Gene Expression and its Discontents: Developmental disorders as dysfunctions of epigenetic cognition

Systems biology presently suffers the same mereological and sufficiency fallacies that haunt neural network models of high order cognition. Shifting perspective from the massively parallel space of gene matrix interactions to the grammar/syntax of the time series of expressed phenotypes using a cognitive paradigm permits import of techniques from statistical physics via the homology between information source uncertainty and free energy density. This produces a broad spectrum of possible statistical models of development and its pathologies in which epigenetic regulation and the effects of embedding environment are analogous to a tunable enzyme catalyst. A cognitive paradigm naturally incorporates memory, leading directly to models of epigenetic inheritance, as affected by environmental exposures, in the largest sense. Understanding gene expression, development, and their dysfunctions will require data analysis tools considerably more sophisticated than the present crop of simplistic models abducted from neural network studies or stochastic chemical reaction theory

Darwin's Rainbow: Evolutionary radiation and the spectrum of consciousness

Evolution is littered with paraphyletic convergences: many roads lead to functional Romes. We propose here another example - an equivalence class structure factoring the broad realm of possible realizations of the Baars Global Workspace consciousness model. The construction suggests many different physiological systems can support rapidly shifting, sometimes highly tunable, temporary assemblages of interacting unconscious cognitive modules. The discovery implies various animal taxa exhibiting behaviors we broadly recognize as conscious are, in fact, simply expressing different forms of the same underlying phenomenon. Mathematically, we find much slower, and even multiple simultaneous, versions of the basic structure can operate over very long timescales, a kind of paraconsciousness often ascribed to group phenomena. The variety of possibilities, a veritable rainbow, suggests minds today may be only a small surviving fraction of ancient evolutionary radiations - bush phylogenies of consciousness and paraconsciousness. Under this scenario, the resulting diversity was subsequently pruned by selection and chance extinction. Though few traces of the radiation may be found in the direct fossil record, exaptations and vestiges are scattered across the living mind. Humans, for instance, display an uncommonly profound synergism between individual consciousness and their embedding cultural heritages, enabling efficient Lamarkian adaptation

Institutional Cognition

We generalize a recent mathematical analysis of Bernard Baars' model of human consciousness to explore analogous, but far more complicated, phenomena of institutional cognition. Individual consciousness is limited to a single, tunable, giant component of interacting cogntivie modules, instantiating a Global Workspace. Human institutions, by contrast, seem able to multitask, supporting several such giant components simultaneously, although their behavior remains constrained to a topology generated by cultural context and by the path-dependence inherent to organizational history. Surprisingly, such multitasking, while clearly limiting the phenomenon of inattentional blindness, does not eliminate it. This suggests that organizations (or machines) explicitly designed along these principles, while highly efficient at certain sets of tasks, would still be subject to analogs of the subtle failure patterns explored in Wallace (2005b, 2006). We compare and contrast our results with recent work on collective efficacy and collective consciousness

Without magic bullets: the biological basis for public health interventions against protein folding disorders

Protein folding disorders of aging like Alzheimer's and Parkinson's diseases currently present intractable medical challenges. 'Small molecule' interventions - drug treatments - often have, at best, palliative impact, failing to alter disease course. The design of individual or population level interventions will likely require a deeper understanding of protein folding and its regulation than currently provided by contemporary 'physics' or culture-bound medical magic bullet models. Here, a topological rate distortion analysis is applied to the problem of protein folding and regulation that is similar in spirit to Tlusty's (2010a) elegant exploration of the genetic code. The formalism produces large-scale, quasi-equilibrium 'resilience' states representing normal and pathological protein folding regulation under a cellular-level cognitive paradigm similar to that proposed by Atlan and Cohen (1998) for the immune system. Generalization to long times produces diffusion models of protein folding disorders in which epigenetic or life history factors determine the rate of onset of regulatory failure, in essence, a premature aging driven by familiar synergisms between disjunctions of resource allocation and need in the context of socially or physiologically toxic exposures and chronic powerlessness at individual and group scales. Application of an HPA axis model is made to recent observed differences in Alzheimer's onset rates in White and African American subpopulations as a function of an index of distress-proneness