This paper is aimed at identifying how a model’s explanatory power is constructed and identified, particularly in the practice of template-based modeling (Humphreys, Philos Sci 69:1–11, 2002; Extending ourselves: computational science, empiricism, and scientific method, 2004), and what kinds of explanations models constructed in this way can provide. In particular, this paper offers an account of non-causal structural explanation that forms an alternative to causal–mechanical accounts of model explanation that are currently popular in philosophy of biology and cognitive science. Clearly, (...) defences of non-causal explanation are far from new (e.g. Batterman, Br J Philos Sci 53:21–38, 2002a; The devil in the details: asymptotic reasoning in explanation, reduction, and emergence, 2002b; Pincock, Noûs 41:253–275, 2007; Mathematics and scientific representation 2012; Rice, Noûs. doi:10.1111/nous.12042, 2013; Biol Philos 27:685–703, 2012), so the targets here are focused on a particular type of robust phenomenon and how strong invariance to interventions can block a range of causal explanations. By focusing on a common form of model construction, the paper also ties functional or computational style explanations found in cognitive science and biology more firmly with explanatory practices across model-based science in general. (shrink)

The philosophical literature on scientific explanation in neuroscience has been dominated by the idea of mechanisms. The mechanist philosophers often claim that neuroscience is in the business of finding mechanisms. This view has been challenged in numerous ways by showing that there are other successful and widespread explanatory strategies in neuroscience. However, the empirical evidence for all these claims was hitherto lacking. Empirical evidence about the pervasiveness and uses of various explanatory strategies in neuroscience is particularly needed because examples and (...) case studies that are used to illustrate philosophical claims so far tend to be hand-picked. The risk of confirmation bias is therefore considerable: when looking for white swans, all one finds is that swans are white. The more systematic quantitative and qualitative bibliometric study of a large body of relevant literature that we present in this paper can put such claims into perspective. Using bibliometric tools, we identify the typical linguistic patterns used in the alleged mechanistic, dynamical, and topological explanations in the literature, their preponderance and how they change over time. Our findings show abundant use of mechanistic language, but also the presence of a significant neuroscience literature using topological and dynamical explanatory language, which grows over time and increasingly differentiates from each other and from mechanistic explanations. (shrink)

According to mainstream philosophical views causal explanation in biology and neuroscience is mechanistic. As the term ‘mechanism’ gets regular use in these fields it is unsurprising that philosophers consider it important to scientific explanation. What is surprising is that they consider it the only causal term of importance. This paper provides an analysis of a new causal concept—it examines the cascade concept in science and the causal structure it refers to. I argue that this concept is importantly different from the (...) notion of mechanism and that this difference matters for our understanding of causation and explanation in science. (shrink)

Journal of Social Philosophy, EarlyView.

This dissertation argues that cognition is a kind of natural agency. Natural agency is the capacity that certain systems have to act in accordance with their own norms. Natural agents are systems that bias their repertoires in response to affordances in the pursuit of their goals. Cognition is a special mode of this general phenomenon. Cognitive systems are agents that have the additional capacity to actively take their worlds to be certain ways, regardless of whether the world is really that (...) way. In this way, cognitive systems are desituated. Desituatedness is the root of specifically cognitive capacities for representation and abstraction. There are two main reasons why this view needs defending. First, natural agency is typically viewed as incompatible with natural science because it is committed to a teleological mode of explanation. Second, cognition is typically held to be categorically distinct from natural agency. This dissertation argues against both of these views. It argues against the incompatibility of agency and natural science by demonstrating that systems biology, general systems theory, and sciences that deal with complex systems have typically underappreciated conceptual and theoretical resources for grounding agency in the causal structure of the world. These conceptual resources do not, however, reduce agency to systems theory because the normativity inherent in agency demands descriptive resources beyond those of even the most sophisticated systems theory. It argues against the categorical difference between natural agency and cognition by pointing out that separating cognition from a richer web of situated, ecologically embedded relations between the agent and the world generates the frame problem, which is an insuperable obstacle to making cognition that is sufficiently responsive to the complexity of the world. Rooting cognition in natural agency is a more robust empirical bet for theorizing cognition and artificial intelligence. (shrink)

We provide three innovations to recent debates about whether topological or “network” explanations are a species of mechanistic explanation. First, we more precisely characterize the requirement that all topological explanations are mechanistic explanations and show scientific practice to belie such a requirement. Second, we provide an account that unifies mechanistic and non-mechanistic topological explanations, thereby enriching both the mechanist and autonomist programs by highlighting when and where topological explanations are mechanistic. Third, we defend this view against some powerful mechanist objections. (...) We conclude from this that topological explanations are autonomous from their mechanistic counterparts. (shrink)

