Editorial
Available even from snippets of human skin, stem cells capable of forming tolerably respectable neurones are, as it were, on the lips of every person expecting—both from the professional and personal viewpoints—that structure and function can now be restored in the context of damage and disease. The opportunity to produce very many fate-restricted progeny from one or a few cells not only promises the provision of re-building blocks suitable for brain repair but also offers mediators of therapeutic plasticity and immune modulation, methods to study human development, reagents for modelling disease, and a resource for drug discovery. The stakes are high for stem cells in regenerative neurology and, hence, in fuelling the expectations of society. This issue of Brain contains several articles that deal with the emerging story of stem and precursor cells as architects of repair in neurological disease.Roland Martin from Hamburg, Germany, (page 1181) comments on the lessons learned from autologous haematopoetic stem-cell transplantation in patients with multiple sclerosis reported by Imke Metz and colleagues from Göttingen (Germany), Rochester, Indianapolis and Duarte (USA), Ottawa (Canada), Madrid (Spain) and Vienna (Austria). They studied brain pathology in patients who died shortly after this procedure providing histological support for a lesson already learned from clinical trials: once the cascade of events initiating the neurodegenerative component of tissue injury is triggered, even profound anti-inflammatory measures will not bolt the stable door after the horse has gone (page 1254). Alexis Joannides and investigators from Cambridge and Cardiff (United Kingdom) characterize the environmental signals determining neural and glial fates to which human embryonic stem cells respond in vitro and in normal rodent brain tissue, and reveal how these lineage choices and the temporal profile of maturation are altered in models of inflammatory and neurodegenerative disease, respectively (page 1263). Stefania Corti and a team from Milan and Lecco (Italy) investigate whether neural stem cells, shown to generate cholinergic motor neurons in vitro repair the superoxide dismutase (SOD1)-G93A transgenic mouse model of amyotrophic lateral sclerosis (page 1289): treated mice have an improved clinical phenotype and show evidence both for integration of grafted motor neurons and enhanced survival of host cells through release of neurotrophins. Detlev Boison and investigators from Portland (USA) and Bonn (Germany) consider whether stem cells engineered to release the inhibitory molecule adenosine and differentiated as neural precursors suppress epilepsy in a rodent kindling model (page 1276): there is a beneficial effect on seizure activity and this is attributed directly to adenosine release in hippocampal structures. Waldy San Sebastián and colleagues from Pamplona, Spain, describe the effects of carotid body cell aggregate derived glial cell derived nerve growth factor on the clinical course and histological outcome of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) lesioning of the monkey striatum (page 1306): grafted animals boast more striatal and commisural tyroxine hydroxylase immunoreactive dopaminergic interneurons and a favourable course to the parkinsonism so induced. Claire Kelly and investigators from Cardiff (United Kingdom) tidy up existing confusion on the preferred cell type – neural precursors or primary foetal striatum – for restoring circuitry in models of Huntington's disease, coming out strongly in favour of human neural precursors (page 1263).
In his book essay on the ‘neurobiological basis of language’, David Caplan reviews Broca's region edited by Yosef Grodzinsky and Katrin Amunts, Towards an evolutionary biology of language by Philip Lieberman, and Constructing a language: a usage based theory of language by Michael Tomasello (page 1442). Through work in behavioural and cognitive neurology, linguistics and psychology, in Montreal and in Boston and now as director of the neuropsychology laboratory at the Massachusetts General Hospital, Dr Caplan is well-qualified to wrestle with issues that inform debates on the evolution, acquisition and neural organization of language. He presents the contrasting views. According to the ‘motor theories of speech perception’, human language is a lucky dividend from things that happened in evolution to the vocal tract—descent of the root of the tongue into the oropharynx—allowing vocalization and changes (dependent on FOXP2) in the neural circuitry that support these motor opportunities for building on the grunts and barkings of non-human species. In time, this potential provided the substrate for cultural influences to fashion the five elements of language that enable expression of the impetus to communicate. But for David Caplan this analysis—competing as it does with Naom Chomsky's concept of an innate ‘universal grammar’ built on abstract domain specific representations and processes—will not quite do. Better to relate language to neural structures and their function. These details are set out by the contributors to Broca's region who survey the neuroanatomy of Brodmann's areas 44 and 45, and functions of brain regions that, with some dissent, provide a substrate for Chomsky's theory of syntactic representations and their processing in language production and comprehension. Broca's region reprints 10 classic papers, in translation, on this brain region and its functions. This issue of Brain contains three further contributions to the anatomy and neurology of language, one of much historical interest.
Jessica Deleon and colleagues from Baltimore (USA) suggest that picture naming is a localized human attribute (page 1408): they use discriminant function analysis to match imaging appearances with success and failure in cognitive tasks carried out during the acute phase of stroke and thereby provide a network for naming pictures that has distributed responsibility for separate components of this complex performance. David Weintrob and investigators from Melbourne (Australia) study aspects of verbal learning in patients undergoing left hemisphere resections that spare the hippocampus to show that cases with loss of the perirhinal and enterorhinal cortices, but not those with resections of the anterolateral and inferior temporal neocortex, have impaired word learning (page 1423). Nina Dronkers and a group from San Diego (USA) and Paris (France) have retrieved the specimens that Paul Broca used in his original description ‘sur le siège de la faculté du language articulé’ and subjected these to high resolution magnetic resonance imaging (page 1432): they find that Messrs Leborgne and Lelong had lesions extending into medial regions of the brain and away from the surface abnormalities that Broca described—revealing inconsistency between the region designated by Broca and that now assigned to him eponymously. This is not our first excursion into the neurology of Broca's area. In ‘From the Archives’, Jan van Gijn reviews ‘The pathology of sensory aphasia, with an analysis of fifty cases in which Broca's centre was not diseased’ by M Allen Starr (Brain 1889; 12: 82–99): ‘A remarkable case of aphasia. Acute and complete destruction by embolic softening of the left motor-vocal speech centre (Broca's convolution) in a right-handed man: transient motor aphasia, marked inability to name objects and especially persons, considerable agraphia and slight word-blindness’ by Byrom Bramwell (Brain 1898; 21: 343–373); and ‘Recent work on aphasia’ by James Collier (Brain 1909; 31: 523–549).
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