2 Out of 3 Methods Find No Correlation Between Alzheimer's and Hippocampus Volume

 Scientists have no coherent story to tell of how a brain could store a memory or instantly retrieve a memory or maintain a memory in a brain that replaces its proteins at a rate of about 3% per day (an effect that should prevent you from remembering anything for more than two months, if your brain stored your memories).  The phrases they mutter about such things make no sense. Asked to explain a mechanism of neural memory storage,  a neuroscientist may mutter some phrase such as "synapse strengthening," which makes no sense as an explanation of memory formation.  Strengthening is not information storage.  And the idea that you stored memories in synapses because they were strengthened makes no more sense than the idea that you store memories in your arm biceps when they strengthen.  There is no robust evidence that synapses strengthen more when you learn something. 

Having no real evidence on a cellular level to support their claims of neural memory storage, neuroscientists sometimes resort to claims about parts of the brain, claiming that some-such part of the brain is needed for memory.  Such claims usually involve claims that the hippocampus is crucial for memory. The experimental evidence has never supported such claims.  People with no hippocampus or a damaged hippocampus usually perform fairly well on tests of memory. 

In my widely-read long post here (entitled "Studies Debunk Hippocampus Memory Myths")  I discuss very many scientific papers that discredit the claim that the hippocampus has some big relation to memory. That post is very thorough in reviewing the relevant literature, but I recently noticed that is has one omission: it fails to discuss what relation (if any) there is between the volume of the hippocampus and a person's tendency to have the severe cognitive disorder known as Alzheimer's disease.  Let us look at that very issue, using a 2023 paper entitled "MRI measurements of brain hippocampus volume in relation to mild cognitive impairment and Alzheimer disease A systematic review and meta-analysis" which you can read here. 

The paper does a meta-analysis of different studies comparing hippocampus volume, Alzheimer's disease and mild cognitive impairment or MCI. The paper comes to different conclusions, based on the different methods used. 

I can explain the different methods:

(1) One method involves a simple method that is only checking the "raw volume" of the hippocampus. This is the easiest and simplest method. 

(2) Another more sophisticated method factors in the "total intercranial volume" of subjects in addition to the hippocampus volume. This is called the "hippocampus volume measured by MRI TIV Correction" method. An AI Overview states, "Total Intracranial Volume (TIV) correction in MRI is a critical preprocessing step in neuroimaging that normalizes brain structural volumes (such as gray matter, white matter, or hippocampus) to account for variations in individual head size."

(3) Another method is called the "hippocampus measured by MRI ICA Correction" method. An AI Overview states, "Independent Component Analysis (ICA) in MRI is a data-driven, blind source separation technique used to isolate and remove noise sources (artifacts) from imaging data to enhance signal quality. It is highly effective at separating artifacts like motion, respiration, and large vessel signals from functional (fMRI) or dynamic susceptibility contrast (DSC-MRI) data, improving diagnostic accuracy." People are supposed to remain totally motionless when they undergoing an MRI scan, but they often fail to be totally motionless; and this can affect the quality of the MRI. This "MRI ICA Correction" helps fix that data quality problem. 

Here are the results for the left hippocampus when these three methods were used. 

Method 1: "The left hippocampus volume measured by MRI Raw volume was negatively correlated with MCI and AD (OR = 0.58, 95%CI: 0.42, 0.75)." So when the simplest and least sophisticated method was used, a correlation was reported between hippocampus volume and mild cognitive impairment (MCI) and Alzheimer's Disease (AD). 

Method 2: "Results of meta-analysis showed no correlation between left hippocampus volume measured by MRI TIV Correction and MCI and AD (OR = 0.90, 95%CI: 0.62, 1.19), as shown in Figure 4." So when the first of the two more sophisticated methods was used, there was  no correlation found between left hippocampus volume and mild cognitive impairment (MCI);  and there was no correlation found between left hippocampus volume and Alzheimer's Disease (AD). 

Method 3:  "Results of meta-analysis showed that the volume of the left hippocampus measured by MRI ICA Correction was not correlated with MCI and AD (OR = 0.92, 95th CI: 0.75, 1.09), as shown in Figure 5." So when the second of the two more sophisticated methods was used, there was  no correlation found between left hippocampus volume and mild cognitive impairment (MCI); and there was no correlation found between left hippocampus volume and Alzheimer's Disease (AD). 

The bottom line here is that two out of the three methods did not find any correlation between left hippocampus volume and mild cognitive impairment (MCI), and did not find any correlation between left hippocampus volume and Alzheimer's Disease.

Here are the results for the right hippocampus when these three methods were used. 

Method 1: "Results of meta-analysis showed that the right hippocampus volume measured by MRI Raw volume method was not correlated with MCI and AD (OR = 0.87, 95%CI: 0.56, 1.18), as shown in Figure 7." So when the simplest and least sophisticated method was used, no correlation was reported between right hippocampus volume and mild cognitive impairment (MCI); and there was no correlation found between right hippocampus volume and Alzheimer's Disease (AD). 

Method 2: "Results of meta-analysis showed no correlation between the right  hippocampus volume measured by MRI TIV Correction and  MCI and AD (OR = 0.81, 95%CI: 0.49, 1.12), as shown in Figure 8." So when the first of the two more sophisticated methods was used, there was  no correlation found between right  hippocampus volume and mild cognitive impairment (MCI);  and there was no correlation found between right hippocampus volume and Alzheimer's Disease (AD). 

Method 3:  "Results of meta-analysis showed that the volume of the right hippocampus measured by MRI ICA Correction was negatively correlated with MCI and AD (OR = 0.49, 95%CI: 0.35, 0.62), as shown in Figure 9." So when the second of the two more sophisticated methods was used, there was  a correlation found between right hippocampus volume and mild cognitive impairment (MCI) and Alzheimer's Disease (AD). 

The bottom line here is that two out of the three methods did not find any correlation between right hippocampus volume and mild cognitive impairment (MCI), and did not find any correlation between right hippocampus volume and Alzheimer's Disease.

Overall, the results here are quite consistent with my claims that memory is not a brain function, and that memories are not stored in brains. 

Men Have Faster-Shrinking Brains, But Women Get an Alzheimer's Diagnosis About Twice as Often as Men

 In the October 13, 2025 online edition of the journal Nature, we have an article with a headline of "Men's brains shrink faster than women's; what that means for Alzheimer's."  Alzheimer's is a disease involving a decline in mental function, and for older people the term is basically equivalent to dementia. 

Now, under the hypothesis that the brain makes the mind and that brains store memories, if men's brains shrink faster than women's as people age, there should be a higher rate of Alzheimer's disease in men. But the article tells us that the opposite is true. The article says, "Nearly twice as many women are diagnosed with Alzheimer’s disease as men." 

