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1.
Int J Mol Sci ; 22(24)2021 Dec 19.
Article in English | MEDLINE | ID: covidwho-1580688

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) triggered the pandemic Coronavirus Disease 19 (COVID-19), causing millions of deaths. The elderly and those already living with comorbidity are likely to die after SARS-CoV-2 infection. People suffering from Alzheimer's disease (AD) have a higher risk of becoming infected, because they cannot easily follow health roles. Additionally, those suffering from dementia have a 40% higher risk of dying from COVID-19. Herein, we collected from Gene Expression Omnibus repository the brain samples of AD patients who died of COVID-19 (AD+COVID-19), AD without COVID-19 (AD), COVID-19 without AD (COVID-19) and control individuals. We inspected the transcriptomic and interactomic profiles by comparing the COVID-19 cohort against the control cohort and the AD cohort against the AD+COVID-19 cohort. SARS-CoV-2 in patients without AD mainly activated processes related to immune response and cell cycle. Conversely, 21 key nodes in the interactome are deregulated in AD. Interestingly, some of them are linked to beta-amyloid production and clearance. Thus, we inspected their role, along with their interactors, using the gene ontologies of the biological process that reveals their contribution in brain organization, immune response, oxidative stress and viral replication. We conclude that SARS-CoV-2 worsens the AD condition by increasing neurotoxicity, due to higher levels of beta-amyloid, inflammation and oxidative stress.


Subject(s)
Alzheimer Disease/genetics , COVID-19/complications , COVID-19/genetics , Alzheimer Disease/complications , Alzheimer Disease/virology , Amyloid beta-Peptides/metabolism , Brain/virology , COVID-19/physiopathology , Comorbidity/trends , Databases, Factual , Gene Expression/genetics , Gene Expression Profiling/methods , Humans , Inflammation/metabolism , Neurotoxicity Syndromes/metabolism , Oxidative Stress/physiology , Pandemics , SARS-CoV-2/metabolism , SARS-CoV-2/pathogenicity , Transcriptome/genetics
2.
J Alzheimers Dis ; 85(2): 729-744, 2022.
Article in English | MEDLINE | ID: covidwho-1518457

ABSTRACT

BACKGROUND: COVID-19 pandemic is a global crisis which results in millions of deaths and causes long-term neurological sequelae, such as Alzheimer's disease (AD). OBJECTIVE: We aimed to explore the interaction between COVID-19 and AD by integrating bioinformatics to find the biomarkers which lead to AD occurrence and development with COVID-19 and provide early intervention. METHODS: The differential expressed genes (DEGs) were found by GSE147507 and GSE132903, respectively. The common genes between COVID-19 and AD were identified. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein interactions (PPI) network analysis were carried out. Hub genes were found by cytoscape. A multivariate logistic regression model was constructed. NetworkAnalyst was used for the analysis of TF-gene interactions, TF-miRNA coregulatory network, and Protein-chemical Interactions. RESULTS: Forty common DEGs for AD and COVID-19 were found. GO and KEGG analysis indicated that the DEGs were enriched in the calcium signal pathway and other pathways. A PPI network was constructed, and 5 hub genes were identified (ITPR1, ITPR3, ITPKB, RAPGEF3, MFGE8). Four hub genes (ITPR1, ITPR3, ITPKB, RAPGEF3) which were considered as important factors in the development of AD that were affected by COVID-19 were shown by nomogram. Utilizing NetworkAnalyst, the interaction network of 4 hub genes and TF, miRNA, common AD risk genes, and known compounds is displayed, respectively. CONCLUSION: COVID-19 patients are at high risk of developing AD. Vaccination is required. Four hub genes can be considered as biomarkers for prediction and treatment of AD development caused by COVID-19. Compounds with neuroprotective effects can be used as adjuvant therapy for COVID-19 patients.


