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The ability to organize and memorize the unfolding of events over time is a fundamental feature of cognition, which develops concurrently with the maturation of the brain. Nonetheless, how temporal processing evolves across the lifetime as well as the links with the underlying neural substrates remains unclear. Here, we intend to retrace the main developmental stages of brain structure, function, and cognition linked to the emergence of timing abilities. This neurodevelopmental perspective aims to untangle the puzzling trajectory of temporal processing aspects across the lifetime, paving the way to novel neuropsychological assessments and cognitive rehabilitation strategies. A new neurodevelopmental perspective of temporal processing aiming to untangle the puzzling trajectory of temporal processing's aspects throughout the lifetime. [ABSTRACT FROM AUTHOR]

Background: Alzheimer's disease is a neurodegenerative disorder associated with the abnormal deposition of pathological processes, such as amyloid-ß and tau, which produces nonlinear changes in the functional connectivity patterns between different brain regions across the Alzheimer's disease continuum. However, the mechanisms underlying these nonlinear changes remain largely unknown. Here, we address this question using a novel method based on temporal or delayed correlations and calculate new whole-brain functional networks to tackle these mechanisms. Methods: To assess our method, we evaluated 166 individuals from the ADNI database, including amyloid-beta negative and positive cognitively normal subjects, patients with mild cognitive impairment, and patients with Alzheimer's disease dementia. We used the clustering coefficient and the global efficiency to measure the functional network topology and assessed their relationship with amyloid and tau pathology measured by positron emission tomography, as well as cognitive performance using tests measuring memory, executive function, attention, and global cognition. Results: Our study found nonlinear changes in the global efficiency, but not in the clustering coefficient, showing that the nonlinear changes in functional connectivity are due to an altered ability of brain regions to communicate with each other through direct paths. These changes in global efficiency were most prominent in early disease stages. However, later stages of Alzheimer's disease were associated with widespread network disruptions characterized by changes in both network measures. The temporal delays required for the detection of these changes varied across the Alzheimer's disease continuum, with shorter delays necessary to detect changes in early stages and longer delays necessary to detect changes in late stages. Both global efficiency and clustering coefficient showed quadratic associations with pathological amyloid and tau burden as well as cognitive decline. Conclusions: This study suggests that global efficiency is a more sensitive indicator of network changes in Alzheimer's disease when compared to clustering coefficient. Both network properties were associated with pathology and cognitive performance, demonstrating their relevance in clinical settings. Our findings provide an insight into the mechanisms underlying nonlinear changes in functional network organization in Alzheimer's disease, suggesting that it is the lack of direct connections that drives these functional changes. [ABSTRACT FROM AUTHOR]

In a recent study on visual episodic memory (Desaunay, Clochon, et al., 2020), we have shown event‐related potentials (ERPs) differences associated with priming (150–300 msec), familiarity (350–470 msec), and recollection (600–700 msec), in young people with autism spectrum disorders (ASD) compared with typical development (TD). To go further into the study of the processes of storage and retrieval of the memory trace, we re‐analyzed Desaunay, Clochon, et al's data using time‐frequency analysis, that is, event‐related synchronization and desynchronization (ERS/ERD). This allows a decomposition of the spectral power within frequency bands associated with these ERPs. We focused both on the same time windows and the same regions of interest as previously published. We mainly identified, in ASD compared with TD, reduced ERS in low‐frequencies (delta, theta) in early time‐windows, and non‐significant differences in ERD in higher frequencies (alpha, beta1) in all time‐windows. Reduced ERS during recognition confirmed previously reported diminution of priming effects and difficulties in manipulation and retrieval of both semantic and episodic information. Conversely, preserved ERD corroborates a preservation of memory storage processes. These observations are consistent with a cognitive model of memory in ASD, that suggests difficulties in cognitive operations or executive demand at retrieval, subsequent to successful long‐term storage of information. Lay Summary: We assessed the EEG synchronization and desynchronization, during visual episodic recognition. We observed, in youth with Autism, reduced synchronization in low‐frequencies (delta, theta), suggesting reduced access to and manipulation of long‐term stored information. By contrast, non‐significant differences in desynchronization at higher frequencies (alpha, beta frequency bands), that support long‐term stored semantic and episodic information, suggested preserved memory traces. [ABSTRACT FROM AUTHOR]