The article tells us that the conclusion that men's brains shrink faster than women's is based on a large study involving 12,500 MRI scans from 4,726 people who had at least two scans per person, taken an average of three years apart. We are given an example of the shrinkage rate: the claim that the postcentral cortex in men shrinks by 2% per year for men, versus 1.2% per year for women. 

The article's findings are contrary to claims that dementia or Alzheimer's disease is proportional to brain tissue loss. It is therefore very misleading for the article to include a visual like the visual it has. The visual shows a normal brain and a shrunken brain, with a caption of "A healthy brain and a brain affected by Alzheimer's disease." This is an old propaganda technique long used by those trying to suggest that brains are the source of minds and that brains are the storage place of memories. The technique involves showing photos of a normal brain and a shrunken brain, with a caption saying that the shrunken brain is the brain of the person with Alzheimer's. 

Contrary to the impression created by such a photo pair, a book on dementia says on page 35 that "there are many reports of people carefully diagnosed...as clearly having the clinical symptoms of dementia and yet showing no evidence of brain pathology."  On the same page the book gives this quote from a neuroscientist named Robert Terry:

"Over the years, investigators have sought assiduously for lesions or tissue alterations in the Alzheimer's brain which...might at least correlate with clinical determinants of the disease severity....Despite 30 years of such efforts, clinico-pathologic correlations have been so weak or entirely lacking that determination of the proximate, let alone the ultimate, cause of Alzheimer's disease (AD) has not been possible."

I may note that studies on the relation between dementia and brain volume are often guilty of various flaws. One flaw sometimes occurring is when the brains of people diagnosed with dementia or Alzheimer's are compared to the brains of healthy controls. If such a diagnosis was made after brains scans of subjects were done, the state of the brain may have influenced what type of diagnosis a person got, making the diagnosis a poor way of independently comparing brain states and mental states. A better technique is to judge dementia or Alzheimer's purely on the basis of performance on mental tests such as the MMSE, and to compare performance on such tests with brain states. The MMSE is the Mini-Mental State Examination, and is the most common test for cognitive impairment. 

The paper here shows graphs comparing MMSE scores and gray matter volumes, and shows no strong correlation between the two. We have in Figure 2 a scatter plot showing dots, each of which represents a correlation between gray matter in some region of the brain, and the corresponding MMSE scores. None of the correlations are strong, with none being higher than .5. Almost all of the correlations are weak, being well under .5; and the average correlation is only about .25.  A strong correlation is one such as .8 or .9. 

We do not have in the paper a graph showing negative correlations between regions of the brain and the corresponding MMSE scores. If such a graph had been given, we would probably have seen just as many or almost as many negative correlations (between brain volumes in different regions and MMSE scores) as positive correlations. Using the phrase "gray matter atrophy" to refer to brain shrinkage, the paper states, "The associations between gray matter atrophy, hypoperfusion, and cognitive impairment in AD [Alzheimer's disease] are still unknown, especially the causal pathways between them." The Nature article discussed in this post makes it all the more clear that there is no clear causal relation between brain shrinkage and dementia or Alzheimer's disease.

Below is interesting data from Table 1 of the paper here. We have data on six elderly female subjects called "super-agers." The MMSE number is the score on the Mini-Mental State Examination, a test of cognitive ability including short-term recall and also long-term semantic memory.  The maximum score on the test is 30. Notice the lack of correlation between brain weight and IQ, and the lack of correlation between brain weight and the MMSE score. The  MMSE scores for the 1st and 2nd subjects are identical, with the 2nd subject being very slightly smarter, even though the second subject has a brain weight 25% smaller. That same 2nd subject has an IQ of 135 -- in the 99th percentile for humans -- despite her  brain being very far below the average female brain size of about 1200 grams. The 4th subject has a brain much smaller than the fifth subject, but has the same perfect MMSE score, and an IQ score 10% higher. These results are consistent with the idea that your brain is not the source of your mind, and not the explanation of your memory powers. 

NAME	AGE	MMSE (MAX=30)	IQ	BRAIN WEIGHT (GRAMS)
SA1	87	29	133	1240
SA2	90	29	135	990
SA3	99	25	112	1020
SA4	87	30	119	1090
SA5	81	30	107	1269
SA6	90	29	111	1100

A similar table with data for 50 subjects can be found in the year 2021 paper "Is there a correlation between the number of brain cells and IQ?" We read this summary of the results:

"In our sample of 50 male brains, IQ scores did not correlate significantly with the total number of neurons (Fig. 1A), oligodendrocytes (Fig. 1B), astrocytes (Fig. 1C) or microglia (Fig. 1D) in the neocortex, nor with the cortical volume (Fig. 2A), surface area (Fig. 2B) and thickness (Fig. 2C). This also applied to estimates of the four separate lobes (frontal-, temporal-, parietal-, and occipital cortices; see Supplementary Material). Neither did IQ score correlate significantly with the volumes of white matter (Fig. 2D), central gray matter (Fig. 2E) or lateral ventricles (Fig. 2F), nor with the brain weight (Fig. 3A), or body height (Fig. 3B). All of these correlation coefficients were less than 0.2." 

Can we imagine a more complete research failure of the "brains make minds" hypothesis?

Appendix: In the scientific paper entitled, “A guide to appropriate use of Correlation coefficient in medical research,” we read the following: “A correlation coefficient of 0.2 is considered to be negligible correlation while a correlation coefficient of 0.3 is considered as low positive correlation.” Below is Table 1 from that paper, which has the heading of "Rule of Thumb for Interpreting the Size of a Correlation Coefficient."

Size of Correlation	Interpretation
.90 to 1.00 (−.90 to −1.00)	Very high positive (negative) correlation
.70 to .90 (−.70 to −.90)	High positive (negative) correlation
.50 to .70 (−.50 to −.70)	Moderate positive (negative) correlation
.30 to .50 (−.30 to −.50)	Low positive (negative) correlation
.00 to .30 (.00 to −.30)	negligible correlation

If you do a Google image search for "correlation coefficient interpretation," you will find several tables or guidelines that list all correlation coefficients of 0.2 or less as either "negligible," "very poor," or "very weak," and some of them (like the table above) actually list all correlation coefficients of .3 or less as "negligible.

The Dubious Dogma That Brains Make Decisions

Neuroscientists like to claim that thoughts and ideas come from your brain, that your memories are stored in your brain, and that when you remember you are retrieving information from your brain. I have discussed in other posts why such claims are not well founded in observations, and why there are strong reasons for rejecting or doubting all such claims. In this post I will discuss another dogmatic claim made about the brain: the claim that the brain is the source of human decisions. I will discuss eight reasons for thinking that this claim is no better founded than dogmatic claims about the brain being the storage place of memories or the source of human abstract thoughts.

Reason #1: Scientists have no understanding of how neurons could make a decision.

