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.