Alzheimer's risk factor; COVID-19; SARS-CoV-2; caregiver burden; delerium; longitudinal cohort; systemic inflammation; Caregivers/psychology; Communicable Disease Control; Humans; Alzheimer Disease/epidemiology; Alzheimer Disease/genetics; Cognitive Dysfunction; Alzheimer Disease; Caregivers; Epidemiology; Health Policy; Developmental Neuroscience; Neurology (clinical); Geriatrics and Gerontology; Cellular and Molecular Neuroscience; Psychiatry and Mental Health
Abstract :
[en] COVID-19 causes lasting neurological symptoms in some survivors. Like other infections, COVID-19 may increase risk of cognitive impairment. This perspective highlights four knowledge gaps about COVID-19 that need to be filled to avoid this possible health issue. The first is the need to identify the COVID-19 symptoms, genetic polymorphisms and treatment decisions associated with risk of cognitive impairment. The second is the absence of model systems in which to test hypotheses relating infection to cognition. The third is the need for consortia for studying both existing and new longitudinal cohorts in which to monitor long term consequences of COVID-19 infection. A final knowledge gap discussed is the impact of the isolation and lack of social services brought about by quarantine/lockdowns on people living with dementia and their caregivers. Research into these areas may lead to interventions that reduce the overall risk of cognitive decline for COVID-19 survivors.
Disciplines :
Neurology
Author, co-author :
Gordon, Marcia N; Dept of Translational Neuroscience, Michigan State University, 400 Monroe Ave NW, Grand Rapids, MI, 49503, USA
HENEKA, Michael ; Dept. of Neurodegenerative Disease and Geriatric Psychiatry/Neurology, University of Bonn Medical Center, Sigmund-Freud Str. 25, 53127 Bonn, Germany
Le Page, Lydia M; Departments of Physical Therapy and Rehabilitation Science, and Radiology and Biomedical Imaging, University of California, San Francisco, USA
Limberger, Christian; Graduate Program in Biological Sciences: Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil
Morgan, David ; Dept of Translational Neuroscience, Michigan State University, 400 Monroe Ave NW, Grand Rapids, MI, 49503, USA
Tenner, Andrea J; Molecular Biology and Biochemistry, Neurobiology and Behavior and Pathology and Laboratory Medicine, University of California, Irvine, USA
Terrando, Niccolò; Department of Anesthesiology, Cell Biology, and Immunology, Duke University Medical Center, Durham, NC, 27710, USA
Willette, Auriel A; Food Science and Human Nutrition, Iowa State University, Ames, IA, USA
Willette, Sara A; IAC Tracker Inc., Ames, IA, USA
External co-authors :
yes
Language :
English
Title :
Impact of COVID-19 on the Onset and Progression of Alzheimer's Disease and Related Dementias: A Roadmap for Future Research.
Publication date :
May 2022
Journal title :
Alzheimer's and Dementia: the Journal of the Alzheimer's Association
This manuscript was facilitated by the Alzheimer's Association International Society to Advance Alzheimer's Research and Treatment (ISTAART), through the Immunity and Neurodegeneration Professional Interest area (PIA). The views and opinions expressed by authors in this publication represent those of the authors and do not necessarily reflect those of the PIA membership, ISTAART or the Alzheimer's Association. AW was funded by Iowa State University, NIH R00 AG047282, and AARGD‐17‐529552. CL received a scholarship from Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) [131409/2020‐4]. NT was supported by the National Institutes of Health (NIH) grants R01 AG057525, R01 AG057525‐04S1, R21 AG055877‐01A1, R03 AG064260, 3P01‐AT009968‐01A1, and the Alzheimer's Association. AT is supported by NIA R01 AG060148 and U54 U54 AG054349. MNG is supported by NIH R01 AG062217 and the Spectrum Health‐MSU Alliance Corporation. DM is supported by R01 AG‐051500, R01AG070349, R44AG058330, and the MSU Foundation. LLP is supported by Supported by an Alzheimer's Association Research Fellowship, a BrightFocus postdoctoral fellowship award and R01AG064170.This manuscript was facilitated by the Alzheimer's Association International Society to Advance Alzheimer's Research and Treatment (ISTAART), through the Immunity and Neurodegeneration Professional Interest area (PIA). The views and opinions expressed by authors in this publication represent those of the authors and do not necessarily reflect those of the PIA membership, ISTAART or the Alzheimer's Association. AW was funded by Iowa State University, NIH R00 AG047282, and AARGD-17-529552. CL received a scholarship from Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) [131409/2020-4]. NT was supported by the National Institutes of Health (NIH) grants R01 AG057525, R01 AG057525-04S1, R21 AG055877-01A1, R03 AG064260, 3P01-AT009968-01A1, and the Alzheimer's Association. AT is supported by NIA R01 AG060148 and U54 U54 AG054349. MNG is supported by NIH R01 AG062217 and the Spectrum Health-MSU Alliance Corporation. DM is supported by R01 AG-051500, R01AG070349, R44AG058330, and the MSU Foundation. LLP is supported by Supported by an Alzheimer's Association Research Fellowship, a BrightFocus postdoctoral fellowship award and R01AG064170.
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