When they try to present low-level explanations for a how a brain could do some of the things that they attribute to brains, our neuroscientists falter and fail. An example is their complete failure to credibly explain either how memories could be encoded in neural states, how memories could be permanently stored in brains, or how memories could be instantly recalled by brains. Neuroscientists also cannot credibly explain how a person could make a decision when faced with multiple choices. 

When I did a Google search for "what happens in the brain when a decision is made," I got a bunch of articles with confident sounding titles. But reading the stories I read mainly what sounded like  bluffing, hype, promissory sounds,  and the kind of talk someone uses to persuade you he understands something he doesn't actually understand (along with some references to brain scanning studies that aren't robust for reasons discussed later in this post).  At no one point in these articles do we ever reach someone who makes us think, "This guy really understands how a brain could reach a decision." 

Let us consider a simple example. Joe says to himself, “Today I can either go to the library or go to see a movie.” He then decides to go to the library, and then starts walking towards the library.

To explain this neurally, we would have to explain several different things:

Item 1: How Joe's brain could hold two different ideas, the idea about the possibility of going to the movie, and the idea of going to the library.

Item 2: The appearance in Joe's brain of a third idea, an idea that he will go today to the library.

Item 3: Some neural act that causes his muscles to move in a way corresponding to his idea about going to a library.

The first two of these things cannot be credibly explained through any low-level explanation involving neurons or synapses. See my post “No One Understands How a Brain Could Generate Ideas” for a discussion of the failure of neuroscientists to present any credible explanations of how brains could generate ideas. In that post, I cite some “expert answers” pages on which the experts address exactly the question of how a brain could generate ideas, and sound exactly as if they have no understanding of such a thing.

On one of the “expert answers” pages that I cite, we have this revealing answer:

“ 'How does the 'brain' forms new ideas?' is the wrong question. We don't actually know how the brain codes old ideas.”

That is correct, which means that neither Item 1 in my list above can be explained neurally, nor Item 2. Since we do not understand how a brain could either hold ideas or form new ideas, we do not have any understanding of how a brain could make a decision.

Reason #2: Hemispherectomy patients can still make decisions just fine.

Hemispherectomy is an operation done on patients with severe epileptic seizures. In an hemispherectomy operation, half of the brain is removed. I can find no studies that have specifically studied decision-making ability in hemispherectomy patients. However, I have cited here and here and here and here scientific papers that show results for intelligence tests taken “before” and “after” a hemispherectomy operation. Such papers show, surprisingly, that removing half of a brain has little effect on intelligence as measured in IQ tests.

Written IQ tests are typically tests of not just intelligence but also decision making ability. For example, the Wechsler IQ test is by far the most common one used by scientists, and it is a multiple-choice test. Every single time a person has to pencil in one of the little ovals in a multiple-choice test, he has to make a decision. So standard IQ tests are very much tests of not just intelligence but also decision-making ability (which may be considered an aspect of intelligence).

Since IQ tests done on hemispherectomy patients show little damage to IQ scores after removing half of a brain, we can only conclude that removing half of a brain has little or no effect on decision making ability. We would not expect such a thing to be true if your brain is what makes your decisions.

Reason #3: Some people who lost most of their brains could still make decisions normally.

Cases of removal of half of the brain by surgical hemispherectomy are not at all the most dramatic cases of brain damage known to us. There are cases of patients who lost almost all of their brains due to diseases such as hydrocephalus, a disease that converts brain tissue to a watery fluid. Many such cases were studied by the physician John Lorber. He found that most of his patients were actually of above-average intelligence. Similarly, a French person working as a civil servant was found in recent years to have almost no functional brain.

Such cases seem to show that you can lose more than 75% of your brain and still have a normal decision making ability. This argues against claims that your brain is what is making your decisions.

Reason #4: Split brain patients don't have their decision making harmed.

The two hemispheres of the brain are connected by a set of thick fibers called the corpus callosum. In rare operations this set of fibers is surgically severed. The result is what called a split-brain patient. Despite the erroneous claims that are sometimes made about this topic, the fact is that such an operation absolutely does not result in anything like a split personality or a split consciousness or a split mind. Such an operation does not result in two minds causing conflicting decisions.

The scientific paper here (entitled "The Myth of Dual Consciousness in the Brain") sets the record straight, as did a scientific study published in 2017. The research was done at the University of Amsterdam by Yair Pinto. A press release entitled “Split Brain Does Not Lead to Split Consciousness” stated, “The researchers behind the study, led by UvA psychologist Yair Pinto, have found strong evidence showing that despite being characterised by little to no communication between the right and left brain hemispheres, split brain does not cause two independent conscious perceivers in one brain.”  Their study (entitled "Split brain: divided perception but undivided consciousness") can be read here. “We have shown that severing the cortical connections between the two brain hemispheres does not seem to lead to two independent conscious agents within one brain,” the researchers said.

In 2014 the wikipedia.org article on split-brain patients stated the following:

“In general, split-brained patients behave in a coordinated, purposeful and consistent manner, despite the independent, parallel, usually different and occasionally conflicting processing of the same information from the environment by the two disconnected hemispheres...Often, split-brained patients are indistinguishable from normal adults.”

In the video here we see a split-brain patient who seems like a pretty normal person, not at all someone with “two minds." And at the beginning of the video here the same patient says that after such a split-brain operation “you don't notice it” and that you don't feel any different than you did before – hardly what someone would say if the operation had produced “two minds” in someone. And the video here about a person with a split brain from birth shows us what is clearly someone with one mind, not two. In these interviews, every single time the split-brain patients answer questions normally, they are showing their ability to make decisions normally. The mere act of answering questions always involves decisions about what to say and how to say it.

But this is not at all what we should expect from the assumption that the brain is the source of our decisions. If that assumption were true, a split-brain operation should cause two independent sources of decision-making that would have a tendency to conflict with each other.

Reason #5: “Decision zig-zag" is almost never observed in pressure situations, but we would expect it to be very common if different parts of the brain (or halves of the brain) were causing decisions. 

Here's a quick mental test I'd like you to try. If you can answer all the questions real quickly, in a small number of seconds, it will tend to show you're a smart person who can think fast.  Try it. 

1. Pick a color.

2. Pick a number between 1 and 10. 

3. Pick a planet.  

4. Pick a continent.

5. Pick a city.

Did you skip the test? No fair. It's easy -- go back and try it. 

Now, if you are like 90% of my readers, you were able to do this exercise real quickly, in less than 10 or 15 seconds. But we would not expect such a thing to be possible if your brain was making your decisions. For in that case, we would expect that different parts of the brain would be coughing up different decisions, leading to a result rather like this:

Pick a color? Uh, red -- no green - no blue - okay, red! 

Pick a number? Uh, 8! No, 6 ! No -- uh, 4!  No, 2!

Pick a planet? Merc -- no Jupiter -- no, Earth, no wait...

Pick a continent?  North -- no South -- no Eur -- no Afri -- no Asia!

