Patients with Alzheimer's disease (AD) often exhibit motion processing deficits. It is unclear whether the localization of moving objectsa perceptual process tightly linked to motionis impaired or intact in AD. In this study, we used the phenomenon of illusory shift of position induced by motion as a behavioural paradigm to probe how the spatial representation differs between AD patients and healthy elderly controls. We measured the magnitudes of motion-induced position shift in a group of AD participants (N = 24) and age-matched elderly observers (N = 24). We found that AD patients showed weakened position mis-localization, but only for motion stimuli of slow speeds. For fast motion, the position mis-localization did not differ significantly between groups. Furthermore, we showed that the magnitudes of position mis-localization can predict the severity of AD; that is, patients with more severe symptoms had less preserved position mis-localization. Our results suggest that AD pathology impacts not only motion processing per se, but also the perceptual process related to motion such as the localization of moving objects.
Objects
Carotid atherosclerotic plaques are the manifestation of atherosclerosis in the carotid arteries and can significantly increase the incidence of cerebrovascular disease. Macrophages and smooth muscle cells are crucial for their development. Our research aimed to reveal the mechanism of carotid atherosclerotic plaque formation.
Methods
The collected carotid plaques were processed to extract RNA and create a DNA library. After completing these steps, Single-nucleus RNA Sequencing analysis was performed using R language to analyze cell subpopulations. KEGG pathway, cellular communication, and the proposed time-series analysis were performed for differential genes.
Results
we performed single-cell nuclear sequencing of the carotid plaque tissue and identified 11 cell types, and the macrophages were divided into five different macrophage subpopulations. The macrophages and smooth muscle cells in the patients with symptomatic carotid atherosclerotic plaques caused intraplaque cell death via the mitochondrial autophagic pathway, resulting in plaque instability and rupture, which in turn led to clinical cardiovascular and cerebrovascular events.
Conclusions
The findings provide new insights into carotid atherosclerosis formation, and this may provide new directions for the prevention and treatment of carotid atherosclerosis.
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