We welcome network theory as a tool for modelling the multi-directional interactions that characterise disease. However, we feel that Cramer et al. have neglected one important aspect: how diseases change over developmental time. We discuss principles such as fan in, fan out, bottlenecks, and common pathways, and argue that modelling these developmental aspects can be vital, particularly in deriving properly targeted treatments.

In this response, we consider four main issues arising from the commentaries to the target article. These include further details of the theory of interactive specialization, the relationship between neuroconstructivism and selectionism, the implications of neuroconstructivism for the notion of representation, and the role of genetics in theories of development. We conclude by stressing the importance of multidisciplinary approaches in the future study of cognitive development and by identifying the directions in which neuroconstructivism can expand in the Twenty-first Century.

In the multidisciplinary field of developmental cognitive neuroscience, statistical associations between levels of description play an increasingly important role. One example of such associations is the observation of correlations between relatively common gene variants and individual differences in behavior. It is perhaps surprising that such associations can be detected despite the remoteness of these levels of description, and the fact that behavior is the outcome of an extended developmental process involving interaction of the whole organism with a variable environment. Given (...) that they have been detected, how do such associations inform cognitive-level theories? To investigate this question, we employed a multiscale computational model of development, using a sample domain drawn from the field of language acquisition. The model comprised an artificial neural network model of past-tense acquisition trained using the backpropagation learning algorithm, extended to incorporate population modeling and genetic algorithms. It included five levels of description—four internal: genetic, network, neurocomputation, behavior; and one external: environment. Since the mechanistic assumptions of the model were known and its operation was relatively transparent, we could evaluate whether cross-level associations gave an accurate picture of causal processes. We established that associations could be detected between artificial genes and behavioral variation, even under polygenic assumptions of a many-to-one relationship between genes and neurocomputational parameters, and when an experience-dependent developmental process interceded between the action of genes and the emergence of behavior. We evaluated these associations with respect to their specificity, to their developmental stability, and to their replicability, as well as considering issues of missing heritability and gene–environment interactions. We argue that gene–behavior associations can inform cognitive theory with respect to effect size, specificity, and timing. The model demonstrates a means by which researchers can undertake multiscale modeling with respect to cognition and develop highly specific and complex hypotheses across multiple levels of description. (shrink)

Neuroconstructivism: How the Brain Constructs Cognition proposes a unifying framework for the study of cognitive development that brings together (1) constructivism (which views development as the progressive elaboration of increasingly complex structures), (2) cognitive neuroscience (which aims to understand the neural mechanisms underlying behavior), and (3) computational modeling (which proposes formal and explicit specifications of information processing). The guiding principle of our approach is context dependence, within and (in contrast to Marr [1982]) between levels of organization. We propose that three (...) mechanisms guide the emergence of representations: competition, cooperation, and chronotopy; which themselves allow for two central processes: proactivity and progressive specialization. We suggest that the main outcome of development is partial representations, distributed across distinct functional circuits. This framework is derived by examining development at the level of single neurons, brain systems, and whole organisms. We use the terms encellment, embrainment, and embodiment to describe the higher-level contextual influences that act at each of these levels of organization. To illustrate these mechanisms in operation we provide case studies in early visual perception, infant habituation, phonological development, and object representations in infancy. Three further case studies are concerned with interactions between levels of explanation: social development, atypical development and within that, developmental dyslexia. We conclude that cognitive development arises from a dynamic, contextual change in embodied neural structures leading to partial representations across multiple brain regions and timescales, in response to proactively specified physical and social environment. (shrink)

The broad issue in this paper is the relationship between cognitive psychology and neuroscience. That issue arises particularly sharply for cognitive neurospsychology, some of whose practitioners claim a methodological autonomy for their discipline. They hold that behavioural data from neuropsychological impairments are sufficient to justify assumptions about the underlying modular structure of human cognitive architecture, as well as to make inferences about its various components. But this claim to methodological autonomy can be challenged on both philosophical and empirical grounds. A (...) priori considerations about (cognitive) multiple realisability challenge the thesis on philosophical grounds, and neuroscientific findings from developmental disorders substantiate that challenge empirically. The conclusion is that behavioural evidence alone is inadequate for scientific progress since appearances of modularity can be thoroughly deceptive, obscuring both the dynamic processes of neural development and the endstate network architecture of real cognitive systems. (shrink)