Pick a city? New ... uh, no Shang... no Paris -- oops, no Moscow! 

As mentioned above, people who have half of their brains removed in hemispherectomy operations can make decisions normally. It therefore cannot be maintained that a decision requires a full brain. If you think that brains make decisions, you are forced to the idea that part of a brain (half a brain or less) can make a decision. But such an idea makes us ask: should not then people be overwhelmed by conflicting decision signals, sent by different parts of a brain? 

Consider the organization of the brain. There are two identical halves. Under the hypothesis that a half of a brain or less can make a decision, we would therefore expect to see very often something that we can call "decision zig-zag."  This would involve behavior in which an organism was flipping back and forth between two possible decisions, as if two physical areas of the brain were conflicting with each other, coming to separate decisions. We would expect to see this particularly often in "coin flip" kind of decisions in which one choice is not obviously better than another. 

But we rarely see such behavior in humans, whenever there is time pressure. It is true that given some important choice, and given the luxury of time to deliberate, a person may kind of go back-and-forth in his mind about what to do. For example, if you are accepted by two different colleges, you may kind of go back-and-forth in your mind, first favoring one choice, then another.  But whenever there is a tight time pressure, and people know there is only a very short time for a decision, humans typically behave with very little indecision. 

Scores on standardized tests such as SAT tests are an excellent gauge of how very infrequently high-performing humans engage in "decision zig-zag" under pressure situations.  In the reading and writing part of an SAT test, a student has to answer more than 100 questions in less than two hours. The questions are multiple choice questions, so doing the test requires making 100 decisions, each a decision about which of the choices to select. Each question typically requires 30 seconds or more of reading.  There is very little time for indecision. Every one who performs very well on the test (in the 90th percentile or higher) is making 100 or more decisions (about which answer to choose) with very little indecision.  Under such pressure situations, humans do not at all perform like they would perform if different halves or different parts of your brain were sending you different signals about what to do.  Humans instead act like beings with a single unified mind.  It would seem that if different parts or halves of a brain were determining what decision to make, there would be so much indecision and "decision zig-zag" that the average SAT score in the US would be at least 200 points lower than it is. 

Reason #6: There is no particular region of the brain that seems to be crucial to non-muscular decision making.

Some particular regions of the brain have been strongly associated with particular functions. For example, we know that the brain stem is strongly associated with autonomic activity that keeps the heart and lungs working. Any major damage to the brain stem usually causes death. We also know that the visual cortex is strongly associated with vision. But no strong associations have been established between any part of the brain and calm non-muscular decision making.  By "non-muscular decision making" I mean the type of thing that goes on when you silently pick a number between 1 and 10 or silently choose in the morning what you will eat for dinner.  

To get an idea of how weak is the neuroscience case that your brain makes decisions, we can look at an article in Psychology Today entitled “The Neuroscience of Making a Decision.” After referring to some brain region that might be involved in addiction, which has no general relevance to the issue of whether brains make decisions, we are referred to a study claiming that the striatum is involved in decision-making. It's a study used that only 7 rats, Since this is less half of the minimum number of animals per study group recommended for a modestly convincing result, the study provides no good evidence for a neural involvement in decision making.

Then the Psychology Today article refers to a brain-scanning study attempting to show that regions called the dorsolateral prefrontal cortex and the ventromedial prefrontal cortex have something to do with decision making. These are the two regions that are most commonly cited as being involved in decision making. A brain scanning study could only give robust evidence for some region being heavily involved in some activity if it were to show a strong percent signal change, rather than the weak signal change of only 1% or less that brain scanning studies typically show. In this case, the study does not even give a figure for the percent signal change. So it does not provide any robust evidence that the the dorsolateral prefrontal cortex or the ventromedial prefrontal cortex have something to do with decision making

Our Psychology Today article then concludes, having provided no real evidence that there is any such thing as a “neuroscience of decision making.”

This study examined six patients with damage to the dorsolateral prefrontal cortex, and found that they had an average IQ of 104, above the average of 100. Since filling out a written IQ test requires many cases of decision making (in regard to the answer given), such a result is incompatible with claims that the dorsolateral prefrontal cortex is some part of the brain particularly involved in decision making. This study says, “We have studied numerous patients with bilateral lesions of the ventromedial prefrontal (VM) cortex” and that “most of these patients retain normal intellect, memory and problem-solving ability in laboratory settings.” The meta-analysis here says that the ventromedial prefrontal cortex is the region of the brain "most commonly implicated in moral decision making," but says that there is a "lack of a significant cluster of activation" in this area, meaning that it doesn't actually light up more during brain scans. 

Failing to report any actual figures for percent signal changes (the number we need to know to judge whether some area of the brain is more involved in an activity), the same meta-analysis notes differences between its findings and the findings of other studies, highlighting how much these brain scan studies tend to conflict with each other. We read the following:

"As previously stated, Bzdok et al. (2012) found a cluster of activation in the rTPJ (BA 39), which we did not find. Another discrepancy between our ME activation clusters and Bzdok et al.’s (2012) for moral cognition are that they found a cluster of activation in the left amygdala, which we did not find. Also, Bzdok et al. (2012) reported activation in the precuneus, which was not found to be a cluster of significant activation for the ME experiments in our analysis."

Another example of a report of a supposed “neuroscience of decision making” is a Neuroscience News article here entitled, “Researchers Discover Decision Making Center of Brain.” We again have a reference to a mere brain scanning study. But this time the study has a graph that gives us the percent signal change that we need to judge whether robust evidence has been found. The graph shows that the percent signal change picked up by the brain scanning is only about a fraction of one percent, about 1 part in 300. That's no good evidence for anything, and could easily be the result of pure chance fluctuations.

Similarly weak results are found in this study, trying to use brain scanning to find some region of the brain more involved in decision making. The graph shows that the percent signal change picked up the brain scanning is only about a fraction of one percent, about 1 part in 300. That's no good evidence for anything, and could easily be the result of pure chance fluctuations. 

In Figure 3 of the study here, we get a brain scanning result for the percent signal change in activity for the dorsolateral prefrontal cortex. The graph shows a signal change of only about 1 part in 300 (about .3 percent). That's no good evidence for anything, and could easily be the result of pure chance fluctuations. 

Most of the studies that claim to show neural correlates of decision making are mainly finding either neural correlates of emotion (which can often be entangled with decision making) or neural correlates of muscle activation (often paired with decision making).  When I do a Google search for "neural correlates of motionless decision making," I am unable to find a single study testing such a thing. 

Reason #7: There is no convincing evidence of some type of change of brain state when a calm non-muscular decision is made.

By looking at brain scans, it is impossible to reliably predict when anyone made a non-muscular decision.  We should not be fooled by a certain type of brain scanning experiment with the following characteristics:

(1) The study will not be pre-registered, and will not publish in advance a specification of some particular type of brain activation signal that it is looking for (in some very specific little part of the brain) as a sign of when someone made a decision.

