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1.
Alzheimers Dement (N Y) ; 8(1): e12348, 2022.
Article Dans Anglais | MEDLINE | ID: covidwho-2047953

Résumé

Introduction: Coronavirus disease 2019 (COVID-19) has caused >3.5 million deaths worldwide and affected >160 million people. At least twice as many have been infected but remained asymptomatic or minimally symptomatic. COVID-19 includes central nervous system manifestations mediated by inflammation and cerebrovascular, anoxic, and/or viral neurotoxicity mechanisms. More than one third of patients with COVID-19 develop neurologic problems during the acute phase of the illness, including loss of sense of smell or taste, seizures, and stroke. Damage or functional changes to the brain may result in chronic sequelae. The risk of incident cognitive and neuropsychiatric complications appears independent from the severity of the original pulmonary illness. It behooves the scientific and medical community to attempt to understand the molecular and/or systemic factors linking COVID-19 to neurologic illness, both short and long term. Methods: This article describes what is known so far in terms of links among COVID-19, the brain, neurological symptoms, and Alzheimer's disease (AD) and related dementias. We focus on risk factors and possible molecular, inflammatory, and viral mechanisms underlying neurological injury. We also provide a comprehensive description of the Alzheimer's Association Consortium on Chronic Neuropsychiatric Sequelae of SARS-CoV-2 infection (CNS SC2) harmonized methodology to address these questions using a worldwide network of researchers and institutions. Results: Successful harmonization of designs and methods was achieved through a consensus process initially fragmented by specific interest groups (epidemiology, clinical assessments, cognitive evaluation, biomarkers, and neuroimaging). Conclusions from subcommittees were presented to the whole group and discussed extensively. Presently data collection is ongoing at 19 sites in 12 countries representing Asia, Africa, the Americas, and Europe. Discussion: The Alzheimer's Association Global Consortium harmonized methodology is proposed as a model to study long-term neurocognitive sequelae of SARS-CoV-2 infection. Key Points: The following review describes what is known so far in terms of molecular and epidemiological links among COVID-19, the brain, neurological symptoms, and AD and related dementias (ADRD)The primary objective of this large-scale collaboration is to clarify the pathogenesis of ADRD and to advance our understanding of the impact of a neurotropic virus on the long-term risk of cognitive decline and other CNS sequelae. No available evidence supports the notion that cognitive impairment after SARS-CoV-2 infection is a form of dementia (ADRD or otherwise). The longitudinal methodologies espoused by the consortium are intended to provide data to answer this question as clearly as possible controlling for possible confounders. Our specific hypothesis is that SARS-CoV-2 triggers ADRD-like pathology following the extended olfactory cortical network (EOCN) in older individuals with specific genetic susceptibility.The proposed harmonization strategies and flexible study designs offer the possibility to include large samples of under-represented racial and ethnic groups, creating a rich set of harmonized cohorts for future studies of the pathophysiology, determinants, long-term consequences, and trends in cognitive aging, ADRD, and vascular disease.We provide a framework for current and future studies to be carried out within the Consortium. and offers a "green paper" to the research community with a very broad, global base of support, on tools suitable for low- and middle-income countries aimed to compare and combine future longitudinal data on the topic.The Consortium proposes a combination of design and statistical methods as a means of approaching causal inference of the COVID-19 neuropsychiatric sequelae. We expect that deep phenotyping of neuropsychiatric sequelae may provide a series of candidate syndromes with phenomenological and biological characterization that can be further explored. By generating high-quality harmonized data across sites we aim to capture both descriptive and, where possible, causal associations.

2.
Alzheimer's & Dementia ; 16(S6):e047721, 2020.
Article Dans Anglais | Wiley | ID: covidwho-959104

Résumé

Abstract Background The pandemic of SARS-CoV-2 is focusing all energies on the impact on survival of affected individuals, treatment and prevention, but increasingly attention is focusing on its enduring consequences. We established a global consortium to study a longitudinal representative cohort of individuals, to characterize neurological and neuropsychiatric sequalae from direct viral, immune-, vascular- or accelerated neurodegenerative injury to the central nervous system (CNS). Method We propose to characterize the neurobehavioral phenomenology associated with SARS-CoV-2 in a large, multinational, longitudinal cohort of post COVID-19 infection patients following three sampling strategies: 1) Opportunity sample of patients discharged after hospital admission for COVID-19 related symptoms. 2) A stratified random sample from COVID-19 testing registries (including asymptomatic and negative participants). 3) Ascertaining COVID-19 exposure (antibody) status in ongoing longitudinal, community-based cohort studies that are already collecting biosamples, cognitive, behavioral and neuroimaging data. We will obtain core data within 6 months of discharge or testing. Core characterization will include interviews with the Schedules of Clinical Assessment in Neuropsychiatry (SCAN), neurological exams, emotional reactivity scales and a neurocognitive assessment. Wherever feasible, we will also collect neuroimaging, biosamples and genetic data. Longitudinal follow up will be conducted at 9 and 18 months of the initial evaluation. An mHealth keeping-in-touch process will be set up to minimize attrition rates. The population cohorts provide a large, unbiased, normative and validation sample, albeit with more heterogenous outcome ascertainment. They also permit examination of pre- and post-COVID trends in symptoms and biomarkers. Since some ethnic groups, as well as in individuals with blood type A, are at higher risk of COVID-19 infection and death, a role of genetics in determining susceptibility to infection and poor outcomes seems well supported. We will collect genome-wide genotypes from our cohort individuals to address the role of ancestry and genetic variation on susceptibility to neuropsychiatric sequelae. High rates of mutation in COVID-19 strongly suggest that viral infectivity, including neurotropism, may not be uniform across countries affected by the pandemic. Results Pending. Conclusion Our consortium is in a unique position to address the interaction between genetics (including ancestral DNA), and viral strain variation on CNS sequelae of SARS-CoV-2.

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