Editorial
Science and religion traditionally part company around the issue of evidence. Whilst it is unarguable that the brain encodes belief and is the organ of decision, these attributes are a far cry from concluding that religiosity is entirely hard-wired and no more than a neural construct lacking all mystery. Nor should we be distracted by the revelation that Albert Einstein's dictum ‘science without religion is lame, religion without science is blind’ was not what he thought at all. On May 15, 2008, Bloomsbury Book Auctions (London) realized a hammer price of £170 000 against an upper estimate of £8000 for the manuscript letter from 1954 to his friend the philosopher Eric Gutkind, in which Einstein writes: ‘The word god is for me nothing more than the expression and product of human weaknesses, the Bible a collection of honourable, but still primitive legends which are nevertheless pretty childish.’Neuroscience and religion do not have to fall out. Take as read that the same brain regions are activated when deciding on the veracity of mathematical statements and the accuracy of geographical locations as those that ponder the statement ‘a personal God exists, just as the Bible describes’ (Harris et al., Ann Neurol 2008; 63: 141–147). In fact, none of these cognitive exercises is devoid of mysteriousness. In the March issue, Sir Michael Atiyah reminded us that—far from being the slave of logic—the essence of mathematical creativity is poetry and beauty (Brain 2008; 131: 1156–1160). And remembering Cecil Day-Lewis (‘On not saying everything’, The Room 1965), Peter Stanford—writer, journalist, broadcaster, former editor of the Catholic Herald and author of The Devil: a biography and Heaven: a traveller's guide to the undiscovered country—emphasizes in his 2008 Little Gidding Lecture to the T.S. Eliot Society, that what goes unsaid provides material for the mystery and meaning of poetic and religious imagination.
In ‘God, theologian and humble neurologist’ Alasdair Coles reviews Did my neurons make me do it? Philosophical and neurobiological perspectives on moral responsibility and free will by Nancey Murphy and Warren S. Brown, The soul in the brain: the cerebral basis of language, art and belief by Michael Trimble, Sacred or neural? The potential of neuroscience to explain religious experience by Anne L.C. Runehow and Alone in the world? Human uniqueness in science and theology by J. Wentzel Van Huyssteen (page 1953). In considering the ‘spark of something beyond empiricism’ that is the religious impulse, we can expect a declaration of Faith from the Reverend Dr Coles but, also as a talented clinical neuroscientist and practising neurologist, how much common ground might he agree between science and religion; and where along the way will the materialists, the Cartesian dualists and the Believers part company? Addressing the uniqueness of humans as having God-given rationality, and thereby turning on its head the caricature of any who subscribe to the doctrines of orthodox religions as having lost their reasoning, Alasdair Coles keeps religion and the brain in step by highlighting van Huyssteen's analysis that religious awareness sees human cognition as the gift that constitutes ‘embodied transcendence’. Dr Coles traces the origins of religion and cognition to cave art of the Upper Paleolithic in Europe where humans adopted a symbolic narrative to account for their new-found consciousness and awareness. The evidence suggests that the cavemen of Lascaux started to talk, make music and believe in order to ‘code the invisible’ and ‘experience the unutterable’. Alasdair Coles keeps faith with neuroscience in his preparedness to anatomize this nascent religiosity, but loses patience with the embarrassment of amateur neurotheology—sometimes accounting for religious experience as mere ecstatic epileptic discharges and, elsewhere, confusing brain activation with the mumbo-jumbo of a ‘God centre’. Without insisting that his own position is evidential or trying to unfold the mystery, Alasdair Coles describes an uncertainty—something ‘unsaid’—that is nevertheless brought into critical focus by dialogue between the disciplines of theology, philosophy, anthropology, ethnography and neuroscience.
Amongst four papers on nerve and muscle, Grazia Devigili and investigators from Ferrara, Milan and Brescia (Italy) respond to the difficulty in diagnosing small fibre neuropathy—seen in diabetes, immune-mediated disorders and other contexts—by proposing criteria that use clinical features, quantitative sensory testing and, especially, histology derived from skin biopsies, the data being based on 67 patients whose natural history is studied prospectively over 2 years (page 1912). Mario Nolano and colleagues from Terme and Naples (Italy) and Rochester (USA) challenge the doctrine that sensory abnormalities in Parkinson's disease result from abnormal central processing of intact afferent information to show that the functional deficits are in fact associated with degeneration and regeneration of cutaneous nerve fibres and Meissner corpuscles, abnormalities of peripheral nerve that correlate with severity but not duration or age at onset of Parkinson's disease (page 1903). On neurodegenerative disease, Jaana Koivunen and investigators from Turku, Helsinki and Tampere (Finland) and Uppsala (Sweden) exploit the ability to image beta amyloid in life using the positron emission tomography ligand (11)C Pittsburgh Compound B (PiB) in patients with variant Alzheimer's disease—presenile dementia with spastic paraparesis—to show uptake in the striatum, cingulate gyri, occipital cortex and thalamus that mimics the regional involvement characteristic of cases having presenilin 1 mutations and amyloid precursor protein gene duplication but differing from the pattern of uptake seen in typical Alzheimer's disease (page 1845).