Transdisciplinary research challenges the divide between Indigenous and academic knowledge by bringing together epistemic resources of heterogeneous stakeholders. The aim of this article is to explore causal explanations in a traditional fishing community in Brazil that provide resources for transdisciplinary collaboration, without neglecting differences between Indigenous and academic experts. Semi-structured interviews were carried out in a fishing village in the North shore of Bahia and our findings show that community members often rely on causal explanations for local ecological phenomena with (...) different degrees of complexity. While these results demonstrate the ecological expertise of local community members, we also argue that recognition of local expertise needs to reflect on differences between epistemic communities by developing a culturally sensitive model of transdisciplinary knowledge negotiation. (shrink)

We provide two programmatic frameworks for integrating philosophical research on understanding with complementary work in computer science, psychology, and neuroscience. First, philosophical theories of understanding have consequences about how agents should reason if they are to understand that can then be evaluated empirically by their concordance with findings in scientific studies of reasoning. Second, these studies use a multitude of explanations, and a philosophical theory of understanding is well suited to integrating these explanations in illuminating ways.

The history of developmental biology is interwoven with debates as to whether mechanistic explanations of development are possible or whether alternative explanatory principles or even vital forces need to be assumed. In particular, the demonstrated ability of embryonic cells to tune their developmental fate precisely to their relative position and the overall size of the embryo was once thought to be inexplicable in mechanistic terms. Taking a causal perspective, this Element examines to what extent and how developmental biology, having turned (...) molecular about four decades ago, has been able to meet the vitalist challenge. It focuses not only on the nature of explanations but also on the usefulness of causal knowledge – including the knowledge of classical experimental embryology – for further scientific discovery. It also shows how this causal perspective allows us to understand the nature and significance of some key concepts, including organizer, signal and morphogen. This title is also available as Open Access on Cambridge Core. (shrink)

The received view of computation is methodologically bifurcated: it offers different accounts of computation in the mathematical and physical cases. But little in the way of argument has been given for this approach. This article rectifies the situation by arguing that the alternative, a unified account, is untenable. Furthermore, once these issues are brought into sharper relief we can see that work remains to be done to illuminate the relationship between physical and mathematical computation.

Mechanistic explanations are often said to explain because they reveal the causal structure of the world. Conversely, dynamical models supposedly lack explanatory power because they do not describe causal structure. The only way for dynamical models to produce causal explanations is via the 3M criterion: the model must be mapped onto a mechanism. This framing of the situation has become the received view around the viability of dynamical explanation. In this paper, I argue against this position and show that dynamical (...) models can themselves reveal causal structure and consequently produce nonmechanistic, dynamical explanations. Taking the example of cell fates from systems biology, I show how dynamical models, and specifically the attractor landscapes they describe, identify the causes of cell differentiation and explain why cells select particular fates. These dynamical features of the system better fit Woodward’s (2010, 2018) criteria of specificity and proportionality and make them the best candidate causes of cell fates than mechanisms. I also show how these causes are irreducible and inaccessible to mechanistic models, making 3M unworkable and counterproductive in this case. Dynamical models can reveal dynamical causes and thereby provide causal explanations. (shrink)

I examine to what extent accounts of mechanisms based on formal interventionist theories of causality can adequately represent biological mechanisms with complex dynamics. Using a differential equation model for a circadian clock mechanism as an example, I first show that there exists an iterative solution that can be interpreted as a structural causal model. Thus, in principle, it is possible to integrate causal difference-making information with dynamical information. However, the differential equation model itself lacks the right modularity properties for a (...) full integration. A formal mechanistic model will therefore have to leave out either noncausal or causal explanatory relations. (shrink)

In this paper, we offer reasons to justify the explanatory credentials of dynamical modeling in the context of the metaplasticity thesis, located within a larger grouping of views known as 4E Cognition. Our focus is on showing that dynamicism is consistent with interventionism, and therefore with a difference-making account at the scale of system topologies that makes sui generis explanatory differences to the overall behavior of a cognitive system. In so doing, we provide a general overview of the interventionist approach. (...) We then argue that recent mechanistic attempts at reducing dynamical modeling to a merely descriptive enterprise fail given that the explanatory standard in dynamical modeling can be shown to rest on interventionism. We conclude that dynamical modeling captures features of nested and developmentally plastic cognitive systems that cannot be explained by appeal to underlying mechanisms alone. (shrink)

Rational analysis is an influential but contested account of how probabilistic modeling can be used to construct non-mechanistic but self-standing explanatory models of the mind. In this paper, I disentangle and assess several possible explanatory contributions which could be attributed to rational analysis. Although existing models suffer from evidential problems that question their explanatory power, I argue that rational analysis modeling can complement mechanistic theorizing by providing models of environmental affordances.

