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Einstein’s brain: Gliogenesis in autism?
Medical Hypotheses 72 (2009) 753–761
Contents lists available at ScienceDirect
Medical Hypotheses journal homepage: www.elsevier.com/locate/mehy
Correspondence
Einstein’s brain: Gliogenesis in autism? Ti-Fei Yuan * Department of Anatomy, Li Kai Shing Faculty of Medicine, The University of Hong Kong, 21 Sassoon Road, Pokfulam, Hong Kong
a r t i c l e
i n f o
Article history: Received 21 January 2009 Accepted 25 January 2009
s u m m a r y The hypothesis is that the increased glia/neuron ratio in cortical areas of Einstein’s brain is the sign of autism disorder rather than the evidence that more glial cells make a genius. Ó 2009 Elsevier Ltd. All rights reserved.
Albert Einstein is generally believed to be one of the greatest minds that ever existed. The fortunate analyses of the cortex of this bright scientist lead to the some interesting inspections on the structural bases of minds and intelligence, including a much lower neuron: glial cell ratio [1]. However, here we present the hypothesis that the feature of high glial cell ratio may represent brain disorders, possibly the autism spectrum disorder, rather an index of genius. Albert Einstein’s brain has often been mentioned in courses of neurobiology talking about the function of glial cells, since the discovery of a much higher glial cell ratio in several cortical areas in post-mortem analyses of the brain [1]. However, few people considered this as potential neuropathological features of a great scientist, though Einstein has been known as a lonely child, late speaker and even a ‘‘absent-minded professor” [8,9]. He himself also admitted the social difficulty and the lack of need for direct contacts with other people [10]. Some people had thus proposed that Einstein suffered from Asperger syndrome, which shows the signs of autism but does not lead to learning difficulties [8,9]. Interestingly, autism is one neuropsychiatric disorder that often associated with macrocephaly, a sign of brain enlargement [2]. Consistently, Einstein’s brain, though no bigger than that of an ordinary person, showed enlargement of the inferior parietal lobe [3] that has been found with volumetric increases in patients of autism disorders [4]. Einstein brain also lacks part of the sylvian fissure [3], the dysfunction of which often causes autism syndromes. Besides neurogenesis, glial cell proliferate under exposures to challenging experiences and learning processes, and the altered glial plasticity may contribute to or parallel the abnormal remodeling of the brain in autism patients [5]. The neuroglial responses and neuroinflammation processes can also lead to altered glial cell number in the cortex of autism patients [6,7]. All these
* Tel.: +852 67362793. E-mail address: yuantf@hku
doi:10.1016/j.mehy.2009.01.023
data suggest that the increased glial cells in the brain of Einstein may reflect the pathological neuroglial responses. Possibly, some associated changes of glial cell proliferation, in these specific areas of Einstein’s brain, are functional and improve local trophic state of brain neurons. However, this is difficult to ascertain, and the temporal relationship between the formation of new glial cells and his genius in 1900s require further investigations on carbon-14 content in these cells, for example. Acknowledgement The author thanks Department of Anatomy, The University of Hong Kong, Li Kai Shing Faculty of Medicine for supports. References [1] Diamond MC, Scheibel AB, Murphy Jr GM, Harvey T. On the brain of a scientist: Albert Einstein. Exp Neurol 1985;88:198–204. [2] Bauman ML, Kemper TL. The neuropathology of the autism spectrum disorders: what have we learned? Novartis Found Symp 2003;251:112–22 [discussion 122–118, 281–197]. [3] Witelson SF, Kigar DL, Harvey T. The exceptional brain of Albert Einstein. Lancet 1999;353:2149–53. [4] McCaffery P, Deutsch CK. Macrocephaly and the control of brain growth in autistic disorders. Prog Neurobiol 2005;77:38–56. [5] Dong WK, Greenough WT. Plasticity of nonneuronal brain tissue: roles in developmental disorders. Ment Retard Dev Disabil Res Rev 2004;10:85–90. [6] Fatemi SH, Folsom TD, Reutiman TJ, Lee S. Expression of astrocytic markers aquaporin 4 and connexin 43 is altered in brains of subjects with autism. Synapse 2008;62:501–7. [7] Vargas DL, Nascimbene C, Krishnan C, Zimmerman AW, Pardo CA. Neuroglial activation and neuroinflammation in the brain of patients with autism. Ann Neurol 2005;57:67–81. [8] BBS News: Einstein and Newton ‘had autism’.; 2009 [retrieved 21.01.09]. [9] Wikipedia. People speculated to have been autistic. ; 2009 [retrieved 21.01.09]. [10] Einstein Albert. The world as I see it. The Center for History of Physics. ; 2009 [retrieved 21.01.09. Originally published in Forum and Century, vol. 84. p. 193–194, the thirteenth in the Forum series, Living Philosophies].
