further on einstein's brain

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BRIEF COMMUNICATION Further on Einstein’s Brain Terence Hines Department of Psychology, Pace University, Pleasantville, New York 10570-2799 In 1985 Diamond et al. published a paper reporting a histological analysis of the brain of Albert Einstein. Sections from four different areas of Einstein’s cortex, Broadmann’s areas 9 and 39 from both the left and the right hemispheres, were obtained. As a comparison, sections from these anatomical areas were also taken from the brains of 11 deceased male VA hospital pa- tients. Sections were stained to allow separate visual- ization of neurons and glia. In all four areas examined, the control brains showed a higher neuron to glial cell ratio than did Einstein’s brain. The authors found that this difference was statistically significant in only one area, specifically area 39 from the left hemisphere. Diamond et al. (5, p. 203) suggested that these results show ‘‘a response by glial cells to greater neuronal metabolic need’’ and that this ‘‘might reflect the en- hanced use of this tissue in the expression of his [Einstein’s] unusual conceptual powers in comparison with control brains.’’ The Diamond et al. (5) paper immediately attracted considerable attention in the popular press. It is often cited in introductory psychology texts (i.e., 8) as well as in more advanced texts on neuroscience such as Bear et al. (1) in which two full pages are devoted to the study. It appears that the Diamond et al. (5) study was never subjected to careful scrutiny of the methods used and the claims made. When this is done, it becomes clear that the study is permeated with faulty methods and statistical analyses that render the conclusions drawn invalid. There are two specific areas of criticism of the Diamond et al. (5) study. The first concerns the nature of the control brains used. The second deals with the statistical analyses used. The control brains were from 11 males ‘‘obtained during the last few years from the Veteran’s Administra- tion Hospital in Martinez, California’’ (5, p. 199). The average age at death for these patients was 64 years (range from 47 to 80), while Einstein died at 76 years of age. While very recent research indicates that the degree of neuronal loss with normal aging may not be as great as once thought (i.e., 6), the age difference between Einstein’s brain and that of the control sample may still pose a problem. The authors’ statement that ‘‘chronological age is not necessarily a useful indicator in measuring biological systems’’ (p. 199), a point often made in the aging literature (7), should not be allowed to obscure the fact that there are real correlations between age and numerous biological variables. As but one example, glial proliferation continues during life while neuronal division obviously does not. This effect, alone, could lead to a smaller neuron to glial cell ratio in an older brain. The authors’ descriptions of the patients from which the control brains were obtained leaves much to be desired. These brains were obtained from patients who died of nonneurological causes. But no information is provided on the actual causes of death or whether the patients suffered from some neurological disease, but died of something else. A chronic alcoholic who dies from a cardiac arrest has died from a nonneurological disease. But one would certainly expect the history of alcoholism to have had some effect on the structure of the patient’s cortex. No information on the length of time the control patients were in the hospital is provided. Nothing is said of the patients’ agonal state. Perhaps more impor- tantly, nothing is mentioned about the length of time between death and the removal of the brains, either the control brains or Einstein’s. All of these variables might be expected to influence cortical morphology. Finally, no information is given about the socioeco- nomic and educational status of the control patients. Since these patients were in a VA hospital, it can be assumed that they were of a lower socioeconomic status than was Albert Einstein. This being the case, one might well expect differences in terms of a somewhat more impoverished environment during childhood for the control patients. As Diamond et al. (3) had previ- ously reported, impoverished environments do cause changes in cortical morphology. In addition to the methodological problems noted above, there are statistical problems in Diamond et al. (5). The authors reported four separate t tests compar- ing the neuron to glial cell ratio in the four different brain areas analyzed. Only one was significant. Even if EXPERIMENTAL NEUROLOGY 150, 343–344 (1998) ARTICLE NO. EN976759 343 0014-4886/98 $25.00 Copyright r 1998 by Academic Press All rights of reproduction in any form reserved.

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Page 1: Further on Einstein's Brain

BRIEF COMMUNICATION

Further on Einstein’s Brain

Terence HinesDepartment of Psychology, Pace University, Pleasantville, New York 10570-2799

In 1985 Diamond et al. published a paper reporting ahistological analysis of the brain of Albert Einstein.Sections from four different areas of Einstein’s cortex,Broadmann’s areas 9 and 39 from both the left and theright hemispheres, were obtained. As a comparison,sections from these anatomical areas were also takenfrom the brains of 11 deceased male VA hospital pa-tients. Sections were stained to allow separate visual-ization of neurons and glia. In all four areas examined,the control brains showed a higher neuron to glial cellratio than did Einstein’s brain. The authors found thatthis difference was statistically significant in only onearea, specifically area 39 from the left hemisphere.

Diamond et al. (5, p. 203) suggested that these resultsshow ‘‘a response by glial cells to greater neuronalmetabolic need’’ and that this ‘‘might reflect the en-hanced use of this tissue in the expression of his[Einstein’s] unusual conceptual powers in comparisonwith control brains.’’

The Diamond et al. (5) paper immediately attractedconsiderable attention in the popular press. It is oftencited in introductory psychology texts (i.e., 8) as well asin more advanced texts on neuroscience such as Bear etal. (1) in which two full pages are devoted to the study.

It appears that the Diamond et al. (5) study wasnever subjected to careful scrutiny of the methods usedand the claims made. When this is done, it becomesclear that the study is permeated with faulty methodsand statistical analyses that render the conclusionsdrawn invalid.

There are two specific areas of criticism of theDiamond et al. (5) study. The first concerns the natureof the control brains used. The second deals with thestatistical analyses used.