This article examines three candidate cases of non-causal explanation in computational neuroscience. I argue that there are instances of efficient coding explanation that are strongly analogous to examples of non-causal explanation in physics and biology, as presented by Batterman, Woodward, and Lange. By integrating Lange’s and Woodward’s accounts, I offer a new way to elucidate the distinction between causal and non-causal explanation, and to address concerns about the explanatory sufficiency of non-mechanistic models in neuroscience. I also use this framework to (...) shed light on the dispute over the interpretation of dynamical models of the brain. _1_ Introduction _1.1_ Efficient coding explanation in computational neuroscience _1.2_ Defining non-causal explanation _2_ Case I: Hybrid Computation _3_ Case II: The Gabor Model Revisited _4_ Case III: A Dynamical Model of Prefrontal Cortex _4.1_ A new explanation of context-dependent computation _4.2_ Causal or non-causal? _5_ Causal and Non-causal: Does the Difference Matter? (shrink)

Batterman and Rice ([2014]) argue that minimal models possess explanatory power that cannot be captured by what they call ‘common features’ approaches to explanation. Minimal models are explanatory, according to Batterman and Rice, not in virtue of accurately representing relevant features, but in virtue of answering three questions that provide a ‘story about why large classes of features are irrelevant to the explanandum phenomenon’ ([2014], p. 356). In this article, I argue, first, that a method (the renormalization group) they propose (...) to answer the three questions cannot answer them, at least not by itself. Second, I argue that answers to the three questions are unnecessary to account for the explanatoriness of their minimal models. Finally, I argue that a common features account, what I call the ‘generalized ontic conception of explanation’, can capture the explanatoriness of minimal models. (shrink)

Although it has been argued that mechanistic explanation is compatible with abstraction, there are still doubts about whether mechanism can account for the explanatory power of significant abstract models in computational neuroscience. Chirimuuta has recently claimed that models describing canonical neural computations must be evaluated using a non-mechanistic framework. I defend two claims regarding these models. First, I argue that their prevailing neurocognitive interpretation is mechanistic. Additionally, a criterion recently proposed by Levy and Bechtel to legitimize mechanistic abstract models, and (...) also a criterion proposed by Chirimuuta herself aimed to distinguish between causal and non-causal explanation, can be employed to show why these models are explanatory only under this interpretation. Second, I argue that mechanism is able to account for the special epistemic achievement implied by CNC models. Canonical neural components contribute to an integrated understanding of different cognitive functions. They make it possible for us to explain these functions by describing different mechanisms constituted by common basic components arranged in different ways. (shrink)

In the last 20 years or so, since the publication of a seminal paper by Watts and Strogatz :440–442, 1998), an interest in topological explanations has spread like a wild fire over many areas of science, e.g. ecology, evolutionary biology, medicine, and cognitive neuroscience. The topological approach is still very young by all standards, and even within special sciences it still doesn’t have a single methodological programme that is applicable across all areas of science. That is why this special issue (...) is important as a first systematic philosophical study of topological explanations and their relation to a well understood and widespread explanatory strategy, such as mechanistic one. (shrink)

Though the realm of biology has long been under the philosophical rule of the mechanistic magisterium, recent years have seen a surprisingly steady rise in the usurping prowess of process ontology. According to its proponents, theoretical advances in the contemporary science of evo-devo have afforded that ontology a particularly powerful claim to the throne: in that increasingly empirically confirmed discipline, emergently autonomous, higher-order entities are the reigning explanantia. If we are to accept the election of evo-devo as our best conceptualisation (...) of the biological realm with metaphysical rigour, must we depose our mechanistic ontology for failing to properly “carve at the joints” of organisms? In this paper, I challenge the legitimacy of that claim: not only can the theoretical benefits offered by a process ontology be had without it, they cannot be sufficiently grounded without the metaphysical underpinning of the very mechanisms which processes purport to replace. The biological realm, I argue, remains one best understood as under the governance of mechanistic principles. (shrink)

