Processing quantities such as the number of objects in a set, size, spatial arrangement and time is an essential means of structuring the external world and preparing for action. The theory of magnitude suggests that number and time, among other continuous magnitudes, are linked by a common cortical metric, and their specialization develops from a single magnitude system. In order to investigate potentially shared neural mechanisms underlying numerosity and time processing, we used visual adaptation, a method which can reveal the existence of a dedicated processing system. We reasoned that cross-adaptation between numerosity and duration would concur with the existence of a common processing mechanism, whereas the absence of cross-adaptation would provide evidence against it. We conducted four experiments using a rapid adaptation protocol where participants adapted to either visual numerosity or visual duration and subsequently performed a numerosity or duration discrimination task. We found that adapting to a low numerosity altered the estimation of the reference numerosity by an average of 5 dots, compared to adapting to a high numerosity. Similarly, adapting to a short duration altered the estimation of the reference duration by an average of 43 msec, compared to adapting to a long duration. In the cross-dimensional adaptation conditions, duration adaptation altered numerosity estimation by an average of 1 dot, whereas there was not sufficient evidence to either support or reject the effect of numerosity adaptation on duration judgments. These results highlight that there are partially overlapping neural mechanisms which are dedicated for processing both numerosity and time.
Structural brain abnormalities and cognitive deficits have been reported in patients with schizophrenia and to a lesser extent in their first-degree relatives (FDRs). Here we investigated whether brain abnormalities in nonpsychotic relatives differ per type of FDR and how these abnormalities are related to intelligent quotient (IQ). Nine hundred eighty individuals from 5 schizophrenia family cohorts (330 FDRs, 432 controls, 218 patients) were included. Effect sizes were calculated to compare brain measures of FDRs and patients with controls, and between each type of FDR. Analyses were repeated with a correction for IQ, having a nonpsychotic diagnosis, and intracranial volume (ICV). FDRs had significantly smaller ICV, surface area, total brain, cortical gray matter, cerebral white matter, cerebellar gray and white matter, thalamus, putamen, amygdala, and accumbens volumes as compared with controls (ds < −0.19, q < 0.05 corrected). Offspring showed the largest effect sizes relative to the other FDRs; however, none of the effects in the different relative types survived correction for multiple comparisons. After IQ correction, all effects disappeared in the FDRs after correction for multiple comparisons. The findings in FDRs were not explained by having a nonpsychotic disorder and were only partly explained by ICV. FDRs show brain abnormalities that are strongly covarying with IQ. On the basis of consistent evidence of genetic overlap between schizophrenia, IQ, and brain measures, we suggest that the brain abnormalities in FDRs are at least partly explained by genes predisposing to both schizophrenia risk and IQ.
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