“…More broadly, our approach has identied a method for generating testable hypotheses in the space of developmental bioelectricity, which has implications for birth defects, traumatic injury, and cancer. 57,[105][106][107] Future work will incorporate this kind of workow into machine science pipelines, and empirically test the creative products of exploring the structures of concepts among diverse elds of inquiry. It is clear however that this approach in exploring the latent space around existing scientic literature extends far beyond bioelectricity and can be applied to numerous domains.…”
Artificial intelligence is a powerful tool that could be deployed to accelerate the scientific enterprise. Here we address a major unmet need: use of existing scientific literature to generate novel...
“…More broadly, our approach has identied a method for generating testable hypotheses in the space of developmental bioelectricity, which has implications for birth defects, traumatic injury, and cancer. 57,[105][106][107] Future work will incorporate this kind of workow into machine science pipelines, and empirically test the creative products of exploring the structures of concepts among diverse elds of inquiry. It is clear however that this approach in exploring the latent space around existing scientic literature extends far beyond bioelectricity and can be applied to numerous domains.…”
Artificial intelligence is a powerful tool that could be deployed to accelerate the scientific enterprise. Here we address a major unmet need: use of existing scientific literature to generate novel...
“…to the rat hosts in which we can implant them. The lessons we learn will likely be actionable for making new kinds of truly bio-inspired AI architectures [178], and also help design strategies for regenerative biomedicine that target how cells and tissues interpret the interventions we provide in the form of biochemical and bioelectrical stimuli [101,179,180].…”
Many studies of memory focus on the material substrate in which data can be stored and reliably read out. Here, I focus on the complementary aspects: the need for agents to dynamically re-interpret and modify memories to suit their ever-changing selves and environment. Using examples from developmental biology, evolution, and synthetic bioengineering, in addition to neuroscience, I propose that a perspective on memory as preserving salience, not fidelity, is applicable to many phenomena on scales from cells to societies. I focus on continuous commitment to confabulation, from the molecular to the behavioral levels, as the answer to the persistence paradox as it applies to individuals and whole lineages. I also speculate that a substrate-independent, processual view of life and mind suggests that memories, as patterns in the excitable medium of cognitive systems, could be seen as active agents in the sense-making process. I explore a view of life and agency as a diverse set of embodied Perspectives – nested agents who interpret each other’s and their own past messages and actions as best as they can (polycomputation). This synthesis suggests unifying symmetries across scales and disciplines, of relevance to research programs in diverse intelligence and the engineering of novel embodied minds.
“…This process requires multiple synapses and neurotransmitters for learning and plasticity to occur. These neurotransmitters and synapses essential for plasticity include gamma-aminobutyric acid (GABA), glutamate, acetylcholine, and dopamine [ 8 , 9 ]. Glutamine (excitatory) and GABA (inhibitory) ratios are balanced in normal individuals.…”
Cognitive impairment is among the most challenging characteristics of autism spectrum disorder (ASD). Although ASD is one of the common neurodevelopmental disorders, we are still behind in diagnosing and treating cognitive impairment in ASD. Cognitive impairment in ASD varies, meaning it could be at the sensory perception level to cognitive processing, learning, and memory. There are no diagnostic criteria for cognitive impairment that are specific to ASD. The leading causes of cognitive impairment in ASD could be neurological, immune, and gastrointestinal dysfunction. Immune dysfunction might lead to neuroinflammation, affecting neural connectivity, glutamate/gamma-aminobutyric acid (GABA) balance, and plasticity. The gut-brain axes are essential in the developing brain. Special retinal changes have recently been detected in ASD, which need clinical investigation to find their possible role in early diagnosis. Early intervention is crucial for ASD cognitive dysfunction. Due to the heterogeneity of the disease, the clinical manifestation of ASD makes it difficult for clinicians to develop gold-standard diagnostic and therapeutic criteria. We suggest a triad for diagnosis, which includes clinical tests for immune and gastrointestinal dysfunction biomarkers, clinical examination for the retina, and an objective neurocognitive evaluation for ASD, and to develop a treatment strategy involving these three aspects. Developing clear treatment criteria for cognitive impairment for ASD would improve the quality of life of ASD people and their caregivers and would delay or prevent dementia-related disorders in ASD people.
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