Philosophers have traditionally treated physicalism as an empirically informed metaphysical thesis. This approach faces a well-known problem often referred to as Hempel’s dilemma: formulations of physicalism tend to be either false or indeterminate. The generally preferred strategy to address this problem involves an appeal to a hypothetical complete and ideal physical theory. After demonstrating that this strategy is not viable, I argue that we should redefine physicalism as an interdisciplinary research program seeking to explain the mental in terms of the (...) physical that encompasses the physical sciences, the psychological and brain sciences, and philosophy. Redefining physicalism in this way improves upon previous reconstructive accounts while avoiding the indeterminacy associated with orthodox forms of futurist physicalism. (shrink)

Most philosophical debate over mental causation has been concerned with reconciling commonsense intuitions that there are causal interactions between the mental and the physical with philosophical theories of the nature of the mental that seem to suggest otherwise. My concern is with a different and more practical problem. We often confront some cognitive, affective, or bodily phenomenon, and wonder about its source – its etiology or its underlying causal basis. For instance, you might wonder whether your queasiness due to something (...) you ate, or whether it is just nervousness, or whether your aunt’s memory loss is a neurological problem or a psychological response to trauma. Such questions attempt to localize the causes of a phenomenon at some level in the complex multi-level systems that we human animals are. In this paper I will attempt to tease out the sense of level implicit in such questions, and to show how it is related to current mechanistic accounts of levels. I will argue that the explanation of our practices of level attribution is deeply pragmatic. Such attributions are often attempts to locate the causes of problems, and to identify interventions that could solve those problems. (shrink)

In robustness analysis, hypotheses are supported to the extent that a result proves robust, and a result is robust to the extent that we detect it in diverse ways. But what precise sense of diversity is at work here? In this paper, I show that the formal explications of evidential diversity most often appealed to in work on robustness – which all draw in one way or another on probabilistic independence – fail to shed light on the notion of diversity (...) relevant to robustness analysis. I close by briefly outlining a promising alternative approach inspired by Horwich’s (1982) eliminative account of evidential diversity. (shrink)

This paper examines the adequacy of causal graph theory as a tool for modeling biological phenomena and formalizing biological explanations. I point out that the causal graph approach reaches it limits when it comes to modeling biological phenomena that involve complex spatial and structural relations. Using a case study from molecular biology, DNA-binding and -recognition of proteins, I argue that causal graph models fail to adequately represent and explain causal phenomena in this field. The inadequacy of these models is due (...) to their failure to include relevant spatial and structural information in a way that does not render the model non-explanatory, unmanageable, or inconsistent with basic assumptions of causal graph theory. (shrink)

Colombo’s (Phenomenology and the Cognitive Sciences, 2013) plea for neural representationalism is the focus of a recent contribution to Phenomenology and Cognitive Science by Daniel D. Hutto and Erik Myin. In that paper, Hutto and Myin have tried to show that my arguments fail badly. Here, I want to respond to their critique clarifying the type of neural representationalism put forward in my (Phenomenology and the Cognitive Sciences, 2013) piece, and to take the opportunity to make a few remarks of (...) general interest concerning what Hutto and Myin have dubbed “the Hard Problem of Content.”. (shrink)

Recent work in explainable artificial intelligence (XAI) attempts to render opaque AI systems understandable through a divide-and-conquer strategy. However, this fails to illuminate how trained AI systems work as a whole. Precisely this kind of functional understanding is needed, though, to satisfy important societal desiderata such as safety. To remedy this situation, we argue, AI researchers should seek mechanistic interpretability, viz. apply coordinated discovery strategies familiar from the life sciences to uncover the functional organisation of complex AI systems. Additionally, theorists (...) should accommodate for the unique costs and benefits of such strategies in their portrayals of XAI research. (shrink)

A tension exists between those who do—e.g. Meyer (The British Journal for the Philosophy of Science 71:959–985, 2020 ) and Chemero ( 2011 )—and those who do not—e.g. Kaplan and Craver (Philosophy of Science 78:601–627, 2011 ) Piccinini and Craver (Synthese 183:283–311, 2011 )—afford nonmechanistic explanations a role in cognitive science. Here, I argue that one’s perspective on this matter will cohere with one’s interpretation of the tasks of cognitive science; that is, of the actions for which cognitive scientists are (...) specially fitted. To make this point concrete, I consider two tasks of cognitive science—establishing causal claims and unifying—and show how these tasks are interpreted differently by mechanists and nonmechanists respectively. I then argue that, as a result of these different interpretations, we cannot expect to resolve the tension between mechanists and nonmechanists by appeal to cognitive scientific practice. I conclude that we should give up on the debate between mechanists and nonmechanists, and search for progress elsewhere. (shrink)