The control brains were from 11 males ‘‘obtainedduring the last few years from the Veteran’s Administra-tion Hospital in Martinez, California’’ (5, p. 199). Theaverage age at death for these patients was 64 years(range from 47 to 80), while Einstein died at 76 years ofage. While very recent research indicates that thedegree of neuronal loss with normal aging may not beas great as once thought (i.e., 6), the age differencebetween Einstein’s brain and that of the control sample

may still pose a problem. The authors’ statement that‘‘chronological age is not necessarily a useful indicatorin measuring biological systems’’ (p. 199), a point oftenmade in the aging literature (7), should not be allowedto obscure the fact that there are real correlationsbetween age and numerous biological variables. As butone example, glial proliferation continues during lifewhile neuronal division obviously does not. This effect,alone, could lead to a smaller neuron to glial cell ratio inan older brain.

The authors’ descriptions of the patients from whichthe control brains were obtained leaves much to bedesired. These brains were obtained from patients whodied of nonneurological causes. But no information isprovided on the actual causes of death or whether thepatients suffered from some neurological disease, butdied of something else. A chronic alcoholic who diesfrom a cardiac arrest has died from a nonneurologicaldisease. But one would certainly expect the history ofalcoholism to have had some effect on the structure ofthe patient’s cortex.

No information on the length of time the controlpatients were in the hospital is provided. Nothing issaid of the patients’ agonal state. Perhaps more impor-tantly, nothing is mentioned about the length of timebetween death and the removal of the brains, either thecontrol brains or Einstein’s. All of these variables mightbe expected to influence cortical morphology.

Finally, no information is given about the socioeco-nomic and educational status of the control patients.Since these patients were in a VA hospital, it can beassumed that they were of a lower socioeconomic statusthan was Albert Einstein. This being the case, onemight well expect differences in terms of a somewhatmore impoverished environment during childhood forthe control patients. As Diamond et al. (3) had previ-ously reported, impoverished environments do causechanges in cortical morphology.

In addition to the methodological problems notedabove, there are statistical problems in Diamond et al.(5). The authors reported four separate t tests compar-ing the neuron to glial cell ratio in the four differentbrain areas analyzed. Only one was significant. Even if

EXPERIMENTAL NEUROLOGY 150, 343–344 (1998)ARTICLE NO. EN976759

343 0014-4886/98 $25.00Copyright r 1998 by Academic Press

All rights of reproduction in any form reserved.

Page 2: Further on Einstein's Brain

these four reported t tests were the only ones per-formed, there would be a problem in that the authorsdid not take into account that performing multiple ttests increases the chances of finding a significantresult. But, it appears that many more than four t testswere done, or at least considered. The authors statethat not only were raw neuron and glial cell countsmade, but also separate counts were done for astrocytesand oligodendrocytes. Further, separate neuron/astro-cyte and neuron/oligodendrocyte ratios were calcu-lated. Thus, it appears that seven different dependentmeasures were actually used; four different raw cellcounts (neurons, astrocytes, oligodendrocytes, and thecombined number of astrocytes and oligodendrocytes)and three different rations (neurons/astrocytes, neurons/oligodendrocytes, and neurons/total glial count). Sincefour different brain areas were examined, this yields atotal of 28 different possible t tests that could have beenperformed. It would be surprising indeed if from a totalof 28 different t tests one did not obtain at least one‘‘significant’’ result purely by chance alone.

It thus appears that Diamond et al. (5) tried severaldifferent dependent measures until they hit upon onewhich yielded a ‘‘significant’’ result. It is interesting inthis regard to note that in several previous papersexaming the effects of environmental deprivation andage on cortical morphology in rats, Diamond and co-workers usually reported simple cell counts, not ratios(i.e., 2, 3, 4). From a total of 57 comparisons in thesethree papers, only 9 (16%) are comparisons of ratios.

A further problem exists with the use of a t test in theanalysis of data such as that reported in Diamond et al.(5). One of the major assumptions of the parametric ttest is that the variances of the two distributions beingcompared are approximately equal. In practice, thisusually means that the variance in one distribution

should not be more than twice that of the otherdistribution. But the data in Diamond et al. (5) are aspecial case where one distribution contains only asingle number. Therefore, the variance of this distribu-tion must be zero. And the variance of the otherdistribution will, by definition, be twice greater thanzero. It may be that the authors attempted to getaround this problem by transforming the scores, asdescribed on page 201 of their report. Unfortunately,the description of this procedure is such that it isimpossible to determine exactly what was done withthe data.

In summary, the Diamond et al. (5) paper is soseriously flawed that its conclusions should not beaccepted.

REFERENCES

1. Bear, M., Conners, B., & Paradiso, M. (1996). Neuroscience:Exploring the brain. Baltimore: Williams and Wilkins.

2. Diamond, M. et al. (1964). Effects of an enriched environment onthe histology of the rat cerebral cortex. Journal of ComparativeNeurology, 123, 111–120.

3. Diamond, M. et al. (1966). Increases in cortical depth and glianumbers in rats subjected to enriched environments. Journal ofComparative Neurology, 128, 117–126.

4. Diamond et al. (1977). Changes in neuron number and size andglia number in the young and aging rat medial occipital cortex.Behavioral Biology, 20, 409–418.

5. Diamond, M. et al. (1985). On the brain of a scientist: AlbertEinstein. Experimental Neurology, 88, 198–204.

6. Gomez-Isla, T. et al. (1998). Neuronal loss correlates with butexceeds neurofibrillary tangles in Alzheimer’s Disease. Annalsof Neurology, 41, 17–24.

7. Schneider, E. et al. (1989). Handbook of the psychology of aging.3rd edition. Orlando: Academic Press.

8. Wade, C., & Tavris, C. (1990). Psychology. 2nd edition. NewYork: Harper and Row.

344 BRIEF COMMUNICATION