Cognitive sequealae of COVID-19 is not predicted by SARS-CoV-2 variants

Background: The long term sequelae of COVID-19 in older adults are only beginning to be clarified, and its predictors and underlying molecular mechanisms may shed light on the relationship between viral infections and Alzheimer\u27s disease and related dementia. Method: A prospective cohort of 874 older adult Amerindians from Argentina with COVID-19 illness confirmed by PCR of nasal swabs as well as controls, was established during the first year of the COVID-19 pandemic. We obtained data on the severity of the acute illness, as well as extensive neuropsychiatric and cognitive assessments, neurological exams (including quantitative hyposmia/anosmia), plasma for biomarkers and preliminary brain MRI images using the ADNI-3 protoco (n=300)l,and whole genome sequencing (n=300). Isolates from SARS-CoV-2 were obtained by the provincial Direction of Epidemiology and sequenced by the national Ministry of Health. Variants of interest/concern were allocated to each case on the basis of the prevalent community isolate at the time of confirmed positive PCR. A deep learning strategy was used to identify predictive factors of cognitive and clinical outcomes. Result: Four distinctive cognitive profiles were identified. Greater cognitive impairment was associated with older age (p = E-9), worse acute COVID-19 illness (p=0.008), unvaccinated status (p = E-7), and severity of anosmia (p = E-5). SARS-CoV-2 variant was associated with severity of acute illness ((p = E-6) but notably not with cognitive impairment. Preliminary analysis of genomic and brain imaging data will be presented. Conclusion: Our data strongly suggest that all SARS-CoV-2 variants of interest up to the omicron wave seem equally likely to result in cognitive impairment in older adults, modulated by the severity of the acute illness

The relationship between pm2.5 and health vulnerability in Argentina in 2010

Abstract: This study aimed to further explore the concept of health vulnerability in Argentina, including environmental pollution in 2010. To this end, we developed a geo-referenced database of PM2.5 concentrations and emissions data from the national emissions inventory to analyze possible correlations with the demographic, activity, education, and health data from the 2010 national census. In addition, to provide a more complete picture of health vulnerability in Argentina, an extended index (SVI + PM2.5) was constructed and mapped, including PM concentration. We obtained data for annual PM2.5 values emissions and air concentrations in Argentina from public sources (GEEAAEIv3.0M for emissions and the Atmospheric Composition Analysis Group V5.GL.03 dataset for surface PM2.5). We evaluated health vulnerability using the “Sanitary Vulnerability Index” (SVI). PM2.5 emissions are concentrated in urban and intensive agricultural areas of Argentina. PM2.5 air concentrations were acceptable (≤10 µg/m3 ) in only 15% of the Argentinean territory. The newly developed SVI + PM2.5 index showed that exposure to particulate material significantly increases the vulnerability shown by SVI in almost all census blocks. These results indicate that the new SVI + PM2.5 index might help identify populations that are at risk because of social issues or air pollution

Service learning as a pedagogy during the pandemic : the UCA gives you a hand ’ project

Resumen: La Pontificia Universidad Católica Argentina (UCA) se ha propuesto articular y complementar la formación académica brindada a sus alumnos con una opción de vida auténtica, que los mueva a construir un mundo más justo dando respuestas a las demandas sociales de los sectores vulnerables de la sociedad. A partir de la pandemia ocasionada por el COVID-19, la UCA ha trabajado para dar respuesta a algunas de las nuevas problemáticas que hoy nos afectan. En esa línea se fueron desarrollando estrategias que nos permitieron continuar trabajando con la comunidad aún durante el período de aislamiento social, preventivo y obligatorio. En el marco del Programa ”UCA + Comunidad en época de pandemia” surge el proyecto “UCA te da la Mano”, realizado conjuntamente por el Departamento de Psicología de la Facultad de Psicología y Psicopedagogía y la Dirección de Compromiso Social y Extensión de la Pontificia Universidad Católica Argentina, el cual tiene el doble objetivo de brindar un espacio de reflexión y orientación para el personal de primera línea de respuesta y ser un espacio de aprendizaje para los alumnos de la carrera de psicología. Participan de ella, docentes, graduados y alumnos.Abstract: One of the main objectives of Pontificia Universidad Católica Argentina (UCA) is to articulate and complement the academic training provided to its studentswith an authentic lifestyle choice , that would encourage them to build a fairer world by responding to the specific social demands coming from vulnerable sectors of society. The university has thus worked to respond to some of the new problems that now affect us as a society due to the COVID-19 pandemic. As a result, strategies have been developed to allow us to continue working with the community even during this period of social, preventive and compulsory isolation. Within the framework of the program ‘UCA + Comunidad en época de pandemia’(UCA + Community in times of a pandemic), UCA has developed a project that we will discuss in this paper: ‘UCA te da la mano’(UCA gives you a hand). The project, was jointly carried out by the Department of Psychology of the Faculty of Psychology and Psychopedagogy and the Directorate of Social Commitment and Outreach of the UCA, and it had a dual objective: providing a space for reflection and orientation for first-line response personnel and becoming a learning space for psychology students

Olfactory dysfunction and chronic cognitive impairment following SARS-CoV-2 infection in a sample of older adults from the Andes mountains of Argentina

