PubMed · 9847765
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B McMahon. Calm down.. https://doi.org/10.7748/ns.13.1.18.s33
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The Nash equilibrium, the main solution concept in analytical game theory, cannot make precise predictions about the outcome of repeated mixed-motive games. Nor can it tell us much about the dynamics by which a population of players moves from one equilibrium to another. These limitations, along with concerns about the cognitive demands of forward-looking rationality, have motivated efforts to explore backward-looking alternatives to analytical game theory. Most of the effort has been invested in evolutionary models of population dynamics. We shift attention to a learning-theoretic alternative. Computational experiments with adaptive agents identify a fundamental solution concept for social dilemmas--stochastic collusion--based on a random walk from a self-limiting noncooperative equilibrium into a self-reinforcing cooperative equilibrium. However, we show that this solution is viable only within a narrow range of aspiration levels. Below the lower threshold, agents are pulled into a deficient equilibrium that is a stronger attractor than mutual cooperation. Above the upper threshold, agents are dissatisfied with mutual cooperation. Aspirations that adapt with experience (producing habituation to stimuli) do not gravitate into the window of viability; rather, they are the worst of both worlds. Habituation destabilizes cooperation and stabilizes defection. Results from the two-person problem suggest that applications to multiplex and embedded relationships will yield unexpected insights into the global dynamics of cooperation in social dilemmas.
The fragile X syndrome is caused by an unstable CGG repeat sequence in the 5' untranslated region of the X-linked, FMR1 gene. When the number of repeats exceeds 200, the region is hypermethylated and the gene is silenced. The lack of the protein produced by the FMR1 gene, FMRP, causes the fragile X syndrome. Recent evidence suggests that FMR1 alleles with unmethylated long repeat tracks (40-200 repeats) may cause a specific somatic phenotype in women, premature ovarian failure, and may cause variation in the levels of FMR1 mRNA and FMRP. Because FMR1 is known to be involved in the regulation of subset of genes expressed in the brain, we investigated the variation in cognitive and/or behavioral performance among carriers of high repeat alleles. Specifically, we administered cognitive, behavioral, and adaptive performance tests to children identified with high repeat alleles who attended special education classes in Atlanta, Georgia public schools and to those with < 40 repeats drawn from the same population. Overall, we found no significant effect of repeat size and the psychometric measures in our test battery after adjustment for multiple comparisons. All scales were found to be within 1 SD standard deviation of the mean. We did find an intriguing, albeit marginally statistically significant, association in the cognitive profile among males and not females, consistent with an X-linked effect. After adjusting for the overall cognitive abilities score, Verbal Ability scores decreased and Nonverbal Reasoning scores increased with repeat number to a greater extent in males than females. Spatial Ability scores were not associated with repeat number.
The advantages of agent-based modeling for a general theory of intelligence at the individual and social level are emphasized over other existing approaches mainly relying on rationality theories. As was pointed out during the National Academy of Sciences Sackler Colloquium session "Implications of Agent-Based Modeling for Understanding Human Rationality and Learning," held in October 2001, properties of social intelligent agents include adaptability and learning capacity, as well as the capacity to produce and employ artifacts and manipulate symbols.