In this essay I propose that what design principles in systems biology and systems neuroscience do is to present abstract characterizations of mechanisms, and thereby facilitate mechanistic explanation. To show this, one design principle in systems neuroscience, i.e., the multilayer perceptron, is examined. However, Braillard contends that design principles provide a sort of non-mechanistic explanation due to two related reasons: they are very general and describe non-causal dependence relationships. In response to this, I argue that, on the one hand, all (...) mechanisms are more or less general, and on the other, many design principles are causal systems. (shrink)

The emphasis on the organization of entities and their activities and interactions has been labeled one of the most distinct contributions of mechanistic philosophy. In this paper I discuss the manner in which the organization of entities and their activities and interactions participates in bringing about phenomena. I present a well-known example from molecular biology—the functioning of the genetic switch in phage lambda—and discuss Marco J. Nathan’s notion of causation by concentration. Nathan introduces causation by concentration to account for the (...) irreducible causal role that the concentration ratio between two kinds of proteins possesses in the genetic switch mechanism in phage lambda. I discuss what the irreducibility of this causal role amounts to and provide a mechanistic interpretation of Nathan’s causation by concentration; that is, I explain this irreducible causal role as one organizational feature of this mechanism. The paper concludes that biological mechanisms need a causal pluralist framework [similar to Glennan’s account in (2009), (2010) and (2017) but slightly modified] where organizational features such as the concentration ratio have a causally relevant role, yet all the causally productive relations occur at the level of entities or individuals. (shrink)

This article demonstrates that non-mechanistic, dynamical explanations are a viable approach to explanation in the special sciences. The claim that dynamical models can be explanatory without reference to mechanisms has previously been met with three lines of criticism from mechanists: the causal relevance concern, the genuine laws concern, and the charge of predictivism. I argue, however, that these mechanist criticisms fail to defeat non-mechanistic, dynamical explanation. Using the examples of Haken et al.’s model of bimanual coordination, and Thelen et al.’s (...) dynamical field model of infant perseverative reaching, I show how each mechanist criticism fails once the standards of Woodward’s interventionist framework are applied to dynamical models. An even-handed application of Woodwardian interventionism reveals that dynamical models are capable of producing genuine explanations without appealing to underlying mechanistic details. 1Introduction2Interventionism and Mechanistic Explanation 2.1Causal relevance and ideal interventions2.2Invariance2.3Explanation3Covering-Laws and Dynamical Explanation 3.1Dynamical models3.2Covering-law explanation3.3Prediction4Causal Relevance 4.1The causal relevance concern4.2Intervening on dynamical models4.3Test case I: The Haken–Kelso–Bunz model4.4Test case II: Dynamical field model5Genuine Laws 5.1The genuine laws concern5.2Using invariance in place of laws5.3Test case I: The Haken–Kelso–Bunz model5.4Test case II: Dynamical field model6Prediction 6.1Predictivism6.2Crude and invariant prediction7Interventionist Criticism of the Haken–Kelso–Bunz Model8Dynamical Explanation8Conclusion. (shrink)

This paper defends three claims about concrete or physical models: these models remain important in science and engineering, they are often essentially idealized, in a sense to be made precise, and despite these essential idealizations, some of these models may be reliably used for the purpose of causal explanation. This discussion of concrete models is pursued using a detailed case study of some recent models of landslide generated impulse waves. Practitioners show a clear awareness of the idealized character of these (...) models, and yet address these concerns through a number of methods. This paper focuses on experimental arguments that show how certain failures to accurately represent feature X are consistent with accurately representing some causes of feature Y, even when X is causally relevant to Y. To analyse these arguments, the claims generated by a model must be carefully examined and grouped into types. Only some of these types can be endorsed by practitioners, but I argue that these endorsed claims are sufficient for limited forms of causal explanation. (shrink)