Abstract: Background: COVID-19 has affected more than 150 million people. The causal coronavirus, SARS-CoV-2 has infected twice as many individuals who have remained asymptomatic. COVID-19 includes central nervous system (CNS) manifestations and may result in chronic neuropsychiatric sequelae. Risk factors for COVID-19 sequelae overlap with those for Alzheimer’s disease (AD), particularly older age and ApoE4 status. The Alzheimer’s Association Consortium on Chronic Neuropsychiatric Sequelae of SARS-CoV-2 infection (CNS SC2) established harmonized definitions, ascertainment and assessment methodologies to evaluate and longitudinally follow up cohorts of older adults with variable exposure to COVID-19. We present preliminary data from CNS SC2 in a prospective cohort of 234 older adult Amerindians from Argentina. Method: Participants are ≥ 60 years recruited from the health registry of the Province of Jujuy containing all SARS-CoV-2 testing data (regardless of clinical status and of the result of the testing). We randomly invite older adults stratified by testing status regardless of symptom severity, a minimum of 3 months after clinical recovery (maximum 6 months); refusal to participate is <45%. Assessment includes interview with the Schedules for Clinical Assessment in Neuropsychiatry (SCAN) and Clinical Dementia Rating scale; neurocognitive assessment; emotional reactivity scale; and neurological assessment including semiquantitative olfactory function test, motor function, coordination and gait. We present here the results of olfactory testing and cognitive assessments. Result: We assessed 233 infected participants and 64 controls. Average duration of formal learning is 9.35 ± 2.6 years and mean age is 66.7 ± 5.13 years. Normative data for the local population were available for Word list, Corsi Blocks, Oral Trails and Five Digit Tests and were used to normalize Z-scores and categorize the sample in 3 groups: normal cognition (NC,44.6%); memory only impairment (MOI,21%); and multiple domain impairment (MDI,34.4%). Individuals with MDI presented severe alterations in short-term memory; semantic memory; naming; executive function and attention compared to NC or MO groups (Table 1). Severity of cognitive impairment was significantly correlated with severity of olfactory dysfunction (χ2 = 13.82; p= 0.003) but not severity of acute COVID-19. Conclusion: Older adults frequently suffer persistent cognitive impairment after recovery from SARS-CoV-2 infection; cognitive impairment is correlated with persistent anosmia

Olfactory dysfunction but not COVID-19 severity predicts severity of cognitive sequelae following SARS-CoV-2 infection in Amerindian older adults

Abstract Background: COVID-19 has affected more than 380 million people. Infections may result in long term sequelae, including neuropsychiatric symptoms. In older adults COVID-19 sequelae resemble early Alzheimer’s disease, and may share risk factors and blood biomarkers with it. The Alzheimer’s Association Consortium on Chronic Neuropsychiatric Sequelae of SARS-CoV-2 infection (CNS SC2) established harmonized definitions, ascertainment and assessment methodologies to evaluate and longitudinally follow up cohorts of older adults with exposure to COVID-19. We present one year data in a prospective cohort from Argentina. Method: Participants (n = 766) are older adults (≥60 years) recruited from the provincial health registry containing all SARS-CoV-2 testing data. We randomly invite older adults stratified by PCR COVID-19 testing status regardless of symptom severity, between 3 and 6 months after recovery. Assessment includes interview with the Schedules for Clinical Assessment in Neuropsychiatry (SCAN) and Clinical Dementia Rating scale (CDR); neurocognitive assessment; emotional reactivity scale; and neurological assessment including semiquantitative olfactory function test, motor function, coordination and gait. Result: We assessed 88.4% infected participants and 11.6 % controls. Education is 10.36 ± 5.6 years and age is 66.9 ± 6.14 years. Level of care during COVID-19 is described in Figure 1. Normalized cognitive Z-scores categorize the cohort in 3 groups with decreased performance compared to normal cognition: memory only impairment (Single-domain,11.7%); impairment in attention+executive function without memory impairment (Two-domain, 8.3%); and multiple domain impairment (Multiple domain,11.6%). Logistic regression showed that severity of anosmia, but not clinical status, significantly predicts cognitive impairment. No controls had olfactory dysfunction. Cognitive impairment is defined as Z-scores below (- 2) (Table 1). Clinical assessment with SCAN revealed functional memory impairment in two thirds of infected patients (CDR ≥ 1), which was severe in half of them. Phone-based follow up at 1 year revealed high adherence (4 participants declined). Five were deceased at follow up. Rates of re-infection (between 10 and 23%) were not affected by the vaccination schedule (Table 2). Conclusion: The longitudinal cohort had very high adherence. Persistent cognitive and functional impairment after SARS-CoV-2 infection is predicted by persistent anosmia but not by the severity of the initial COVID-19 disease

The complete mitochondrial and plastid genomes of Corallina chilensis (Corallinaceae, Rhodophyta) from Tomales Bay, California, USA

Genomic analysis of the marine alga Corallina chilensis from Tomales Bay, California, USA, resulted in the assembly of its complete mitogenome (GenBank accession number MK598844) and plastid genome (GenBank MK598845). The mitogenome is 25,895 bp in length and contains 50 genes. The plastid genome is 178,350 bp and contains 233 genes. The organellar genomes share a high-level of gene synteny to other Corallinales. Comparison of rbcL and cox1 gene sequences of C. chilensis from Tomales Bay reveals it is identical to three specimens from British Columbia, Canada and very similar to a specimen of C. chilensis from southern California. These genetic data confirm that C. chilensis is distributed in Pacific North America

Chronic neuropsychiatric sequelae of SARS‐CoV‐2: Protocol and methods from the Alzheimer's Association Global Consortium

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

Chronic neuropsychiatric sequelae of SARS‐CoV‐2: Protocol and methods from the Alzheimer's Association Global Consortium

Abstract 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