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Background and AimsRecent studies suggest cognitive, emotional, and behavioral impairments occur in patients after SARS-CoV-2 infection. However, studies are limited to case reports or case series and, to our knowledge, few of them have control groups. This study aims to assess the prevalence of neuropsychological and neuropsychiatric impairment in patients after hospitalization.MethodsWe enrolled 29 COVID+ patients (M/F: 17/12; age 58.41 ± 10.00 years; education 11.07 ± 3.77 years, 2 left handers) who needed hospitalization but no IC, about 20 days post-dismission, and 29 COVID− healthy matched controls. Neuropsychological and neuropsychiatric assessments were conducted via teleneuropsychology using the following tests: MMSE, CPM47, RAVLT, CDT, Digit-Span Forward/Backward, Verbal fluencies; BDI-II, STAI. People with previous reported cognitive impairment and neurological or psychiatric conditions were excluded. Clinical and demographics were collected. Comparison between groups was conducted using parametric or non-parametric tests according to data distribution (T-test, Mann Withney-U test; Chi-square goodness of fit). Within COVID+ group, we also evaluated the correlation between the cognitive and behavioral assessment scores and clinical variables collected.ResultsAmong COVID+, 62% had at least one pathological test (vs. 13% in COVID−; p = 0.000) and significantly worst performances than COVID− in RAVLT learning (42.55 ± 10.44 vs. 47.9 ± 8.29, p = 0.035), RAVLT recall (8.79 ± 3.13 vs. 10.38 ± 2.19, p = 0.03), and recognition (13.69 ± 1.47 vs. 14.52 ± 0.63, p = 0.07). STAI II was higher in COVID− (32.69 ± 7.66 vs. 39.14 ± 7.7, p = 0.002). Chi-square on dichotomous values (normal/pathological) showed a significant difference between groups in Digit backward test (pathological 7/29 COVID+ vs. 0/29 COVID−; p = 0.005).ConclusionsPatients COVID+ assessed by teleneuropsychology showed a vulnerability in some memory and executive functions (working memory, learning, delayed recall, and recognition). Intriguingly, anxiety was higher in the control group. Our findings therefore confirm the impact of COVID-19 on cognition even in patients who did not need IC. Follow-up is needed to evaluate the evolution of COVID-19-related cognitive deficit.Clinical Trial Registration[ClinicalTrials.gov], identifier [NCT05143320].

Penetrance estimates of the leucine-rich repeat kinase 2 (LRRK2) p.G2019S mutation for PD vary widely (24%-100%). The p.G2019S penetrance in individuals of Ashkenazi Jewish ancestry has been estimated as 25%, adjusted for multiple covariates. It is unknown whether penetrance varies among different ethnic groups. The objective of this study was to estimate the penetrance of p.G2019S in individuals of non-Ashkenazi Jewish ancestry and compare penetrance between Ashkenazi Jews and non-Ashkenazi Jews to age 80.The kin-cohort method was used to estimate penetrance in 474 first-degree relatives of 69 non-Ashkenazi Jewish LRRK2 p.G2019S carrier probands at 8 sites from the Michael J. Fox LRRK2 Cohort Consortium. An identical validated family history interview was administered to assess age at onset of PD, current age, or age at death for relatives in different ethnic groups at each site. Neurological examination and LRRK2 genotype of relatives were included when available.Risk of PD in non-Ashkenazi Jewish relatives who carry a LRRK2 p.G2019S mutation was 42.5% (95% confidence interval [CI]: 26.3%-65.8%) to age 80, which is not significantly higher than the previously estimated 25% (95% CI: 16.7%-34.2%) in Ashkenazi Jewish carrier relatives. The penetrance of PD to age 80 in LRRK2 p.G2019S mutation carrier relatives was significantly higher than the noncarrier relatives, as seen in Ashkenazi Jewish relatives.The similar penetrance of LRRK2 p.G2019S estimated in Ashkenazi Jewish carriers and non-Ashkenazi Jewish carriers confirms that p.G2019S penetrance is 25% to 42.5% at age 80 in all populations analyzed. © 2017 International Parkinson and Movement Disorder Society.

This fMRI study deals with the neural correlates of spatial and objects working memory (SWM and OWM) in elderly subjects (ESs) and idiopathic Parkinson’s disease (IPD). Normal aging and IPD can be associated with a WM decline. In IPD population, some studies reported similar SWM and OWM deficits; others reported a greater SWM than OWM impairment. In the present fMRI research, we investigated whether compensated IPD patients and elderly subjects with comparable performance during the execution of SWM and OWM tasks would present differences in WM-related brain activations. We found that the two groups recruited a prevalent left frontoparietal network when performing the SWM task and a bilateral network during OWM task execution. More specifically, the ESs showed bilateral frontal and subcortical activations in SWM, at difference with the IPD patients who showed a strict left lateralized network, consistent with frontostriatal degeneration in IPD. The overall brain activation in the IPD group was more extended as number of voxels with respect to ESs, suggesting underlying compensatory mechanisms. In conclusion, notwithstanding comparable WM performance, the two groups showed consistencies and differences in the WM activated networks. The latter underline the compensatory processes of normal typical and pathological aging.