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A growing interest in studying the impact of brain asymmetry on physiological markers and cognition in people with Parkinson's disease (PwPD) recently emerged. The aim of this study was to test the impact of striatal denervation asymmetry on brain markers such as ceramides accumulation (ng/ml), as well as its impact on cognitive performances in early PwPD. We analysed data from 329 PwPD patients at the beginning of the disease (mean 6.9 months after diagnosis) (72 left-asymmetric, 83 right-asymmetric and 174 symmetric PwPD) and 167 healthy controls. Asymmetry was based on the difference in putamen denervation greater than 20%. Patients with genetic mutations were excluded. We performed generalized linear mixed models introducing the amount of cerebrospinal fluid ceramides (ng/ml) and cognitive functions as discriminating factors. Finally, Spearman correlations were used to highlight the relationship between cognition and cerebrospinal fluid ceramides on the whole pathological group and within each sub-group, as a function of striatal denervation asymmetry. First, a reduced concentration of ceramide (C18:0 CER) in the symmetrical group compared to the asymmetrical group and the control group was observed. More specifically left denervation predominant PwPD had significantly more ceramides (C22:0 CER) than the right and controls. Second, poorer cognitive performance for the symmetric group compared to the asymmetric and control groups was reported. Overall, positive correlations between cognition and ceramides (C18:0, C22:0 CER) was observed. Conversely, glucosylceramide correlation (C22:0 GlcCer) showed a negative link with cognition. This study shows that asymmetry of striatal degeneration in early Parkinson's disease is accompanied by metabolic variations related to cognitive processes.

Neuropsychological deficits and brain damage following SARS-CoV-2 infection are not well understood. 110 patients, with either severe, moderate or mild disease in the acute phase underwent neuropsychological and olfactory tests, as well as completed psychiatric and respiratory questionnaires at 223 ± 42 days post-infection. Additionally, a subgroup of 50 patients underwent functional magnetic resonance imaging. Patients in the severe group displayed poorer verbal episodic memory performances, and moderate patients had reduced mental flexibility. Neuroimaging revealed patterns of hypo and hyper functional connectivity in severe patients, while only hyperconnectivity patterns were observed for moderate. The default mode, somatosensory, dorsal attention and cerebellar networks were implicated. Partial least squares correlations analysis confirmed specific association between memory performances and brain functional connectivity. The severity of the infection in the acute phase is a predictor of neuropsychological post-COVID syndrome. SARS-CoV-2 infection causes long-term memory and executive dysfunctions, related to largescale functional brain connectivity alterations.

This meta-analysis was conducted to quantify the risk of patients exhibiting cognitive deficits in the acute phase of COVID-19 at the time of the first variants (i.e., before the vaccine) and quantify the potential vulnerability of older patients and those who experienced more severe respiratory symptoms. To this end, we searched the LitCovid and EMBASE platforms for articles, including preprints, and included all studies (n = 48) that featured a measurement of cognition, which encompassed 2233 cases of COVID-19. Of these, 28 studies reported scores on global cognitive efficiency scales administered in the acute phase of COVID-19 (up to 3 months after infection). We were able to perform a meta-analysis of proportions on 24 articles (Npatients = 943), and a logistic regression on 18 articles (Npatients = 518). The meta-analysis for proportion indicated that 52.31% of patients with COVID-19 exhibited cognitive deficits in the acute phase. This high percentage, however, has to be interpreted taking in consideration the fact that the majority of patients were hospitalized, and some presented neurological complications, such as encephalopathy. A bootstrap procedure with random resampling revealed that an age of 59 was the threshold at which one would be more prone to present cognitive deficits. However, the severity of respiratory symptoms did not influence the scores on a global cognitive efficiency scale. Overall, our results indicated that neuropsychological deficits were a major consequence of the acute phase of the first forms of COVID-19.