(2) The study will scan the brains of people as they made some decision in their minds. 

(3) Scientists will then examine the brain scans, looking for some particular tiny area of the brain that was more a tiny bit more active when the decisions were made. 

(4) The study will involve only a small number of subjects, maybe 10, 15, 20 or 25. 

Let me explain why this type of study is not at all good evidence for anything.  In any random brain there will be random fluctuations in activity from moment to moment.  Let us suppose a researcher has the freedom to compare any of 200 different little areas of the brain, looking for some area that has an increase in activity during some particular moment (such as when a decision is made). We would expect that purely by chance there would be some area that would show a tiny bit more activity during the particular moment being studied, even if it is not your brain that is making a decision. Similarly, if I use a machine that can detect minute fluctuations in temperature in the livers of 20 people while they are making a decision, and I have the freedom to check 200 different little regions of the liver, I will probably be able to find some tiny liver region which (purely by chance) had a minutely higher temperature when some decision was made. But this would do nothing to show that livers make decisions. 

A discussion of this issue can be found around page 23 of the technical paper here, where we read the following:

"With a plausible population correlation of 0.5, a 1000-voxel whole-brain analysis would require 83 subjects to achieve 80% power. A sample size of 83 is five times greater than the average used in the studies we surveyed: collecting this much data in an fMRI experiment is an enormous expense that is not attempted by any except a few major collaborative networks."

In other words, brain imaging studies tend to use only a fraction of the sample size they need, given the techniques they typically use.  It is possible to do a reliable study with a small sample size, if you limit the analysis to only one small tiny area of the brain. But that is almost never done.  

On page 33 the paper above states the following, giving us a strong reason for skepticism about brain scanning studies:

"In short, our exploration of power suggests that across-subject whole-brain correlation experiments are generally impractical: without adequate multiple comparisons correction they will have false positive rates approaching 100%, with adequate multiple comparisons correction they require 5 times as many subjects than what the typical lab currently utilizes."

The study here is an example of the type of unconvincing study I have just discussed. The authors scanned brains, looking for change in signal strength corresponding to whether some type of decision was made.  Having the freedom to check any of 200 or more brain regions (since their study was not a pre-registered study announcing its intention to look in only one little place in the brain), the authors found one or two tiny regions where there is an extremely small greater activation when a decision was made. The difference in signal strength (as reported in Figure 1 and figure 2) was only about .1 of 1 percent, which is about 1 part in 1000.  But we would expect a result as good as that by chance, because of random variations in little parts of the brain, even if brains do not actually make decisions. So the study does nothing at all to provide evidence that brains are making decisions.  The study say it did "whole brain analyses", but it used only 32 subjects, only a small fraction of the 83 subjects recommended above for a mere 1000-voxel "whole brain analysis" study.  

On page 68 of the book "Casting Light on the Dark Side of Brain Imaging," we read about another problem in brain scanning studies:

"Take a guess at how many ways we can analyze data from a single brain scan. Theoretically countless, practically at least 69,000 ways....Brain imaging data usually requires between 6 and 10 steps of general data preparation and analysis. Researchers can perform any of these steps in a variety of ways....Different choices in data processing and analysis can lead to widely divergent results: small variations can quickly sum to form large discrepancies. In some cases, researchers may run many variations of an analysis, but only report results that support their hypothesis. This practice can lead to biased publications that overestimate true effects." 

Here is the kind of thing we would like to have in order to have convincing evidence of greater brain activity when a non-muscular decision is made:

(1) There would have to be many replicated pre-registered studies that all showed that some particular region of the brain activated at a substantially higher level when a decision was made (more than just a fraction of 1 percent). 

(2) In the pre-registration declarations, published prior to the collection of any data, the study authors would have to announce that they were studying only one small region of the brain to see whether it activates more during decision making, rather than giving themselves the freedom to check any brain region they wanted in a "fishing expedition" kind of approach to produce signal variations we would expect by chance.  

(3) In the same  pre-registration declarations, published prior to the collection of any data, the study authors would have to commit to one exact method of data analysis, precisely spelled out, thereby depriving themselves of the freedom to keep "slicing and dicing" the brain scan data until they got a result supporting their hypothesis. 

 Nothing like this has occurred.  Instead we have a succession of little brain scan studies (usually with low statistical power) showing minute less-than-one-percent activation increases in some region that differs from study to study, studies in which researchers are free to look for some minute signal deviation in any brain region, and free to try dozens of data analysis methods until something that can be called a neural correlation coughs up.  The results of such studies are what what we would expect to get by chance even if brains are not actually making decisions. 

In short, we have no robust evidence that brains make decisions. Nature never told us that decisions are made by brains. It is merely neuroscientists who told us such a thing, without ever having adequate evidence for such a claim. 

Reason #8: Humans can make decisions many times more quickly than they would make if decisions were being made by brains subject to several severe signal slowing factors and severe signal noise. 

Humans can make decisions very, very fast. Every time some one drives in the city, he is making important decisions very quickly, such as whether to brake at a particular moment. Every time some one speaks very quickly in conversation, he is making many instantaneous decisions about what words to use. People such as  quarterbacks and soccer players, standardized test takers,  chess players in special "speed" matches, and players of the Jeopardy TV show are making decisions at a very fast speed, often instantaneously. 

If you tried my previous selection game, you probably made decisions at a rate of about one decision per one or two seconds (each time you picked one of the possibilities, you were making a decision on what to pick).  If it took you 15 seconds to do that test, about two-thirds of that was reading and memory recall; and you were making a decision at a rate of about one decision per second.  A baseball hitter typically makes a decision (on whether to swing) in only a small fraction of a second. According to this scientific paper, "The average speech rate of adults in English is between 150 and 190 words per minute (Tauroza and Allison 1990), although in conversation this figure may rise considerably, reaching 200 wpm (Walker 2010; Laver 1994)."  Someone speaking in conversation at 200 words per minute is making decisions at a rate of three per second, each a decision on which word to use.  

But we have strong reasons for believing that brains should not be fast enough for instantaneous decisions. The "100 meters per second" claim often made about brain signal speed is not at all accurate, as it completely ignores very serious slowing factors such as the 200-times-slower speed of transmission through dendrites, the very serious slowing factor caused by cumulative synaptic delays, and the additional very serious slowing factor caused by what is called synaptic fatigue. A realistic calculation of brain signal speed (such as I have made here) leads to the conclusion that brains should be far too slow to allow extremely rapid or instantaneous decisions, and that if a brain were making a non-muscular decision (not involving a reflex), it should take at least five or ten seconds for any such decision.  

We also know that the brain has multiple sources of very severe signal noise, as discussed here. It would seem that all this noise would be a huge factor preventing different parts of a brain from reaching a single decision quickly, just as it would greatly decrease the chance of a classroom of 30 people reaching the same decision very quickly if all of the people were blaring different podcasts, videos and rock songs from their smartphones. 

