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MIGLIOR ARTICOLO DEL MESE CON PRIMO AUTORE ITALIANO
Giacomo Tondo, Cecilia Boccalini, Emilia Giovanna Vanoli, Luca Presotto, Cristina Muscio, Valentina Ciullo, Nerisa Banaj, Federica Piras, Graziella Filippini, Pietro Tiraboschi, Fabrizio Tagliavini, Giovanni Battista Frisoni, Stefano F. Cappa, Gianfranco Spalletta, Daniela Perani.
Selezionato dal lettore: Dott. Lorenzo Fontanelli
MOTIVATION: Subjective Cognitive Decline is self-reported confusion or memory problems that have been happening more often or getting worse in the past months. On the other hands, patients with pre-Mild Cognitive Impairment (pre-MCI) exhibit mild functional changes, but their objective cognitive change is within normal range and does not meet MCI criteria. Little is still known about SCD and pre-MCI and their possible evolution to dementia.
In this multicenter study, Tondo and colleagues enrolled 105 patients with SCD and pre-MCI all of which underwent cognitive and neurobehavioral evaluation, FDG-PET, and, amyloid-PET. Moreover, authors correlated several neuropsychological and neuropsychiatric dimensions with different brain metabolism patterns.
In details, an high proportion of patients had neuropsychiatric symptoms, more than half had evidence of brain hypomethabolism and about one fifth had increased brain amyloid load. Executive and visuo-motor impairment correlated with hypometabolism in frontal, occipital cortices and basal ganglia; Memory impairment correlated with hypometabolism in temporo-parietal regions; and visuo-spatial impairment correlated with hypometabolism in fronto-parietal cortices.
This study is interesting because indicates that SCD and pre-MCI represent heterogeneous populations with different neuropsychological and neuroimaging findings leading to further studies of these very mild symptomatic patients, in order to better understand their risk of progression to dementia.
MIGLIOR ARTICOLO IN ASSOLUTO
Cheng-Ying Ho, Mohammad Salimian, Julia Hegert, Jennifer O’Brien, Sun Gyeong Choi, Heather Ames, Meaghan Morris, John C. Papadimitriou, Joseph Mininni, Peter Niehaus, Allen Burke, Leyla Canbeldek, Jonathan Jacobs, Autumn LaRocque, Kavi Patel, Kathryn Rice, Ling Li, Robert Johnson, Alexandra LeFevre, Thomas Blanchard, CiaraM. Shaver, Ann Moyer, Cinthia Drachenberg
JAMA Neurol. doi: 10.1001/jamaneurol.2022.0154 Published online on April 11, 2022.
Selezionato dal lettore: Dott.ssa Silvy Pilotto
Motivation: Olfactory tract dysfunction is a common symptom in SARS-CoV2 infection even in the early stages of the disease and reported in more than 10% of patients. Although in most cases the symptom tends to resolve spontaneously, a proportion of patients refers the persistence of olfactory impairment even beyond one year after infection.
The exact pathophysiological mechanism underling olfactory impairment associated with SARS-CoV2 infection is still obscure although the two main pivotal hypotheses point on direct cellular virus damage or on a secondary mechanism of inflammation against olfactory cells.
This study represents the first attempt at investigating ultrastructural alterations of the olfactory bulb and olfactory tract in patients with COVID-19. It consists of a multicenter postmortem cohort study that included deceased patients with COVID-19 and olfactory impairment and related control subjects matched for age and disease severity. Ultrastructural and histopathological analysis were performed on olfactory tissues collected from 23 cases and 14 controls from April 7, 2020, to September 11, 2021.
Tissue examinations demonstrate the presence of axonal disruptions and losses, as well as microvascular changes in cases but not in controls. Furthermore, results suggest an association between pathological alterations of the olfactory tract and severity of olfactory symptoms reported ante mortem. However, ultrastructural as well as histopathologic findings do not appear to be associated with severity and duration of infection nor with the presence of virus in the tissues examined. Based on these findings, pathophysiological alterations seem to be caused more by a secondary inflammatory mechanism rather than a direct viral action. Such considerations could have important implications in the therapeutic field in patients with COVID-19 and severe olfactory dysfunction.