Subject(s)
Alzheimer Disease/genetics , COVID-19/virology , Protein Interaction Maps/genetics , SARS-CoV-2/pathogenicity , Alzheimer Disease/complications , Alzheimer Disease/metabolism , Alzheimer Disease/virology , Computational Biology/methods , Databases, Genetic , Gene Expression Profiling/methods , Humans , SARS-CoV-2/genetics
3.
Int J Mol Sci ; 22(14)2021 Jul 06.
Article in English | MEDLINE | ID: covidwho-1485149

ABSTRACT

Chronic neurodegenerative diseases are complex, and their pathogenesis is uncertain. Alzheimer's disease (AD) is a neurodegenerative brain alteration that is responsible for most dementia cases in the elderly. AD etiology is still uncertain; however, chronic neuroinflammation is a constant component of brain pathology. Infections have been associated with several neurological diseases and viruses of the Herpes family appear to be a probable cause of AD neurodegenerative alterations. Several different factors may contribute to the AD clinical progression. Exogeneous viruses or other microbes and environmental pollutants may directly induce neurodegeneration by activating brain inflammation. In this paper, we suggest that exogeneous brain insults may also activate retrotransposons and silent human endogenous retroviruses (HERVs). The initial inflammation of small brain areas induced by virus infections or other brain insults may activate HERV dis-regulation that contributes to neurodegenerative mechanisms. Chronic HERV activation in turn may cause progressive neurodegeneration that thereafter merges in cognitive impairment and dementia in genetically susceptible people. Specific treatment for exogenous end endogenous pathogens and decreasing pollutant exposure may show beneficial effect in early intervention protocol to prevent the progression of cognitive deterioration in the elderly.


Subject(s)
Alzheimer Disease/pathology , Alzheimer Disease/virology , Brain/pathology , Brain/virology , Endogenous Retroviruses/pathogenicity , Virus Diseases/pathology , Virus Diseases/virology , Animals , Cognition Disorders/pathology , Cognition Disorders/virology , Encephalitis/pathology , Encephalitis/virology , Humans
4.
Arch Virol ; 166(3): 733-753, 2021 Mar.
Article in English | MEDLINE | ID: covidwho-1064515

ABSTRACT

The chronic dysfunction of neuronal cells, both central and peripheral, a characteristic of neurological disorders, may be caused by irreversible damage and cell death. In 2016, more than 276 million cases of neurological disorders were reported worldwide. Moreover, neurological disorders are the second leading cause of death. Generally, the etiology of neurological diseases is not fully understood. Recent studies have related the onset of neurological disorders to viral infections, which may cause neurological symptoms or lead to immune responses that trigger these pathological signs. Currently, this relationship is mostly based on epidemiological data on infections and seroprevalence of patients who present with neurological disorders. The number of studies aiming to elucidate the mechanism of action by which viral infections may directly or indirectly contribute to the development of neurological disorders has been increasing over the years but these studies are still scarce. Comprehending the pathogenesis of these diseases and exploring novel theories may favor the development of new strategies for diagnosis and therapy in the future. Therefore, the objective of the present study was to review the main pieces of evidence for the relationship between viral infection and neurological disorders such as Alzheimer's disease, Parkinson's disease, Guillain-Barré syndrome, multiple sclerosis, and epilepsy. Viruses belonging to the families Herpesviridae, Orthomyxoviridae, Flaviviridae, and Retroviridae have been reported to be involved in one or more of these conditions. Also, neurological symptoms and the future impact of infection with SARS-CoV-2, a member of the family Coronaviridae that is responsible for the COVID-19 pandemic that started in late 2019, are reported and discussed.


