studies will show only extremely small changes in brain activity, involving changes of smaller than one half of one percent.  Such variations of only about  one part in 200 or smaller are no robust evidence that brains produce thinking or produce recall. We would expect to get variations of such a size given random moment-to-moment fluctuations in brains, variations that would occur even if a person was not thinking and not recalling anything. And the fact that the vast majority of fMRI-based neural correlate studies use way-too-small study group sizes means that such studies are not robust evidence of anything.  As discussed here, a recent large study was announced with a headline of "Brain studies show thousands of participants are needed for accurate results," but a typical fMRI-based neural correlate study will not even use dozens of participants. 

But there is an entirely different way in which neuroscientists can look for neural correlates of memory recall and thinking. Rather than using big fMRI machines to scan the brain, a neuroscientist can hook up brains to electroencephalography machines (EEG machines) that read electrical activity of the brain.  To produce such readings, many different electrodes will be attached to the heads of subjects who are being tested. The output is not an image of the brain, but a reading showing lines that go up and down.  A neuroscientist can study such lines, looking for some neural correlate of thinking or recall that shows up as a difference in a wiggly line. 

Scientists studying such EEG outputs are looking for what they call an event-related potential or ERP.  In theory an ERP is some EEG pattern that might be repeated whenever some mental event occurs such as recognition or recall or concentration. In the literature an ERP is typically described as some blip occurring over less than a second. Figure 5 of the paper here gives us a "heat map" of various claimed ERP effects relating to cognition. The claimed effects have various names listed on the right side of the heat-map, names such as N400 and CDA (standing for contralateral delay activity). 

What typically goes on is a cherry-picking affair.  A neuroscientist will typically use a type of EEG device with 128 electrodes, each of which is attached to a different part of the head.  After the device records neural activity,  there will be 128 different readings, each from a different part of the head.  Each reading will be some long wavy line.  Imagine a paper scroll about three inches high and 100 meters long, with a wavy line stretching from beginning to end, and you'll have a rough idea of the output from any electrode.  Neuroscientists will not typically show us some graph showing the statistical average of all of these lines. Instead, they will be free to choose any group of electrodes, to try to show some correlation effect.  

Imagine you are a neuroscientist. Did you fail to get any correlation effect from averaging the outputs from electrodes 98, 99, 100 and 101? Then you can just keep playing around with electrode combinations until you get something that looks like an effect. For example, maybe you'll get something that looks like an effect if you average the results of electrodes 34, 35, 37 and 38.  If the studies were properly designed, using a pre-registration in which an exact methods description was published before data gathering, such dubious "slice and dice until you get a desired result" techniques would not be possible. But we almost never see any such pre-registration in these EEG neural correlate studies. Also, there's no rule that you cannot cherry-pick two or three electrodes that were not adjacent. 

So, for example, in the study here in Figure 3 we have a diagram showing two graphs of nice-looking ERP effects. The caption tells us the first graph is from electrode 65, and that the second graph is from electrode 91. But Figure 2 shows that 128 electrodes were used, and that electrode 65 is on the other side of the head, nowhere close to electrode 91.  Our authors have apparently cherry-picked the results from 128 electrodes, looking for the results that would best show the desired effect.  

A scientific paper about the shortfalls of studies looking for these ERP effects tells us the following:

"An example of this issue is described in a recent paper by Luck and Gaspelin (2017), who demonstrated how 'researcher degrees of freedom' could influence statistical analysis of ERP data. ERP recordings typically employ dozens of electrodes and result in hundreds of time points, which results in an almost unlimited variety of possible data analysis approaches, and, consequently, in the probability of a false significant finding approaching certainty."

Many such studies have been done, but they have failed to produce any robust evidence that human brains produce memory recall or thinking. Let us look at some of these studies, and the results that have been claimed. I will use the "heat map" in Figure 5 of the paper here to select the best-reported claimed ERP effects for cognitive activity. According to that figure, the best-reported ERP effects relating to cognition are:

(1) A CDA or contralateral delay effect having something to do with memory;

(2) an FN400/N400 effect (also called an "ERP old/new effect) having something to do with recognition;

(3) an N170 effect having something to do with categorization;

(4) a P100 effect  (also called a P1 effect) having something to do with attention.

