Study aims to understand how SARS-CoV-2 affects the brain in the long term

To date, coronavirus disease 2019 (COVID-19), which occurs due to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has claimed more than 6.5 million lives in the world. Most people infected with SARS-CoV-2 remain asymptomatic or have mild to moderate symptoms; however, some people have severe symptoms that require hospitalization.

Study: Chronic neuropsychiatric sequelae of SARS-CoV-2: Protocol and Methods from the Alzheimer’s Association Global Consortium. Image Credit: Gorodenkoff /


In addition to the lungs, COVID-19 also affects the central nervous system (CNS) through anoxic mechanisms, viral neurotoxicity, inflammation, and cerebrovascular mechanisms. As a result, about a third of patients with COVID-19 develop different neurological problems, such as seizures, loss of smell or taste, and stroke.

The risk of developing neuropsychiatric or cognitive complications appears to be independent of the initial severe lung disease caused by COVID-19. However, a recent Translational research and clinical interventions The study formulated a method to identify molecular and systemic factors linking COVID-19 to short- and long-term neurological diseases.

About the study

The authors reviewed the existing literature in the current study and highlighted the documented links between SARS-CoV-2 infection, brain, neurological symptoms, Alzheimer’s disease (AD) and dementias. (SARD). Risk factors and possible viral, inflammatory and molecular pathways associated with COVID-19 were also discussed.

The current study has provided a better understanding of the Alzheimer’s Association Consortium on chronic neuropsychiatric sequelae of SARS-CoV-2 (CNS SC2) infection, which is extremely useful in addressing key neurological issues related to COVID. -19.

Many countries around the world, including Argentina, Austria, Australia, Chile, China, Canada, Germany, Greece, India, Netherlands, United States, Qatar, Thailand, Germany, the United Kingdom and Thailand participated in the study.

Data is collected continuously and more and more countries are joining the study. The main strength of this study is the inclusion of participants from diverse genetic backgrounds and socio-economic strata of society.

Using the global network, the researchers aimed to provide a scientific framework to characterize the neuropsychiatric and neurobehavioral phenomenology related to COVID-19 by designing harmonized, multinational and longitudinal cohorts of patients after recovery from COVID-19. Follow-up data is also recorded at 12 months, 24 months and beyond after the initial SARS-CoV-2 assessment.

The study cohort included both male and female participants aged 50 and older. Previous studies have indicated that most COVID-19 patients who required hospitalization were in this age group, making the cohort appropriate to assess how viral infection influences cognitive decline and dementia. For future meta-analyses and other studies, all consortium members have agreed to share data obtained using the CNS-SC2 methodology.

The present study used the semi-structured interview programs of the World Health Organization (WHO) for Clinical Assessment in Neuropsychiatry (SCAN) to assess psychopathology and neurological symptoms. In addition to the WHO SCAN, neuroimaging, emotional reactivity assessment and biomarker analysis data were obtained

Study results

The consortium proposed a combination of flexible experimental design and statistical data analysis to make inferences about the neuropsychiatric sequelae of COVID-19. Generating high-quality harmonized data would help better elucidate post-COVID-19 neuropsychiatric events. Moreover, in-depth phenotyping of neuropsychiatric sequelae could help identify a series of candidate syndromes with phenomenological and biological characterization, which could be further explored in future research.

No strong evidence supporting the incidence of cognitive impairment post-COVID-19 in the form of SARD or otherwise has been reported. Nonetheless, descriptive observations and, where possible, causal association have advanced understanding of post-COVID-19 neuropsychiatric manifestations.

Clinical assessments, biomarker tools, and imaging data allowed the authors to detect even minor differences in neurobehavioral after SARS-CoV-2 infection. The WHO SCAN technique has uncovered new phenomena or symptoms that had not previously been identified as common neurological events related to COVID-19. In general, structured and semi-structured interviews play an important role in neuropsychiatry.

It is important to minimize cultural biases, as they can influence the performance of the new method. Several studies have highlighted the role of culture in presenting bias in cognitive assessments in a culturally diverse sample. In this context, the consortium proposed that the harmonization of data is important, as well as the development of a better understanding of different capacities across cultures.

The impact of COVID-19 on olfactory, motor and cognitive functions was assessed by semi-quantitative neurological examination. Increased Aβ load was correlated with olfactory impairment in older people with amnesia. SARS-CoV-2 evades the olfactory bulb, which may be responsible for the incidence of anosmia in infected patients.

COVID-19 patients were found to be more susceptible to cognitive decline than controls. Additionally, a change in emotional behavior has been prominently observed in COVID-19 patients.


The proposed matching strategies and study design offered the opportunity to include large samples of underrepresented racial and ethnic groups. This should help determine pathophysiological factors, cognitive aging patterns, long-term consequences, ADRD and vascular disease in the future.

Journal reference:

  • DeErausquin, AG, Snyder, H., Brugha, TS, et al. (2022) Chronic Neuropsychiatric Sequelae of SARS-CoV-2: Protocol and Methods from the Alzheimer’s Association Global Consortium. Translational research and clinical interventions. 8(1). doi:10.1002/trc2.12348.

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