In the last two decades few topics in philosophy of science have received as much attention as mechanistic explanation. A significant motivation for these accounts is that scientists frequently use the term “mechanism” in their explanations of biological phenomena. While scientists appeal to a variety of causal concepts in their explanations, many philosophers argue or assume that all of these concepts are well understood with the single notion of mechanism. This reveals a significant problem with mainstream mechanistic accounts– although philosophers (...) use the term “mechanism” interchangeably with other causal concepts, this is not something that scientists always do. This paper analyses two causal concepts in biology–the notions of “mechanism” and “pathway”–and how they figure in biological explanation. I argue that these concepts have unique features, that they are associated with distinct strategies of causal investigation, and that they figure in importantly different types of explanation. (shrink)

Completeness is an important but misunderstood norm of explanation. It has recently been argued that mechanistic accounts of scientific explanation are committed to the thesis that models are complete only if they describe everything about a mechanism and, as a corollary, that incomplete models are always improved by adding more details. If so, mechanistic accounts are at odds with the obvious and important role of abstraction in scientific modelling. We respond to this characterization of the mechanist’s views about abstraction and (...) articulate norms of completeness for mechanistic explanations that have no such unwanted implications. _1_ Introduction _2_ A Balancing Act: When Do Details Matter? _3_ The Norms of Causal Explanation _4_ The Norms of Constitutive Explanation _5_ Salmon-Completeness _6_ From More Details to More Relevant Details _7_ Non-explanatory Virtues of Abstraction _8_ From Explanatory Models to Explanatory Knowledge _9_ Mechanistic Completeness Reconsidered _10_ Conclusion. (shrink)

It is widely assumed that mechanistic explanations are causal explanations. Many prominent new mechanists endorse interventionism as the correct analysis of explanatory causal models in biology and other fields. This article argues that interventionism is not entirely satisfactory in this regard. A case study of Jacob and Monod’s operon model shows that at least some important mechanistic explanations in biology present significant contrasts with the interventionist account. This result motivates a more inclusive approach to mechanistic explanation, allowing for noncausal aspects.

This paper argues that in some explanations mathematics are playing an explanatory rather than a representational role, and that this feature unifies many types of non-causal or non-mechanistic explanations that some philosophers of science have been recently exploring under various names. After showing how mathematics can play either a representational or an explanatory role by considering two alternative explanations of a same biological pattern—“Bergmann’s rule”—I offer an example of an explanation where the bulk of the explanatory job is done by (...) a mathematical theorem, and where mechanisms involved in the target systems are not explanatorily relevant. Then I account for the way mathematical properties may function in an explanatory way within an explanation by arguing that some mathematical propositions involving variables non directly referring to the target system features constitute constraints to which a whole class of systems should comply, provided they are describable by a mathematical object concerned by those propositions. According to such “constraint account”, those mathematical facts are directly entailing the explanandum, as a consequence of such constraints. I call those explanations “structural”, because here properties of mathematical structures are accounting for the explanandum; various kinds of mathematical structures thereby define various types of structural explanations. (shrink)

It is a widespread assumption in philosophy of science that data is what is explained by theory—that data itself is not explanatory. I draw on instances of representational and explanatory practice from mammalian chronobiology to suggest that this assumption is unsustainable. In many instances, biologists employ representations of data in explanatory ways that are not reducible to constraints on or evidence for representations of mechanisms. Data graphs are used to exemplify relationships between quantities in the mechanism, and often these representations (...) are necessary for explaining particular aspects of the phenomena under study. I argue that this kind of representation is distinct from representing laws or generalizations, and its primary purpose is to convey particular types or patterns of quantitative relationships. The benefit of the analysis is two-fold. First, it provides a more accurate account of explanatory practice in broadly mechanistic analysis in biology. Second, it suggests that there is not an explanatory “fundamental” type of representation in biology. Rather, the practice of explanation consists in the construction of different types of representations and their employment for distinct explanatory purposes. (shrink)

In addition to theorizing about the role and value of mechanisms in scientific explanation or the causal structure of the world, there is a fundamental task of getting straight what a ‘mechanism’ is in the first place. Broadly, this paper is about the challenge of application: the challenge of aligning one's philosophical account of a scientific concept with the manner in which that concept is actually used in scientific practice. This paper considers a case study of the challenge of application (...) as it pertains to the concept of a mechanism: the debate about whether natural selection is a mechanism. By making clear what is and is not at stake in this debate, this paper considers various strategies for dealing with the challenge of application and makes a case for definitional pluralism about mechanism concepts. (shrink)