In this study we present a self‐organizing connectionist model of early lexical development. We call this model DevLex‐II, based on the earlier DevLex model. DevLex‐II can simulate a variety of empirical patterns in children's acquisition of words. These include a clear vocabulary spurt, effects of word frequency and length on age of acquisition, and individual differences as a function of phonological short‐term memory and associative capacity. Further results from lesioned models indicate developmental plasticity in the network's recovery from damage, in (...) a non‐monotonic fashion. We attribute the network's abilities in accounting for lexical development to interactive dynamics in the learning process. In particular, variations displayed by the model in the rate and size of early vocabulary development are modulated by (a) input characteristics, such as word frequency and word length, (b) consolidation of lexical‐semantic representation, meaning‐form association, and phonological short‐term memory, and (c) delayed processes due to interactions among timing, severity, and recoverability of lesion. Together, DevLex and DevLex‐II provide an accurate computational account of early lexical development. (shrink)

In this study we present a self-organizing connectionist model of early lexical development. We call this model DevLex-II, based on the earlier DevLex model. DevLex-II can simulate a variety of empirical patterns in children's acquisition of words. These include a clear vocabulary spurt, effects of word frequency and length on age of acquisition, and individual differences as a function of phonological short-term memory and associative capacity. Further results from lesioned models indicate developmental plasticity in the network's recovery from damage, in (...) a non-monotonic fashion. We attribute the network's abilities in accounting for lexical development to interactive dynamics in the learning process. In particular, variations displayed by the model in the rate and size of early vocabulary development are modulated by (a) input characteristics, such as word frequency and word length, (b) consolidation of lexical-semantic representation, meaning-form association, and phonological short-term memory, and (c) delayed processes due to interactions among timing, severity, and recoverability of lesion. Together, DevLex and DevLex-II provide an accurate computational account of early lexical development. (shrink)

Nativists about syntactic processing have argued that linguisticprocessing, understood as the implementation of a rule-basedcomputational architecture, is spared in Williams syndrome, (WMS)subjects – and hence that it provides evidence for a geneticallyspecified language module. This argument is bolstered by treatingSpecific Language Impairments (SLI) and WMS as a developmental doubledissociation which identifies a syntax module. Neuroconstructivists haveargued that the cognitive deficits of a developmental disorder cannot beadequately distinguished using the standard gross behavioural tests ofneuropsychology and that the linguistic abilities of the (...) WMS subject canbe equally well explained by a constructivist strategy of neurallearning in the individual, with linguisitic functions implemented in anassociationist architecture. The neuroconstructivist interpretation ofWMS undermines the hypothesis of a double dissociation between SLI andWMS, leaving unresolved the question of nativism about syntax. Theapparent linguistic virtuosity of WMS subjects is an artefact ofenhanced phonological processing, a fact which is easier to demonstratevia the associationist computational model embraced byneuroconstructivism. (shrink)

Some evolutionary psychologists (EP) are strong nativists about Theory of Mind (TOM). They argue that the development of specialised cognitive competence required for TOM requires genetic specification of the developmental trajectory of a specialised cognitive system. EP arrives at this conclusion via conceptual arguments concerning the inadequacy of blank slate neuroconstructivism (strong neuroconstructivism) and empirical evidence from developmental and neuropsychology. I argue that the correct understanding of the conceptual argument applied to the case of TOM supports a moderate form of (...) neuroconstructivism which does not itself require genetic prespecification. In this respect there is no useful analogy with arguments which support stron nativism about linguistic competence. Understanding this debate has consequences for our understanding of modularity, autism, developmental disorders and nativism about high level cognition. (shrink)

