“…Fig. 10(From [51]). Growth of a GP module, based on the coincidence between an inner-flow and incoming stimuli.…”
Section: Methodsmentioning
confidence: 99%
“…When initiated in 1983, the Guided Propagation (GP) system implemented concept-cells named Event - Detectors ( EDs ), considered as potential targets for inner - flows of activity. The other main feature of this deterministic approach was the recruitment of new cells for growing the memory paths ending in EDs, in response to requests of a dynamic learning algorithm [51]. In this formalism, the direction/path taken by a given inner-flow depends on the occurrence of afferent stimuli, one after the other, hence the expression: “guided propagation”.…”
Background
Environmental factors can modify the expression of genes, including those involved in the metabolism of neurotransmitters. Accounting for a control role of monoamine neurotransmitters, the guided propagation (GP) memory model may contribute to investigate the consequences of neuromodulation impairments on development disorders such as autism. A prenatal transient excess of ‘monoamine oxidase A’ enzyme is assumed here to trigger persistent epigenetic regulations that would induce imbalanced metabolisms of synaptic monoamines. When imported into the ‘offline’ encoding cycles of a GP model, the consequent ‘serotoninergic noise’ leads to aberrant memory structures that can be linked with autism symptoms.ResultsIn computer experiments, different levels of uncoupling between representations of monoamines correlate with the amount of impaired GP modules, the severity of irrelevant connections, as well as network overgrowth. Two types of faulty connections are respectively assumed to underlie autism traits, namely repetitive behavior and perceptual oversensitivity. Besides computational modelling, a genetic family-tree shows how the autism sex-ratio can result from combinations of pharmacological and epigenetic features.ConclusionsThese results suggest that the current rise of autism is favored by three possible sources of biological masking: (1) during sleep, when cyclic variations of monoamines may undergo disrupted enzymatic activities; (2) across generations of ‘healthy carriers’ protected by the X-chromosome silencing and a specific genetic variant; (3) early in life, as long as the brain development draws on pools of neurons born when the transient enzymatic excess and its persistent epigenetic regulation overlapped, and as long as the B type of monoamine oxidase does not significantly impact dopamine. A disease-modifying therapy can be derived from this study, which involves relevant biomarkers to be first monitored over several months of clinical trial.Electronic supplementary materialThe online version of this article (10.1186/s12868-018-0477-1) contains supplementary material, which is available to authorized users.
“…Fig. 10(From [51]). Growth of a GP module, based on the coincidence between an inner-flow and incoming stimuli.…”
Section: Methodsmentioning
confidence: 99%
“…When initiated in 1983, the Guided Propagation (GP) system implemented concept-cells named Event - Detectors ( EDs ), considered as potential targets for inner - flows of activity. The other main feature of this deterministic approach was the recruitment of new cells for growing the memory paths ending in EDs, in response to requests of a dynamic learning algorithm [51]. In this formalism, the direction/path taken by a given inner-flow depends on the occurrence of afferent stimuli, one after the other, hence the expression: “guided propagation”.…”
Background
Environmental factors can modify the expression of genes, including those involved in the metabolism of neurotransmitters. Accounting for a control role of monoamine neurotransmitters, the guided propagation (GP) memory model may contribute to investigate the consequences of neuromodulation impairments on development disorders such as autism. A prenatal transient excess of ‘monoamine oxidase A’ enzyme is assumed here to trigger persistent epigenetic regulations that would induce imbalanced metabolisms of synaptic monoamines. When imported into the ‘offline’ encoding cycles of a GP model, the consequent ‘serotoninergic noise’ leads to aberrant memory structures that can be linked with autism symptoms.ResultsIn computer experiments, different levels of uncoupling between representations of monoamines correlate with the amount of impaired GP modules, the severity of irrelevant connections, as well as network overgrowth. Two types of faulty connections are respectively assumed to underlie autism traits, namely repetitive behavior and perceptual oversensitivity. Besides computational modelling, a genetic family-tree shows how the autism sex-ratio can result from combinations of pharmacological and epigenetic features.ConclusionsThese results suggest that the current rise of autism is favored by three possible sources of biological masking: (1) during sleep, when cyclic variations of monoamines may undergo disrupted enzymatic activities; (2) across generations of ‘healthy carriers’ protected by the X-chromosome silencing and a specific genetic variant; (3) early in life, as long as the brain development draws on pools of neurons born when the transient enzymatic excess and its persistent epigenetic regulation overlapped, and as long as the B type of monoamine oxidase does not significantly impact dopamine. A disease-modifying therapy can be derived from this study, which involves relevant biomarkers to be first monitored over several months of clinical trial.Electronic supplementary materialThe online version of this article (10.1186/s12868-018-0477-1) contains supplementary material, which is available to authorized users.
“…"Teenager"-cells would then form chains or neutral memory paths in active areas, made thus ready to receive new connections from series of unexpected stimuli at the time they occur. A differentiation episode would thus be restricted to new connections established along preformed memory paths, by following a coincidence-detection criterion [25].…”
Section: Gp Dynamic Learning In Questionmentioning
confidence: 99%
“…This option lessens the role of connection weights among learning actors; emphasis is set instead on the mechanisms that promote and guide the dynamic setting of neural structures. Mainly inspired by the brain spontaneous activity, the Guided Propagation (GP) model implements the continuous growth of memory paths ending in concept cells [25]. Thirdly, at the neuroanatomical level, significant data associate reward circuits with action-selection.…”
“…This type of learning is also called lifelong or never-ending (Beroule, 1988). For example, spam filtering and classification of news feeds with ever changing features are but a few useful applications of lifelong learning (Rennie, 2000;Sahami, Dumais, Heckerman, & Horvitz, 1998).…”
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