An intelligent hypothesis about human decision making is that it comes from an immaterial aspect of human beings, what is commonly called a soul or spirit.  A neuroscientist will protest that it is forbidden to postulate some important reality that we cannot directly see. Such a rule is not at all followed in general by scientists. Astrophysicists and cosmologists nowadays are constantly claiming that most of the universe consists of important realities we cannot see, what they call dark matter and dark energy -- both things that have never been directly observed by any method. 

Postscript: A 2021 paper is entitled "Reduced decision bias and more rational decision making following ventromedial prefrontal cortex damage."  So you make more rational decisions if your front brain is damaged? That's a result incompatible with claims that your brain makes decisions.  In a 2021 article a neuroscientist is quoted as saying, "You realize that neither the term ‘decision-making’ nor the term ‘attention’ actually corresponds to a thing in the brain."

Why Strokes, Alzheimer's Disease and Drunkenness Don't Prove the “Brains Make Minds” Dogma

A person believing that brains generate minds may refer us to cases of Alzheimer's disease, and say this proves this brains make minds and store memories. Or the person may make a similar argument when referring to strokes. Or the person may claim that drunkenness shows your brain makes your mind, because in that we see a physical liquid causing a judgment deterioration. In this post I will address these objections.

Alzheimer's disease could never prove that brains make minds, because we do not see in Alzheimer's disease an actual loss of the self or consciousness.  A mind with very poor memory is still a mind.

In regard to Alzheimer's disease or strokes, we cannot actually tell whether a person has suffered a loss of memories. For it might be that such patients merely experience a difficulty in retrieving memories.

Imagine you are used to visiting cnn.com to get the news each morning. But one day you turn on your computer and find you can no longer access any information at cnn.com. Does this prove that the information stored at cnn.com has been lost? It certainly does not. The problem could merely be an inability for you to retrieve information at cnn.com, perhaps because of a bad internet connection. Similarly, if I write the story of my life, and place it on my bookshelf, I may one day go blind and be unable to access that information. But the information is still there on my bookshelf.

In the same vein, the memories of people with Alzheimer's may be perfectly intact, but such persons may be merely experiencing some difficulty in retrieving their memories. There are, in fact, reports of incidents called terminal lucidity, in which people suffering from memory loss or dementia suddenly regained their memories shortly before dying. Such reports tend to support the idea that memory problems such as Alzheimer's involve difficulties in retrieving memories rather than the actual destruction of memories stored in the brain.

There is actually a way in Alzheimer's may argue against the idea that your memories are all stored in your brain. A doctor reports the following:

One of the big challenges we face with Alzheimer's is that brain cell destruction begins years or even decades before symptoms emerge. A person whose disease process starts at age 50 might have memory loss at 75, but by the time we see the signs, the patient has lost 40 to 50 percent of their brain cells.

If your brain cells were the place your memories were stored, why would you not notice memory loss until 40% or 50% of your brain cells were gone?

The evidence in regard to the cause of Alzheimer's diseases is actually pretty baffling. The most common explanation is that the disease is caused by something called amyloid plaques. But the Chicago Tribune tells us, “Scientists have learned that about a third of people who appear to have Alzheimer's disease do not have high levels of amyloid in their brains.”

A brain study was made of nine very old people who scored particularly high on a memory test. After these people died, their brains were examined. Three of the nine very old “super memory” people were found to have brains filled with the plaques often seen in Alzheimer's patients. These “super memory” people had brains in much worse shape than a large fraction of Alzheimer's patients with very poor memories.

In 2017 there was a news story entitled, "New Discovery Suggests Neuron Death Does Not Kickstart Dementia." The story reported this:

The leading theory in Alzheimer’s disease is that memory loss is the result of neuron death and nerve ending damage, which lead to memory loss, are caused by the formation of toxic protein clumps in the brain, called tau tangles and beta-amyloid plaques. But a new, small study challenges this theory, showing that the loss of neurons in brains of people with dementia is actually very small. What’s more, levels of neuron loss in patients did not indicate how far along the were in the disease, suggesting neuron death has little to do with the symptoms of dementia. 

The news story quotes a scientist saying the following:

Much to our surprise, in studying the fate of eight neuronal and synaptic markers in our subjects’ prefrontal cortices, we only observed very minor neuronal and synaptic losses. Our study therefore suggests that, contrary to what was believed, neuronal and synaptic loss is relatively limited in Alzheimer’s disease. 

A book on dementia says on page 34 that in the pioneering Blessed, Tomlinson and Roth study (1968) "there is only a rather low correlation between the brain plaque count and the test scores among the senile" -- not what we would expect if brain plaques were causing memory loss.  There were four cases with a high plaque count and low dementia. The book tells us that in a well-known study involving nuns and Alzheimer's disease, one of the nuns had high cognitive scores despite having "abundant neurofibrillary tangles and senile plaques." The book tells us that "predicting backwards from autopsy to clinical diagnosis appears unreliable and poorly predictive," which is not what we would expect if dementia was really caused by brain states. 

After telling us on page 35 that "there are many reports of people carefully diagnosed...as clearly having the clinical symptoms of dementia and yet showing no evidence of brain pathology,"  the book gives this quote from a neuroscientist named Robert Terry:

Over the years, investigators have sought assiduously for lesions or tissue alterations in the Alzheimer's brain which...might at least correlate with clinical determinants of the disease severity....Despite 30 years of such efforts, clinico-pathologic correlations have been so weak or entirely lacking that determination of the proximate, let alone the ultimate, cause of Alzheimer's disease (AD) has not been possible. 

The scientific paper here made an examination of 14 brains of recently deceased people who had donated their brains to medical science. Four were controls, five were people with Alzheimer's disease but no dementia, and five were people with Alzheimer's and dementia. The paper made detailed comparisons of the number of neurons in the brains and the total number of cells in the brains as a whole. The "bottom line" of the study is in Figure 6, which is below. The white bars are the controls; the gray bars are those with asymptomatic Alzheimer's; the black bars are those with Alzheimer's and dementia. 

We see here nothing to back up common claims that Alzheimer's is some disease that robs people of large number of neurons. The number of neurons is about the same for all three groups, and the total number of cells is greater for those with Alzheimer's.  Such a study shows that a common visual (showing a normal brain side- by- side with a shrunken Alzheimer's brain) is misleading, and that the idea of very large neuron loss as a hallmark of Alzheimer's is incorrect. 

