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Vergani, A. A.

Publications and source records attributed to Vergani, A. A..

2 recordsLinked to original sources
bioRxiv2024

Event-Related Potential Markers of Subject Cognitive Decline and Mild Cognitive Impairment during a sustained visuo-attentive task

Subjective cognitive decline (SCD), mild cognitive impairment (MCI), or severe Alzheimers disease stages are still lacking clear electrophysiological correlates. In 178 individuals (119 SCD, 40 MCI, and 19 healthy subjects (HS)), we analysed event-related potentials recorded during a sustained visual attention task, aiming to distinguish biomarkers associated with clinical conditions and task performance. We observed condition-specific anomalies in event-related potentials (ERPs) during visual encoding (P1/N1/P2) and decision-making (P300/P600/P900): SCD individuals showed attenuated dynamics compared to HS, while MCI individuals showed amplified dynamics, except for P300, which matched clinical severity. ERP features confirmed a non-monotonic trend, with MCI showing higher neural resource recruitment. Moreover, task performance correlated with condition-specific ERP gain and latencies across early and late ERP components. These findings enhanced the understanding of the neural mechanisms underlying cognitive decline in SCD and MCI and suggested potential biomarkers for early diagnosis and intervention. HighlightsO_LIIn encoding (P1/N1/P2) and decision (P600/P900) ERPs, SCD individuals showed attenuated dynamics compared to HS, while MCI individuals exhibited amplified dynamics compared to SCD. C_LIO_LIP300 dynamics matched clinical severity. C_LIO_LIMCI individuals demonstrated higher recruitment of neural resources, indicating a non-monotonic trend in ERP features between clinical conditions. C_LIO_LITask performance correlated with condition-specific gain and latencies across multiple ERP components. C_LI

neuroscience↗
bioRxiv2022

Dopamine depletion leads to pathological synchronization of distinct basal ganglia loops in the beta band

Motor symptoms of Parkinsons Disease (PD) are associated with dopamine deficits and pathological oscillation of basal ganglia (BG) neurons in the {beta} range ([12-30] Hz). However, how the dopamine depletion affects the oscillation dynamics of BG nuclei is still unclear. With a spiking neurons model, we here captured the features of BG nuclei interactions leading to oscillations in dopamine-depleted condition. We found that both the loop between subthalamic nucleus and Globus Pallidus pars externa (GPe) and the loop between striatal fast spiking and medium spiny neurons and GPe displayed resonances in the {beta} range, and synchronized to a common {beta} frequency through interaction. Crucially, the synchronization depends on dopamine depletion: the two loops were largely independent for high levels of dopamine, but progressively synchronized as dopamine was depleted due to the increased strength of the striatal loop. Our results highlight the role of the interplay between the GPe-STN and the GPe-striatum loop in generating sustained {beta} oscillations in PD subjects, and explain how this interplay depends on the level of dopamine. This paves the way to the design of therapies specifically addressing the onset of pathological {beta} oscillations. Author summaryParkinsons Disease is associated to the death of neurons generating a particular neurotransmitter: the dopamine. Motor symptoms of PD, on the other hand, are known to be due to dysfunctions in a particular subcortical area of the brain, the BG network. In particular, the BG network develops pathological oscillations in a specific frequency range ({beta}: [12-30] Hz). What is unclear is how dopamine depletion leads to these oscillations. In this work we developed a BG network model and we found the actual reason for these abnormal oscillations is the synchronization of two loops within the network that are individually oscillating in the {beta} range. For healthy level of dopamine the two loops are decoupled and the oscillation power is low. When dopamine is depleted (as in PD) the two loops synchronize and originate the pathological oscillations associated with motor symptoms.

neuroscience↗