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Tassone, F.

Publications and source records attributed to Tassone, F..

2 recordsLinked to original sources

Preserved perception-action dissociation but altered visuomotor behaviours in healthy aging.

The two visual pathways hypothesis posits distinct brain systems for vision-for-perception and vision-for-action. While this dissociation is well-established in younger adults, its integrity in healthy aging remains unclear. To address this, younger (n = 25, range: 18-25 years) and older adults (n = 25, range: 65-95 years) completed estimation and grasping tasks in two experiments. In Experiment 1, two rectangular objects with varying lengths (40 mm and 42 mm) were placed on the "far" and "close" surfaces of a Ponzo illusion. Despite age-related changes in grasping kinematics, the perception-action dissociation persisted. The Ponzo illusion influenced estimation such that objects placed on the "far" surface were perceived as longer. In contrast, grasping was not affected by the illusion, and even showed effect in the opposite direction, with larger apertures for objects placed on the "close" surface of the illusion. Experiment 2 tested whether this reversed effect was mediated by the surface size on which the object was placed, rather than perceived distance. To this end, we removed the illusory distance cues and varied only the background surface size ("big" versus "small"). While perceptual estimations were unaffected, surface size modulated grasping in both age groups, with a stronger effect in older adults. These findings indicate that the perception-action dissociation is preserved in aging, but older adults rely more on contextual cues during action, potentially reflecting compensatory mechanisms to maintain visuomotor performance.

neuroscience↗

Episignatures stratifying ADNP syndrome show modest correlation with phenotype

ADNP syndrome, also known as Helsmoortel-van Der Aa syndrome, is a neurodevelopmental condition associated with intellectual disability/developmental delay, autism spectrum disorder, and multiple medical comorbidities. ADNP syndrome is caused by mutations in the activity-dependent neuroprotective protein (ADNP). A recent study identified genome-wide DNA methylation changes in 22 individuals with ADNP syndrome, adding to the group of neurodevelopmental disorders with an epigenetic signature. This methylation signature segregated those with ADNP syndrome into two groups, based on the location of the mutations. Here, we conducted an independent study on 24 individuals with ADNP syndrome and replicated the existence of the two, mutation-dependent ADNP episignatures. To probe whether the two distinct episignatures correlate with clinical outcomes, we used deep behavioral and neurobiological data from two prospective cohorts of individuals with a genetic diagnosis of ADNP syndrome. We found limited phenotypic differences between the two ADNP groups, and no evidence that individuals with more widespread methylation changes are more severely affected. Also, in spite of the methylation changes, we observed no profound alterations in the blood transcriptome of individuals with ADNP syndrome. Our data warrant caution in harnessing methylation signatures in ADNP syndrome as a tool for clinical stratification, at least with regards to behavioral phenotypes.

developmental biology↗