The 2009 study "Comparison of Different MRI Brain Atrophy Rate Measures with Clinical Disease Progression in AD" compared brain shrinkage in 55 normal people and 64 people with Alzheimer's disease.  In Table 2 we see that 40 of the normal people had whole brain shrinkage of 0.4 % per year, and 15 of the normal people had whole brain shrinkage of 0.8 % per year.  For those with Alzheimer's disease, 32 had whole brain shrinkage of 0.6 % per year (less than 1% per year), and that 33 had whole brain shrinkage of 1.4% per year.  In short, there was hardly any difference between the brain shrinkage rates for those with Alzheimer's and the normal people.  The 2019 paper "Lifespan Changes of the Human Brain In Alzheimer’s Disease" presents a model based on brain scans of hundreds of healthy controls and hundreds of people with Alzheimer's disease. Figure 1 of the paper depicts the lifespan changes of white matter and gray matter of those with Alzheimer's disease and normal healthy people. The lines look almost identical. 

Given these conflicting findings, it seems that the evidence is not telling us any clear tale in regard to what causes Alzheimer's. Very many of the people with Alzheimer's have amyloid plaques in the brains, but one third do not. And apparently lots of people with very good memories have amyloid plaques, and many do not. There is also no strong correlation between neuron loss and dementia. Such evidence gives us no clear signal as to whether our memories are stored in our brains.

As for strokes, they can damage an ability to move, speak or understand language. Understanding language is partially based on auditory processing, and speaking language is based on muscular finesse in the vicinity of the tongue and vocal chords. We know that the brain helps the senses do their work, and is involved in muscular control. But an article in US News and World Report says, "It’s important to recognize that strokes do not cause a drop in overall intelligence.” On quora.com, someone states, "My speech therapist was pretty adamant that having a stroke does NOT, in any way, affect your intelligence." That's something we would not expect under the theory that the brain generates the mind. Under that theory, we might expect that people would lose half or more of their intelligence after a stroke.

If our memories were stored in our brains, what we would expect is that people would often get amnesia after a stroke. But such a thing seems to happen only very rarely.  A scientific paper says, "Reports of amnesic syndrome due to unilateral stroke have appeared infrequently." The paper lists some new cases which it claims are new examples, but when we read the examples we find typically only mild things like an inability to recall a daughter's phone number. Speaking of strokes, the paper says, "There have been two reported cases of persistent amnesia following unlitateral infarctions in which there were no other neurological deficits," indicating the rarity of such a thing. The paper also says that of a group of 68 patients who had brain infarctions, there were no cases of amnesia.  Talking about strokes, this paper says, "Amnesia as the main symptom of acute ischemic cerebral events is rare, mostly transient, and easily mistaken for TGA [ transient global amnesia]." 

What about drunkenness? Does drinking alcohol really cause you to “lose your mind”? Not really.

Consider the case of the drunk asked to walk a straight or to touch his finger to his nose. If such a person really had his mind dulled by the alcohol, he would be unable to interpret the police officer's language. But instead such a drunk will normally understand the command just fine, and attempt to follow it.

What we mainly see in drunkenness is a kind of overconfidence and loss of inhibition, along with mood changes and a deterioration of muscle skills. You don't really see people losing their minds or memories while they are drunk. If they did, they would probably forget how to start up their cars (or do something like putting their combs or their fingers in the ignition slot rather than their keys).

A CBS New story says that people who consumed alcohol were actually better at certain creative problems.

In fact, there is no such thing as a “temporary stupid potion” that will cause an intelligent person to regress to the intelligence level of a small child, nor is there any such thing as a “temporary amnesia potion” that will cause you to forget where you grew up or where you live or what your mother's name is. Wikipedia.org has an article on “drug induced amnesia,” but gives us no examples of any such drug other than benzodiazepines (which do not produce retrograde amnesia, the inability to recall old memories) but only help produce antograde amnesia (the inability to make new memories).

But if your memories do actually come from your brain, and your intelligence comes from your brain, we would think that such potions should have been invented already. If your memories do actually come from your brain, and your intelligence comes from your brain, it should have been easy for scientists to create some potion that would temporarily disrupt the chemistry supposedly needed for memory recall and thinking. The nonexistence of any such potion is actually further evidence against the claim that your brain is the source of your thoughts and the storage place of your memories.

Postscript: A recent study (which found no correlation between the number of neurons in the brains of 50 subjects and their IQs) refers to the fact "that highly demented female Alzheimer’s disease patients have normal neocortical neuron numbers (Regeur et al. 1994, Pelvig et al. 2003)`"

Against the objections of its advisory Peripheral and Central Nervous System Drugs Advisory Committee, the FDA approved not long ago a drug for Alzheimer's, the first such drug to be approved since 2003. The drug is fantastically expensive, costing more than $50,000 per year, and there is no compelling evidence that it works. People are arguing that it "provides hope for families," but so would a placebo pill, which would be very inexpensive.  In early 2024 we heard that Biogen is abandoning the drug, apparently because of its low effectiveness. 

Some studies (mostly with small study group sizes such as about 25) have claimed to find smaller volumes in the hippocampus of those with Alzheimer's, with such people having perhaps 15% smaller hippocampus volume. Such studies are problematic partially because of the small number of subjects and also because of the small volume of the hippocampus, which is only about 1/400 (one four-hundredth) the size of the brain. A 2016 study has the title "

No Association of Lower Hippocampal Volume With Alzheimer’s Disease Pathology in Late-Life Depression." It involved more than 50 patients and 50 controls. In a section entitled "Associations between clinical factors, hippocampal volume, and amyloid binding in patients," we read that "No main effects were detected for measures of episodic memory, including total learning, delayed recall, and delayed recognition." The largest study of hippocampal volume is the study here, involving 19,000 people, and showing a decline from about 8000 cubic millimeters at age 50 to about 7200 cubic millimeters at age 75. 

A 2023 press release on a study  tells us that "a University of California, Irvine-led team of researchers have discovered that the oldest-old, those who live to be 90+ and have superior cognitive skills, have similar levels of brain pathology as Alzheimer’s patients." The study is  the paper here entitled "A Population-Based Clinicopathological Study in the Oldest-Old: The 90+ Study." We read this:

"Half of all non-demented participants (49%) and just over half of demented participants (57%) met pathological criteria for AD [Alzheimer's Disease], ... The pathologies examined to date failed to explain all dementia in this cohort, as almost one quarter (22%) of all demented participants did not have significant AD or any other pathology to explain their cognitive loss."

The visual below has a graph from the paper:

Another recent study tells us the number of people with Alzheimer's Disease and the typical brain pathology claimed to cause that disease is even less than the 57% depicted in the graph above, and also tells us that some things described as causes of dementia are found in almost all who died without ever having dementia.. In the study  we read this:

"Pure AD [Alzheimer's Disease] neuropathology is observed in less than half of patients diagnosed with probable AD dementia in life... Some level of AD pathology has also been observed in nearly 40% of dementia patients, who were considered to have non-AD diagnoses during life. Moreover, many elderly individuals considered cognitively normal proximate to the time of death have been demonstrated to have AD pathology at autopsy.....Boyle et al. [90] reported that among 467 individuals who had been studied longitudinally and remained non-demented till autopsy, the vast majority had beta-amyloid, all had tangles, about a quarter had macroscopic infarcts, another quarter had microinfarcts, and between 5 and 10% had neocortical Lewy bodies."