Subject(s)
COVID-19/pathology , Nervous System Diseases/virology , Viral Tropism/physiology , Alzheimer Disease/virology , COVID-19/virology , Epilepsy/virology , Flaviviridae/metabolism , Guillain-Barre Syndrome/virology , Herpesviridae/metabolism , Humans , Multiple Sclerosis/virology , Nervous System Diseases/pathology , Orthomyxoviridae/metabolism , Parkinson Disease/virology , Retroviridae/metabolism , SARS-CoV-2/metabolism
5.
Alzheimers Dement ; 17(6): 1056-1065, 2021 Jun.
Article in English | MEDLINE | ID: covidwho-1008220

ABSTRACT

INTRODUCTION: The increasing evidence of SARS-CoV-2 impact on the central nervous system (CNS) raises key questions on its impact for risk of later life cognitive decline, Alzheimer's disease (AD), and other dementia. METHODS: The Alzheimer's Association and representatives from more than 30 countries-with technical guidance from the World Health Organization-have formed an international consortium to study the short-and long-term consequences of SARS-CoV-2 on the CNS-including the underlying biology that may contribute to AD and other dementias. This consortium will link teams from around the world covering more than 22 million COVID-19 cases to enroll two groups of individuals including people with disease, to be evaluated for follow-up evaluations at 6, 9, and 18 months, and people who are already enrolled in existing international research studies to add additional measures and markers of their underlying biology. CONCLUSIONS: The increasing evidence and understanding of SARS-CoV-2's impact on the CNS raises key questions on the impact for risk of later life cognitive decline, AD, and other dementia. This program of studies aims to better understand the long-term consequences that may impact the brain, cognition, and functioning-including the underlying biology that may contribute to AD and other dementias.


Subject(s)
Brain/virology , COVID-19/complications , Alzheimer Disease/virology , Cognitive Dysfunction/virology , Dementia/virology , Humans , SARS-CoV-2
6.
Med Sci Monit ; 26: e930340, 2020 Dec 16.
Article in English | MEDLINE | ID: covidwho-979224

ABSTRACT

Alterations in complex behavioral patterns during the extended period of the COVID-19 pandemic are predicted to promote a variety of psychiatric disease symptoms due to enforced social isolation and self-quarantine. Accordingly, multifaceted mental health problems will continue to increase, thereby creating a challenge for society and the health care system in general. Recent studies show that COVID-19 can directly or indirectly influence the central nervous system, potentially causing neurological pathologies such as Alzheimer disease and Parkinson disease. Thus, chronic COVID-19-related disease processes have the potential to cause serious mental illnesses, including depression, anxiety, and sleep disorders. Importantly, mental health problems can foster systemic changes in functionally-linked neuroendocrine conditions that heighten a person's susceptibility to COVID-19 infection. These altered defense mechanisms may include compromised "self-control" and "self-care", as well as a "lack of insight" into the danger posed by the virus. These consequences may have serious social impacts on the future of COVID-19 survivors. Compounding the functionally related issues of altered mental health parameters and viral susceptibility are the potential effects of compromised immunity on the establishment of functional herd immunity. Within this context, mental health takes on added importance, particularly in terms of the need to increase support for mental health research and community-based initiatives. Thus, COVID-19 infections continue to reveal mental health targets, a process we must now be prepared to deal with.


Subject(s)
COVID-19/complications , Mental Health , SARS-CoV-2/pathogenicity , Survivors/psychology , Alzheimer Disease/epidemiology , Alzheimer Disease/prevention & control , Alzheimer Disease/virology , Anxiety/epidemiology , Anxiety/prevention & control , Anxiety/psychology , COVID-19/epidemiology , COVID-19/psychology , Depression/epidemiology , Depression/prevention & control , Depression/psychology , Disease Susceptibility/psychology , Humans , Pandemics , Parkinson Disease/epidemiology , Parkinson Disease/prevention & control , Parkinson Disease/virology , Physical Distancing , Self Care/psychology , Self-Control/psychology , Social Isolation/psychology
7.
J Alzheimers Dis ; 77(2): 539-541, 2020.
Article in English | MEDLINE | ID: covidwho-760838