ABSTRACTIn this paper I offer an interventionist perspective on the explanatory structure and explanatory power of dynamical models in cognitive science: I argue that some “pure” dynamical models – ones that do not refer to mechanisms at all – in cognitive science are “contextualized causal models” and that this explanatory structure gives such models genuine explanatory power. I contrast this view with several other perspectives on the explanatory power of “pure” dynamical models. One of the main results is that dynamical (...) models need not refer to underlying mechanisms in order to be explanatory. I defend and illustrate this position in terms of dynamical models of the A-not-B error in developmental psychology as elaborated by Thelen and colleagues, and dynamical models of unintentional interpersonal coordination developed by Richardson and colleagues. (shrink)

We address the question of whether and to what extent explanatory and modelling strategies in systems biology are mechanistic. After showing how dynamic mathematical models are actually required for mechanistic explanations of complex systems, we caution readers against expecting all systems biology to be about mechanistic explanations. Instead, the aim may be to generate topological explanations that are not standardly mechanistic, or to arrive at design principles that explain system organization and behaviour in general, but not specific mechanisms. These abstraction (...) strategies serve various aims, including prediction and control, that are central to understanding the epistemic diversity of systems biology. (shrink)

Causal relations among components and activities are intentionally misrepresented in mechanistic explanations found routinely across the life sciences. Since several mechanists explicitly advocate accurately representing factors that make a difference to the outcome, these idealizations conflict with the stated rationale for mechanistic explanation. We argue that these idealizations signal an overlooked feature of reasoning in molecular and cell biology—mechanistic explanations do not occur in isolation—and suggest that explanatory practices within the mechanistic tradition share commonalities with model-based approaches prevalent in population (...) biology. (shrink)

I examine the adequacy of the causal graph-structural equations approach to causation for modeling biological mechanisms. I focus in particular on mechanisms with complex dynamics such as the PER biological clock mechanism in Drosophila. I show that a quantitative model of this mechanism that uses coupled differential equations – the well-known Goldbeter model – cannot be adequately represented in the standard causal graph framework, even though this framework does permit causal cycles. The reason is that the model contains dynamical information (...) about the mechanism that concerns causal properties but that does not correspond to variables that could be subject to independent interventions. Thus, a representation of the mechanisms as a causal structural model necessarily suppresses causally relevant information. (shrink)

Besides mechanistic explanations of phenomena, which have been seriously investigated in the last decade, biology and ecology also include explanations that pinpoint specific mathematical properties as explanatory of the explanandum under focus. Among these structural explanations, one finds topological explanations, and recent science pervasively relies on them. This reliance is especially due to the necessity to model large sets of data with no practical possibility to track the proper activities of all the numerous entities. The paper first defines topological explanations (...) and then explains why topological explanations and mechanisms are different in principle. Then it shows that they are pervasive both in the study of networks—whose importance has been increasingly acknowledged at each level of the biological hierarchy—and in contexts where the notion of selective neutrality is crucial; this allows me to capture the difference between mechanisms and topological explanations in terms of practical modelling practices. The rest of the paper investigates how in practice mechanisms and topologies are combined. They may be articulated in theoretical structures and explanatory strategies, first through a relation of constraint, second in interlevel theories, or they may condition each other. Finally, I explore how a particular model can integrate mechanistic informations, by focusing on the recent practice of merging networks in ecology and its consequences upon multiscale modelling. (shrink)

An increasing number of philosophers have promoted the idea that mechanism provides a fruitful framework for thinking about the explanatory contributions of computational approaches in cognitive neuroscience. For instance, Piccinini and Bahar :453–488, 2013) have recently argued that neural computation constitutes a sui generis category of physical computation which can play a genuine explanatory role in the context of investigating neural and cognitive processes. The core of their proposal is to conceive of computational explanations in cognitive neuroscience as a subspecies (...) of mechanistic explanations. This paper identifies several challenges facing their mechanistic account and sketches an alternative way of thinking about the epistemic roles of computational approaches used in the study of brain and cognition. Drawing on examples from both low-level and systems-level computational neuroscience, I argue that at least some computational explanations of neural and cognitive processes are partially independent from mechanistic constraints. (shrink)