There is an argument that has recently been deployed in favor of thinking that the mind is mostly (or even exclusively) composed of cognitive modules; an argument that draws from some ideas and concepts of evolutionary and of developmental biology. In a nutshell, the argument concludes that a mind that is massively composed of cognitive mechanisms that are cognitively modular (henceforth, c-modular) is more evolvable than a mind that is not c-modular (or that is scarcely c-modular), since a cognitive mechanism (...) that is c-modular is likely to be biologically modular (henceforth, b-modular), and b-modular characters are more evolvable (e.g., Sperber 2002, Carruthers 2005). In evolutionary biology, the evolvability of a character in an organism is understood as the “organism’s capacity to facilitate the generation of non-lethal selectable phenotypic variation from random mutation” with respect to that character. Here I will argue that the notion of cognitive modularity needed to make this argument plausible will have to be understood in terms of the biological notion of variational independence; that is, it will have to be understood in such a way that a cognitive feature is c-modular only if few or no other morphological changes (cognitive and not) are significantly correlated with variations of that feature arising in members of the relevant population. I will also argue that all –except for (possibly) one—of the connotations contained in a cluster of notions of cognitive modularity widely accepted in some of the mainstream currents of thought in classical cognitive science, are simply irrelevant to the argument. In order to argue for this, I will have to examine the question as to whether there are any strong theoretical connections between (1) those connotations and (2) notions of modularity accepted in biology, specially in evolutionary and in developmental biology, that are thought to be most relevant to arguments to the effect that biological modularity enhances evolvability. (shrink)

I examine an argument that has recently appeared in the cognitive science literature in favor of thinking that the mind is mostly composed of Fodorian-type cognitive modules; an argument that concludes that a mind that is massively composed of classical cognitive mechanisms that are cognitively modular is more evolvable than a mind that is not cognitively modular, since a cognitive mechanism that is cognitively modular is likely to be biologically modular, and biologically modular characters are more evolvable. I argue that (...) the notion of cognitive modularity needed to make this argument plausible will have to be understood in terms of the biological notion of variational independence, as follows: a cognitive feature is cognitively modular only if few or no other morphological changes are significantly correlated with variations of that feature arising in members of the relevant population as a result of ontogeny. I also argue that most of the connotations contained in a cluster of notions of classical cognitive modularity are, as far as we know, irrelevant to the argument, and that only the presence of selective impairments—also known as cognitive dissociations—can be considered as strong indicators of the type of modularity that genuinely enhances evolvability. (shrink)

In this paper we argue that attempts to distinguish between categories of 'dyslexia' and 'poor reader' or 'reading disabled' are scientifically unsupportable, arbitrary and thus potentially discriminatory. We do not seek to veto scientific curiosity in examining underlying factors in reading disability, for seeking greater understanding of the relationship between visual symbols and spoken language is crucial. However, while stressing the potential of genetics and neuroscience for guiding assessment and educational practice at some stage in the future, we argue that (...) there is a mistaken belief that current knowledge in these fields is sufficient to justify a category of dyslexia as a subset of those who encounter reading difficulties. The implications of this debate for large-scale intervention are outlined. (shrink)

In this paper we argue that attempts to distinguish between categories of ‘dyslexia’ and ‘poor reader’ or ‘reading disabled’ are scientifically unsupportable, arbitrary and thus potentially discriminatory. We do not seek to veto scientific curiosity in examining underlying factors in reading disability, for seeking greater understanding of the relationship between visual symbols and spoken language is crucial. However, while stressing the potential of genetics and neuroscience for guiding assessment and educational practice at some stage in the future, we argue that (...) there is a mistaken belief that current knowledge in these fields is sufficient to justify a category of dyslexia as a subset of those who encounter reading difficulties. The implications of this debate for large-scale intervention are outlined. (shrink)

The pivotal problem of comorbidity research lies in the psychometric foundation it rests on, that is, latent variable theory, in which a mental disorder is viewed as a latent variable that causes a constellation of symptoms. From this perspective, comorbidity is a (bi)directional relationship between multiple latent variables. We argue that such a latent variable perspective encounters serious problems in the study of comorbidity, and offer a radically different conceptualization in terms of a network approach, where comorbidity is hypothesized to (...) arise from direct relations between symptoms of multiple disorders. We propose a method to visualize comorbidity networks and, based on an empirical network for major depression and generalized anxiety, we argue that this approach generates realistic hypotheses about pathways to comorbidity, overlapping symptoms, and diagnostic boundaries, that are not naturally accommodated by latent variable models: Some pathways to comorbidity through the symptom space are more likely than others; those pathways generally have the same direction (i.e., from symptoms of one disorder to symptoms of the other); overlapping symptoms play an important role in comorbidity; and boundaries between diagnostic categories are necessarily fuzzy. (shrink)