It is claimed that an "ERP old/new effect" (apparently the same or similar to an FN400/N400 effect) is some EEG sign of recognition.  Looking at the  papers attempting to show this effect, we see nothing that looks very impressive. The claim is that when you have people look at some list of words that includes words they were asked to memorize and words they were not asked to memorize,  that for only about a fifth of a second some type of brain wave looks slightly different when that wave is read from the parietal region of the brain. 

No robust evidence has been provided for such an effect, because the study group sizes used in the studies claiming such an effect are too small. Even if such a fraction of a second effect was observed, it can be explained without assuming that a memory has been retrieved from the brain.  When somebody recognizes something, there can be a kind of "aha" effect in which muscular responses differ very slightly.  For example, after recognizing a face in the crowd, a person's facial expressions can be different than when encountering a stranger, with the difference lasting only an instant. Such a difference could easily be the explanation for some marginal fraction-of-a-second difference showing up in a reading of brain waves. 

In one paper I read claiming to get this fraction of a second "ERP old/new effect," the instructions were for subjects to click an "Old" button if they recognized a word, and a "New" button if they did not. The instructions stated that the "Old" button should only be clicked if the subject was sure he had seen the word before. With such instructions, there easily could be a kind of momentary pausing effect when people thought they recognized a word, during which they were wondering whether they were sure about seeing the word before.  Such a muscular pausing could be the cause of this fleeting "ERP old/new effect," with the effect having nothing to do with a difference in brain activity during recognition. 

This "ERP old/new effect is apparently the same (or involves or is related to) something called the N400 response. A paper described it like this:

"The N400 is a negative-going wave peaking at about 400 ms, whose amplitude is larger after presentation of a stimulus whose probability of occurrence is low within its semantic context (Kutas & Federmeier, 2011). For example 'He spread the warm bread with socks' would elicit a larger N400 than 'He spread the warm bread with butter” (Kutas & Hillyard, 1980).' "

This is another alleged neural correlate of cognitive activity that can easily be explained purely by muscle activity having nothing to do with the mind. The person presented with some crazy sentence may have a different muscle response, perhaps a look of bemusement on his face, or a kind of "huh?" look on his face.  Since the reported N400 response only involves a fraction of a second difference, we can't tell whether evidence is being picked up of brains thinking, or merely evidence of a tiny-bit different muscle response. 

A meta-analysis of studies about this claimed N400 response tells us that the average number of subjects used is only about 15.  Is such a sample size large enough? It is not, judging from the paper here. That paper is devoted to estimating how large a study group size would be needed to detect a particular ERP effect, one similar to the claimed N400 response and the claimed "ERP old/new effect." The paper tells us that to get a fairly good 80% statistical power would require at least "30– 50 clean trials with a sample of 25 subjects." 

There's another claimed ERP effect called the contralateral delay effect or CDA. The effect is claimed to occur as a fraction-of-a-second blip when people are shown screens having colored circles  or colored squared, and asked to identify whether a later screen matches the previous screen. Figure 1 of the paper here shows the type of screens shown.  The visual below shows the kind of screens shown, and how long the inputs were shown.

After taking EEG recording of brain waves of people during such an activity, scientists have claimed that there is some distinctive blip that shows up (lasting only a fraction of a second), something they call a contralateral delay effect or CDA. It has been claimed that such an effect is a correlate of working memory.  But since the alleged effect is extremely short-lived, it provides no evidence that brains store memories. What is showing up could simply be related to vision or to some color persistence effect by which a perceived color will hang around in the mind or brain for a second or two. 

It is well-known that there is something called an "afterimage," in which you can see something after you stopped looking at it.  For example, the web page here has a photo of Amy Whitehouse that is strangely colored. Look at the dot at the center of the photo for 30 seconds, and then look to the blank white area to the right of the photo. You will then see a ghostly afterimage of Amy Whitehouse. Whatever that type of effect is, it isn't memory.  It's just a "lingering of perception" thing.  The claimed CDA effect may merely be picking up that type of short-term thing, not something related to a brain storage or retrieval of memories. 