Current debates about the integration of traditional and academic ecological knowledge struggle with a dilemma of division and assimilation. On the one hand, the emphasis on differences between traditional and academic perspectives has been criticized as creating an artificial divide that brands TEK as “non-scientific” and contributes to its marginalization. On the other hand, there has been increased concern about inadequate assimilation of Indigenous and other traditional perspectives into scientific practices that disregards the holistic nature and values of TEK. The (...) aim of this article is to develop a practice-based account of the epistemic relations between TEK and AEK that avoids both horns of the dilemma. While relations between TEK and AEK are often described in terms of the “holistic” nature of the former and the “mechanistic” character of the latter, we argue that a simple holism–mechanism divide misrepresents the epistemic resources of both TEK and AEK. Based on the literature on mechanistic explanations in philosophy of science, we argue that holders of TEK are perfectly capable of identifying mechanisms that underlie ecological phenomena while AEK often relies on non-mechanistic strategies of dealing with ecological complexity. Instead of generic characterizations of knowledge systems as either mechanistic or holistic, we propose to approach epistemic relations between knowledge systems by analyzing their heuristics in practice. (shrink)

This paper considers the way mathematical and computational models are used in network neuroscience to deliver mechanistic explanations. Two case studies are considered: Recent work on klinotaxis by Caenorhabditis elegans, and a longstanding research effort on the network basis of schizophrenia in humans. These case studies illustrate the various ways in which network, simulation and dynamical models contribute to the aim of representing and understanding network mechanisms in the brain, and thus, of delivering mechanistic explanations. After outlining this mechanistic construal (...) of network neuroscience, two concerns are addressed. In response to the concern that functional network models are non-explanatory, it is argued that functional network models are in fact explanatory mechanism sketches. In response to the concern that models which emphasize a network’s organization over its composition do not explain mechanistically, it is argued that this emphasis is both appropriate and consistent with the principles of mechanistic explanation. What emerges is an improved understanding of the ways in which mathematical and computational models are deployed in network neuroscience, as well as an improved conception of mechanistic explanation in general. (shrink)

Life scientists increasingly rely upon abstraction-based modeling and reasoning strategies for understanding biological phenomena. We introduce the notion of constraint-based reasoning as a fruitful tool for conceptualizing some of these developments. One important role of mathematical abstractions is to impose formal constraints on a search space for possible hypotheses and thereby guide the search for plausible causal models. Formal constraints are, however, not only tools for biological explanations but can be explanatory by virtue of clarifying general dependency-relations and patterning between (...) functions and structures. We describe such situations as constraint-based explanations and argue that these differ from mechanistic strategies in important respects. While mechanistic explanations emphasize change-relating causal features, constraint-based explanations emphasize formal dependencies and generic organizational features that are relatively independent of lower-level changes in causal details. Our distinction between mechanistic and constraint-based explanations is pragmatically motivated by the wish to understand scientific practice. We contend that delineating the affordances and assumptions of different explanatory questions and strategies helps to clarify tensions between diverging scientific practices and the innovative potentials in their combination. Moreover, we show how constraint-based explanation integrates several features shared by otherwise different philosophical accounts of abstract explanatory strategies in biology. (shrink)

Neuroscience constrains psychology, but stating these constraints with precision is not simple. Here I consider whether mechanistic analysis provides a useful way to integrate models of cognitive and neural structure. Recent evidence suggests that cognitive systems map onto overlapping, distributed networks of brain regions. These highly entangled networks often depart from stereotypical mechanistic behaviors. While this casts doubt on the prospects for classical mechanistic integration of psychology and neuroscience, I argue that it does not impugn a realistic interpretation of either (...) type of model. Cognitive and neural models may depict different, but equally real, causal structures within the mind/brain. (shrink)

Medical explanations have often been thought on the model of biological ones and are frequently defined as mechanistic explanations of a biological dysfunction. In this paper, I argue that topological explanations, which have been described in ecology or in cognitive sciences, can also be found in medicine and I discuss the relationships between mechanistic and topological explanations in medicine, through the example of network medicine and medical genetics. Network medicine is a recent discipline that relies on the analysis of various (...) disease networks in order to find organizing principles in disease explanation. My aim is to show how topological explanations in network medicine can help solving the conceptual issues that pure mechanistic explanations of the genetics of disease are currently facing, namely the crisis of the concept of genetic disease, the progressive geneticization of diseases and the dissolution of the distinction between monogenic and polygenic diseases. However, I will also argue that topological explanations should not be considered as independent and radically different from mechanistic explanations for at least two reasons. First, in network medicine, topological explanations depend on and use mechanistic information. Second, they leave out some missing gaps in disease explanation that require, in turn, the development of new mechanistic explanations. Finally, I will insist on the specific contribution of topological explanations in medicine: they push us to develop an explanation of disease in general, instead of focusing on single explanations of individual diseases. This last point may have major consequences for biomedical research. (shrink)