This paper addresses concerns raised recently by Datteri (Biol Philos 24:301–324, 2009) and Craver (Philos Sci 77(5):840–851, 2010) about the use of brain-extending prosthetics in experimental neuroscience. Since the operation of the implant induces plastic changes in neural circuits, it is reasonable to worry that operational knowledge of the hybrid system will not be an accurate basis for generalisation when modelling the unextended brain. I argue, however, that Datteri’s no-plasticity constraint unwittingly rules out numerous experimental paradigms in behavioural and systems (...) neuroscience which also elicit neural plasticity. Furthermore, I propose that Datteri and Craver’s arguments concerning the limitations of prosthetic modelling in basic neuroscience, as opposed to neuroengineering, rests on too narrow a view of the ways models in neuroscience should be evaluated, and that a more pluralist approach is needed. I distinguish organisational validity of models from mechanistic validity. I argue that while prosthetic models may be deficient in the latter of these explanatory virtues because of neuroplasticity, they excel in the former since organisational validity tracks the extent to which a model captures coding principles that are invariant with plasticity. Changing the brain, I conclude, is one viable route towards explaining the brain. (shrink)

Modules are widely held to play a central role in explaining mental development and in accounts of the mind generally. But there is much disagreement about what modules are, which shows that we do not adequately understand modularity. This paper outlines a Fodoresque approach to understanding one type of modularity. It suggests that we can distinguish modular from nonmodular cognition by reference to the kinds of process involved, and that modular cognition differs from nonmodular forms of cognition in being a (...) special kind of computational process. The paper concludes by considering implications for the role of modules in explaining mental development. (shrink)

En las ciencias cognoscitivas, existe una teoría con respecto a la arquitectura computacional de la mente conocida como el modularismo masivo. Esta teoría sostiene que la mente está en su mayoría constituida por mecanismos que son cognoscitivamente modulares. Algunos de los defensores de esta teoría proponen un argumento cuya conclusión es que es muy probable que mecanismos que son cognoscitivamente muy modulares sean más evolucionables que aquellos mecanismos que no son cognoscitivamente modulares. Aquí muestro que para poder defender plausiblemente esta (...) conclusión es necesario añadir a la noción de modularidad cognoscitiva la siguiente característica: "Un sistema cognoscitivo S de organismos de una población P es cognoscitivamente modular sólo si S es variacionalmente modular en P." Defiendo también la idea que una de las características que normalmente se asocian al concepto de modularidad cognoscitiva-i.e., la noción de doble disociación cognoscitiva-es muy cercana a la idea de modularidad variacional. Adicionalmente, argumento que no hay razones positivas, y sí algunas razones negativas, para pensar que las otras características usualmente asociadas al concepto de modularidad cognoscitiva-tales como la especificidad de dominio o la especialización funcional-coadyuven a la evolucionabilidad de los módulos cognoscitivos. In the cognitive sciences, there is a theory concerning the computational architecture of the mind known as massive modularity. This theory holds that the mind is constituted mostly by cognitive modules. Some of the defenders of this theory have put forward an argument whose conclusion is that it is very likely that those mechanisms that are cognitively very modular are more evolvable than mechanisms that are not cognitively modular. Here I show that a plausible defense of this conclusion requires us to add to the usual notion of cognitive modularity the following characteristic: "A cognitive system S of organism of a population P is cognitively modular only if S is variationally modular in P." I also defend the view that one of the characteristics normally associated to the concept of cognitive modularity-namely, the notion of a double dissociation-is conceptually close to the concept of variational modularity. Additionally, I argue that there are not positive reasons-while there are some negative ones-to think that the other characteristics usually associated to cognitive modularity, such as domain specificity or functional specialization, enhance the evolvability of cognitive modules. (shrink)