We publish 11 papers—original articles, a review, scientific commentary and piece ‘From the Archives’—on clinical and experimental aspects of demyelinating disease, representing a semi-thematic issue on multiple sclerosis. Since the application 27 years ago of magnetic resonance imaging with a resolution sufficient to depict the individual lesions of multiple sclerosis (Young et al., Lancet 1981; 2: 1063–1066), neurologists have become familiar with these characteristic MR appearances. But interpretation is sometimes more challenging. On page 1759, Claudia Lucchinetti and colleagues from Rochester (USA), Göttingen (Germany), Istanbul (Turkey) and Vienna (Austria) describe the clinical and radiological correlates of individual demyelinating lesions in 168 patients with multiple sclerosis that were sufficiently ambiguous to justify surgical biopsy; often identified at presentation, these tumefactive lesions usually anticipate later clinical events but, despite initially causing a good deal of alarm and diagnostic confusion, they merge into a rather typical clinical and radiological phenotype and seem not threaten a relatively poor long-term prognosis. Moving down the nervous system, Katrin Weier and colleagues from Basel (Switzerland) report the imaging and clinical characteristics of lesions that mimic stable non-communicating syringomyelia in nine patients with multiple sclerosis, representing a rare (<5%) but—as with the tumefactive lesions—well recognized radiological feature that has no tell-tale clinical correlate and which they (and our referees) consider to be a consequence of spinal cord demyelination and not chance co-morbidity (page 1776).
On mechanisms of demyelinating disease, Don Mahad (named recently by the Times Higher Education Supplement as one of the 10 most promising young scientists working in all disciplines in the UK) and investigators from Newcastle-upon-Tyne (UK) and Vienna (Austria) pursue the hypothesis that the so-called pattern III lesions seen in multiple sclerosis and in Balo's concentric sclerosis result from hypoxia-like cell injury by showing defects of the mitochondrial respiratory chain complex IV (cytochrome c oxidase, COX), manifesting as a deficiency of the catalytic component COX-1, that is not seen in pattern II inflammatory lesions or tissue damaged by stroke (page 1722). Jane Anderson and a team from Cambridge and institutions in London (UK) combine information derived from an experimental model of human demyelinating disease, and tissue from individuals with multiple sclerosis, to show that neuronal and axonal loss are associated with the accumulation of abnormal and insoluble species of phosphorylated tau suggesting a novel and ubiquitous mechanism for the crucial component of the complex cascade of events that underlies disease progression (page 1736). Tanja Kuhlmann and investigators from Münster and Göttingen (Germany) and Montreal (Canada) add precision to the characterization of progenitors and mature oligodendrocytes in the normal and diseased adult central nervous system, using the transcription factors Nkx2.2 and Olig2 and NogoA, to show that—by comparison with the early lesions of multiple sclerosis and the periplaque white matter which are rich in progenitors and mature (presumably remyelinating) oligodendrocytes—the density of progenitors is reduced with chronicity; and those cells that are present fail to mature, substantiating the hypothesis that the reduced remyelination seen in chronic lesions of multiple sclerosis is due to blocked oligodendrocyte differentiation (page 1749). Monique Dubois-Dalcq (Bethesda, USA) and her former colleagues from Paris (France) and Edinburgh (UK) review the story of neurite outgrowth and endogenous remyelination taking an evolutionary approach that explores the molecular basis for successful repair in fish, the ‘Janus face’ of inflammation and the inhibitory molecular machinery of the mammalian adult central nervous system, concluding with a strategy for enhancing remyelination in the context of multiple sclerosis and—to turn full circle within our thematic issue—documenting the anticipated successes with the next generation of brain images (page 1686).
Jan Lünemann and Christian Münz comment on work by Phil de Jager and colleagues from Boston and Cambridge (USA) that uses cytometric profiling to reveal a reduction in CD8lowCD56+ cells in multiple sclerosis (see pages 1681 and 1701). And Samantha Jilek and colleagues from Lausanne (Switzerland) add weight to the evidence implicating Epstein Barr (EBV) virus in triggering demyelinating disease—a story that goes back many years, drawing on epidemiological, serological, immunological and neuropathological sources; in cross-sectional studies and serial observations of individual patients, they show an inverse relationship between disease duration and intensity of peripheral blood CD8 cell responsiveness that is specific and suggests a contribution specifically from EBV early in the illness—not so much ‘hit-and-run’ as ‘caught-at-the-scene-of-the-crime’ (page 1712). Formulating a view on the complex aetiology and pathogenesis of multiple sclerosis, involving the interplay of infections and genetic susceptibility, and culminating in a complex pathogenesis expressed as relapsing–remitting and then progressive disease, has long taxed the minds of imaginative commentators. Many have aired their formulations, with varying degrees of confidence and competence, down the years. In ‘From the Archives’, we review a remarkably forward looking account from 62 years ago—‘The problem of disseminated sclerosis (being the Presidential Address of the Neurological Section, Royal Society of Medicine. October 1946)’ by Douglas McAlpine. Brain 1946; 69: 233–250.