The paper also tells us the following, which doesn't sound like what we would find if the cause of dementia was mainly physical: "Among a cohort of over 1000 elderly individuals without dementia at baseline, followed for an average of 12 years, the rate of global cognitive decline in five domains of cognitive function was reduced by an average of 70% in persons who were at the 90th percentile of social activity, compared to persons who were at the 10th percentile." 

An excellent paper on this topic is the paper "Exploring why 'memory loss' is a misleading descriptor of people living with dementia and can lead to dysfunctional care" by Steven R. Sabat and Alison Warren. The paper points out that there are many types of memory and aspects of memory, and that it is misleading to be using the term "memory loss" for someone who has difficulty with one aspect of memory but who may still have other aspects of memory. We read this:

"Explicit episodic memory is the type of memory most affected by the disease process of AD [Alzheimer's disease], but implicit memory types are relatively spared and can contribute to familiarity that informs recognition (Deason et al., 2019). Explicit and implicit memory are only two of many types of memory. Not only are there several types of memory systems (i.e., short-term; working; long-term; declarative/explicit; nondeclarative/implicit; autobiographical; episodic; emotional, etc.), but also different ways in which they interact in the daily milieu of human existence (Poldrack et al., 2001). ... Remarkably, there have been observations of significant lucidity despite an advanced stage of disease (Griffin et al., 2022; Mashour et al., 2019; Ramirez et al., 2023). The salient concept is that the severity of memory problems, or likewise, the ability to retrieve information from memory, fluctuates greatly. Indeed, persons with dementia have memory difficulties, but to say they have memory loss is clinically inaccurate. Furthermore, the memory difficulties that manifest can vary by dementia type. For example, a person with AD may have difficulty with episodic memory of events and personal experiences, but maintain procedural memory (learned skills, habits) (Kudlicka et al., 2019), while other forms of dementia,...affect memory quite sparingly and instead result in visual deficits (Crutch et al., 2012; DeTure & Dickson, 2019). Regardless of the type of dementia, it has long been known, but rarely discussed, that persons with dementia retain considerable cognitive capacities and are capable of new learning (Kudlicka et al., 2019). For example, studies examining cognitive plasticity and learning potential in persons with MCI and AD have demonstrated improved performance in visual memory, verbal learning, and executive function in all participants (Backman, 1992; Fernandez-Ballesteros et al., 2006), challenging the enduring notion that persons with dementia lose their memory but are also incapable of creating new memories. In addition to the preservation of implicit memory in general, persons with dementia maintain other components under this classification, including emotional memory, emotional communications, a variety of skills, and ability to learn....Furthermore, research supports that even during cognitive decline, persons with cognitive impairments can continue to learn new skills and thus create new memories (Sabat, 2018). Considering the evidence, dementia is a syndrome of memory retrieval difficulties rather than loss and characterizing it as such can have far reaching consequences for persons with dementia, especially how they are treated and the fate of their quality of life."

A paper states this:

"Patients with the same neurological disease and comparable brain damage often display different functional outcomes. For example, more than 25% of elderly individuals with no sign of cognitive impairment met post-mortem pathological criteria of Alzheimer’s disease (AD).1 By the same token, 10–40% of individuals with mild to moderate brain pathology showed no clinical symptoms of dementia."

The 2024 paper "More Similar than Different: Memory, Executive Functions, Cortical Thickness,and Glucose Metabolism in Biomarker-Positive Alzheimer’s Disease and Behavioral Variant Frontotemporal Dementia"  has a Table 5 that lists cortical thickness numbers for 11 regions of the brain. We have these numbers for both 79 people with Alzheimer's disease, and 39 healthy controls. The differences are very small. The 79 subjects with Alzheimer's disease had an average cortical thickness  2.47 millimeters, and the 39 healthy controls had an average cortical thickness of 2.6 millimeters. We have no mention of a blinding protocol in the analysis, and the slight difference could easily be due purely to a tendency to measure the healthy controls as having a greater cortical thickness. The 2008 paper "Frequent Amyloid Deposition Without Significant Cognitive Impairment Among the Elderly" stated this: "Similar to the results of several recent neuropathological studies, we did not find significantly worse cognitive performance among amyloid-positive subjects." It was a claim contradicting the idea that amyloid deposits in the brain cause Alzheimer's, a claim that has soaked up very many millions in research dollars without any effective treatment emerging. 

The MMSE test seems to be the main test used for dementia or cognitive impairment. You can get a score between 0 and 30 on the test, and any score of 25 or higher is considered "normal." It must be remembered that every single time a person answers one of the questions on the test correctly, that is a demonstration of some memory ability -- because any ability to recognize or use language requires some memory skill, skills such as recognition (of words heard) or recall of the correct words you need to use to state a correct answer.   

The scientific paper "Word retrieval in connected speech in Alzheimer’s disease: a review with meta-analyses" has a Table 1 that shows the MMSE scores for more than 1000  Alzheimer’s disease patients. Page 10 of the paper tells us that the average MMSE score for those with Alzheimer's disease (AD) was 19.07, and that the median was also about 19 (18.95). 

Although definitely an indication that Alzheimer's involves some memory difficulty, this data shows what a glaring error it is to speak about such people by saying that they "lack memory" or "have no memory." To the contrary, every single score above 0 on the MMSE is an indication that some memory ability still exists;  and data showing that Alzheimer's patients score an average of about 20 on this test (which has a maximum score of 30) suggests that on average those with Alzheimer's have most of the memory skill that they had in their prime. 

Similar data is found in Table 1 of the paper here, entitled "Brain-age predicts subsequent dementia in memory clinic patients."  We have cognitive performance data on 664 patients classified as "non-dementia," and 476 patients classified with "dementia."  The average MMSE score for those with dementia (about 22 out of 30) is almost as high as the average MMSE score for those classified as "non-dementia," a score of about 24. It would be very wrong to say those classified with dementia were "lacking memory," as you need quite a lot of memory skills to score 22 out of 30 on the MMSE test. The table also gives us figures for brain volume for both groups, and the brain volume for those classified with "dementia" is only slightly less than those classified as "non-dementia." Figure 3 of the paper is the scatter plot below, which tells us no clear tale about any clear relation between "brain age" (largely how much of your brain was loss to atrophy) and whether or not you will have dementia.  The plot is consistent with the idea that your brain is not the source of your mind. 

See my post "Men Have Faster-Shrinking Brains, But Women Get an Alzheimer's Diagnosis About Twice as Often as Men" for a discussion of a new study presenting finding inconsistent with claims of a causal relation between brain shrinkage and Alzheimer's.