The N170 effect is some ERP effect supposedly produced when someone is shown a picture of a face. Referring to a mere fraction of a second, the wikipedia.org article on the effect claims that this alleged effects only lasts "130-200 msec after stimulus presentation." Figure 1 of the paper here has a diagram similar to the schematic diagram below, with the black line representing the response from seeing faces, and the gray line representing the response from seeing objects that are not faces.

This meta-analysis tells us that most of the faces used in studies of the N170 effect have involved emotional faces. The faces shown usually had expressions such as fear, disgust or joy. You can easily explain the fraction-of-a-second blip shown without imagining that viewing faces involves some recognition activity by the brain, and that all that is being picked up is a slight physiological response in regard to emotional stimulus. Studies of the N170 effect do not rule out some scenario like this:

(1) You see a face with an emotional expression, and your mind or soul (not your brain) recognizes the emotion. 

(2) Seeing emotion on someone's face produces a slight physiological response, which shows up as a fleeting blip in brain waves. 

The P100 effect (also called a P1 effect) is also some claimed small-fraction-of-a-second effect supposedly occurring for about 50 milliseconds when a person engages in visual selective attention, such as looking at only the left part of a screen. Eye muscles behave differently when you focus on only one side of a screen. Since such an instantaneous effect can easily be explained in terms of muscle activity involving the eyes, it provides no good evidence that brains are producing mental attention.  

Nothing we have discussed provides any good evidence that brains produce thinking, that brains store memories, or that brains retrieve memories. What kind of test can we imagine that would be a good test of such claims? The test might go something like this:

(1) Subjects wearing EEG electrodes on their head would be asked to look at photos displayed on a computer screen, with each photo shown for five seconds.  Most of the photos would be photos of people who were not famous and could not be recognized. One third of the photos would be photos of famous people with neutral expressions, none of whom were scary or threatening.  A computer program would assure a random shuffling of the photos. 

(2) Subjects would be asked to remain motionless and expressionless. Subjects would be told to simply say in their mind (without speech)  "Go" if they recognized the face, and "No" if they did not. 

(3) Attempts would be made from reading brain waves to determine whether there was any correlation between the perception of recognized faces and the perception of faces that were not recognized. 

Such a test would fail. No robust evidence would be found for a neural correlate of recognition. 

I used the "heat map" in Figure 5 of the paper here to select the best-reported claimed ERP effects for cognitive activity. It is interesting what is not reported in that heat map. According to the map it seems:

(1) There are no strong ERP/EEG effects for learning. 

(2) There are no strong ERP/EEG effects for decision making. 

(3) There are no strong ERP/EEG effects for prediction. 

(4) There are no strong ERP/EEG effects for executive function. 

(5) There are no strong ERP/EEG effects for perception.

(5) There are no strong ERP/EEG effects for speech.

Overall, EEG studies fail to provide robust evidence that thinking or decisions or memory retrieval or memory storage occurs because of the brain. The shape-seeking scientists eagerly looking for these slight, fleeting blip effects in EEG lines can be compared to people eagerly scanning the clouds looking for shapes that resemble animals, to back up some belief that the ghosts of dead animals live in the sky. 

The sample sizes used in these EEG/ERP studies are generally way too small to provide a robust evidence for a real effect. The headline of a news release of an important recent study is "Brain studies show thousands of participants are needed for accurate results." But these EEG/ERP studies typically involve only about 15 subjects per experiment.  A huge defect calling into question the reliability of all such studies is that the researcher is free to scan the results from 120 electrodes, and cherry-pick the output from whatever few electrodes he finds most shows some sub-second effect that is being eagerly sought, doing additional cherry picking that involves looking for some one-second slice of time in which the effect will show the most. This is a recipe for "conjuring phantoms." Given such complete freedom to scan data looking for some fleeting blip in wavy lines, it is easy to find almost any imaginary effect you might be hoping to find. In general, the fleeting ERP blips that are found can be explained as brain involvement in muscle activity and physiological activity, without postulating that brains are the source of thinking and memory.