Cambridge
CiteULike 
Connotea 
Del.icio.us What's this?
Related articles in Brain:
- God, theologian and humble neurologist
- Alasdair Coles
Brain 2008 131: 1953-1959.[Extract] [FREE Full Text] - Sensory deficit in Parkinson's disease: evidence of a cutaneous denervation
- Maria Nolano, Vincenzo Provitera, Anna Estraneo, Mona M. Selim, Giuseppe Caporaso, Annamaria Stancanelli, Anna Maria Saltalamacchia, Bernardo Lanzillo, and Lucio Santoro
Brain 2008 131: 1903-1911.[Abstract] [FREE Full Text] - PET amyloid ligand [11C]PIB uptake shows predominantly striatal increase in variant Alzheimer's disease
- J. Koivunen, A. Verkkoniemi, S. Aalto, A. Paetau, J.-P. Ahonen, M. Viitanen, K. Någren, J. Rokka, M. Haaparanta, H. Kalimo, and J. O. Rinne
Brain 2008 131: 1845-1853.[Abstract] [FREE Full Text] - Non-communicating syringomyelia: a feature of spinal cord involvement in multiple sclerosis
- Katrin Weier, Yvonne Naegelin, Alain Thoeni, Jochen G. Hirsch, Ludwig Kappos, Wolfgang Steinbrich, Ernst-Wilhelm Radue, and Achim Gass
Brain 2008 131: 1776-1782.[Abstract] [FREE Full Text] - Mitochondrial defects in acute multiple sclerosis lesions
- Don Mahad, Iryna Ziabreva, Hans Lassmann, and Douglas Turnbull
Brain 2008 131: 1722-1735.[Abstract] [FREE Full Text] - Abnormally phosphorylated tau is associated with neuronal and axonal loss in experimental autoimmune encephalomyelitis and multiple sclerosis
- J. M. Anderson, D. W. Hampton, R. Patani, G. Pryce, R. A. Crowther, R. Reynolds, R. J. M. Franklin, G. Giovannoni, D. A. S. Compston, D. Baker, M. G. Spillantini, and S. Chandran
Brain 2008 131: 1736-1748.[Abstract] [FREE Full Text] - Differentiation block of oligodendroglial progenitor cells as a cause for remyelination failure in chronic multiple sclerosis
- T. Kuhlmann, V. Miron, Q. Cuo, C. Wegner, J. Antel, and W. Brück
Brain 2008 131: 1749-1758.[Abstract] [FREE Full Text] - From fish to man: understanding endogenous remyelination in central nervous system demyelinating diseases
- Monique Dubois-Dalcq, Anna Williams, Christine Stadelmann, Bruno Stankoff, Bernard Zalc, and Catherine Lubetzki
Brain 2008 131: 1686-1700.[Abstract] [FREE Full Text] - Do natural killer cells accelerate or prevent autoimmunity in multiple sclerosis?
- Jan D. Lünemann and Christian Münz
Brain 2008 131: 1681-1683.[Extract] [FREE Full Text] - Cytometric profiling in multiple sclerosis uncovers patient population structure and a reduction of CD8low cells
- Philip L. De Jager, Elizabeth Rossin, Saumyadipta Pyne, Pablo Tamayo, Linda Ottoboni, Vissia Viglietta, Mira Weiner, Dulce Soler, Elena Izmailova, Lauren Faron-Yowe, Carmeline O’Brien, Sam Freeman, Susana Granados, Alex Parker, Ronenn Roubenoff, Jill P. Mesirov, Samia J. Khoury, David A. Hafler, and Howard L. Weiner
Brain 2008 131: 1701-1711.[Abstract] [FREE Full Text] - Strong EBV-specific CD8+ T-cell response in patients with early multiple sclerosis
- Samantha Jilek, Myriam Schluep, Pascal Meylan, François Vingerhoets, Laurence Guignard, Anita Monney, Joerg Kleeberg, Géraldine Le Goff, Giuseppe Pantaleo, and Renaud A. Du Pasquier
Brain 2008 131: 1712-1721.[Abstract] [FREE Full Text]
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||