ABSTRACT

The ongoing coronavirus disease 2019 (COVID-19) pandemic has substantially affected patients with dementia and their caregivers. However, we found not all Alzheimer's disease (AD) patients were afraid of COVID-19 infection. Therefore, we investigated the association between rate of awareness of COVID-19 and depressive tendency in AD. 126 consecutive outpatients with AD were enrolled in this study from May 25, on the day when the declaration of emergency was lifted in Japan, through June 30, 2020. In addition to routine psychological tests, the participants were asked the following two questions: "Do you know COVID-19?" and "Why are you wearing a face mask?". Moderate to severe AD patients were found to have a low COVID-19 recognition rate and did not fully understand why they were wearing face masks. In addition, because they did not understand the seriousness of the COVID-19 outbreak, their Geriatric Depression Scale scores were also substantially lower. These results may appear to simply indicate that people with severe dementia are unaware of current events. However, these results provide insights into how to care for patients with dementia and how to allocate the time and support of our limited staff during the COVID-19 outbreak.


Subject(s)
Alzheimer Disease , Awareness , Coronavirus Infections , Mental Competency , Pandemics , Patient Care , Pneumonia, Viral , Aged , Alzheimer Disease/diagnosis , Alzheimer Disease/psychology , Alzheimer Disease/virology , Betacoronavirus , COVID-19 , Caregivers/psychology , Communicable Disease Control/organization & administration , Coronavirus Infections/epidemiology , Coronavirus Infections/prevention & control , Coronavirus Infections/psychology , Female , Humans , Japan/epidemiology , Male , Pandemics/prevention & control , Patient Care/methods , Patient Care/trends , Pneumonia, Viral/epidemiology , Pneumonia, Viral/prevention & control , Pneumonia, Viral/psychology , Psychosocial Support Systems , SARS-CoV-2 , Severity of Illness Index
8.
Am J Geriatr Psychiatry ; 28(7): 712-721, 2020 07.
Article in English | MEDLINE | ID: covidwho-72500

ABSTRACT

The COVID-19 pandemic is causing global morbidity and mortality, straining health systems, and disrupting society, putting individuals with Alzheimer's disease and related dementias (ADRD) at risk of significant harm. In this Special Article, we examine the current and expected impact of the pandemic on individuals with ADRD. We discuss and propose mitigation strategies for: the risk of COVID-19 infection and its associated morbidity and mortality for individuals with ADRD; the impact of COVID-19 on the diagnosis and clinical management of ADRD; consequences of societal responses to COVID-19 in different ADRD care settings; the effect of COVID-19 on caregivers and physicians of individuals with ADRD; mental hygiene, trauma, and stigma in the time of COVID-19; and the potential impact of COVID-19 on ADRD research. Amid considerable uncertainty, we may be able to prevent or reduce the harm of the COVID-19 pandemic and its consequences for individuals with ADRD and their caregivers.


Subject(s)
Alzheimer Disease , Caregivers/psychology , Communicable Disease Control , Coronavirus Infections , Dementia , Pandemics , Patient Care Management , Pneumonia, Viral , Aged , Alzheimer Disease/epidemiology , Alzheimer Disease/therapy , Alzheimer Disease/virology , Betacoronavirus , COVID-19 , Communicable Disease Control/methods , Communicable Disease Control/organization & administration , Comorbidity , Coronavirus Infections/epidemiology , Coronavirus Infections/prevention & control , Coronavirus Infections/psychology , Critical Pathways/trends , Dementia/epidemiology , Dementia/therapy , Dementia/virology , Humans , Pandemics/prevention & control , Patient Care Management/methods , Patient Care Management/organization & administration , Patient Care Management/trends , Pneumonia, Viral/epidemiology , Pneumonia, Viral/prevention & control , Pneumonia, Viral/psychology , Risk Assessment , Risk Factors , SARS-CoV-2 , Social Stigma , Vulnerable Populations/psychology
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