Contents lists available at ScienceDirect
Medical Hypotheses journal homepage: www.elsevier.com/locate/mehy
Correspondence
Einstein’s brain: Gliogenesis in autism? Ti-Fei Yuan * Department of Anatomy, Li Kai Shing Faculty of Medicine, The University of Hong Kong, 21 Sassoon Road, Pokfulam, Hong Kong
a r t i c l e
i n f o
Article history: Received 21 January 2009 Accepted 25 January 2009
s u m m a r y The hypothesis is that the increased glia/neuron ratio in cortical areas of Einstein’s brain is the sign of autism disorder rather than the evidence that more glial cells make a genius. Ó 2009 Elsevier Ltd. All rights reserved.
Albert Einstein is generally believed to be one of the greatest minds that ever existed. The fortunate analyses of the cortex of this bright scientist lead to the some interesting inspections on the structural bases of minds and intelligence, including a much lower neuron: glial cell ratio [1]. However, here we present the hypothesis that the feature of high glial cell ratio may represent brain disorders, possibly the autism spectrum disorder, rather an index of genius. Albert Einstein’s brain has often been mentioned in courses of neurobiology talking about the function of glial cells, since the discovery of a much higher glial cell ratio in several cortical areas in post-mortem analyses of the brain [1]. However, few people considered this as potential neuropathological features of a great scientist, though Einstein has been known as a lonely child, late speaker and even a ‘‘absent-minded professor” [8,9]. He himself also admitted the social difficulty and the lack of need for direct contacts with other people [10]. Some people had thus proposed that Einstein suffered from Asperger syndrome, which shows the signs of autism but does not lead to learning difficulties [8,9]. Interestingly, autism is one neuropsychiatric disorder that often associated with macrocephaly, a sign of brain enlargement [2]. Consistently, Einstein’s brain, though no bigger than that of an ordinary person, showed enlargement of the inferior parietal lobe [3] that has been found with volumetric increases in patients of autism disorders [4]. Einstein brain also lacks part of the sylvian fissure [3], the dysfunction of which often causes autism syndromes. Besides neurogenesis, glial cell proliferate under exposures to challenging experiences and learning processes, and the altered glial plasticity may contribute to or parallel the abnormal remodeling of the brain in autism patients [5]. The neuroglial responses and neuroinflammation processes can also lead to altered glial cell number in the cortex of autism patients [6,7]. All these
* Tel.: +852 67362793. E-mail address: yuantf@hku
doi:10.1016/j.mehy.2009.01.023
data suggest that the increased glial cells in the brain of Einstein may reflect the pathological neuroglial responses. Possibly, some associated changes of glial cell proliferation, in these specific areas of Einstein’s brain, are functional and improve local trophic state of brain neurons. However, this is difficult to ascertain, and the temporal relationship between the formation of new glial cells and his genius in 1900s require further investigations on carbon-14 content in these cells, for example. Acknowledgement The author thanks Department of Anatomy, The University of Hong Kong, Li Kai Shing Faculty of Medicine for supports. References [1] Diamond MC, Scheibel AB, Murphy Jr GM, Harvey T. On the brain of a scientist: Albert Einstein. Exp Neurol 1985;88:198–204. [2] Bauman ML, Kemper TL. The neuropathology of the autism spectrum disorders: what have we learned? Novartis Found Symp 2003;251:112–22 [discussion 122–118, 281–197]. [3] Witelson SF, Kigar DL, Harvey T. The exceptional brain of Albert Einstein. Lancet 1999;353:2149–53. [4] McCaffery P, Deutsch CK. Macrocephaly and the control of brain growth in autistic disorders. Prog Neurobiol 2005;77:38–56. [5] Dong WK, Greenough WT. Plasticity of nonneuronal brain tissue: roles in developmental disorders. Ment Retard Dev Disabil Res Rev 2004;10:85–90. [6] Fatemi SH, Folsom TD, Reutiman TJ, Lee S. Expression of astrocytic markers aquaporin 4 and connexin 43 is altered in brains of subjects with autism. Synapse 2008;62:501–7. [7] Vargas DL, Nascimbene C, Krishnan C, Zimmerman AW, Pardo CA. Neuroglial activation and neuroinflammation in the brain of patients with autism. Ann Neurol 2005;57:67–81. [8] BBS News: Einstein and Newton ‘had autism’.