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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
3.
Neuromolecular Med ; 23(4): 561-571, 2021 12.
Article in English | MEDLINE | ID: covidwho-1525619

ABSTRACT

The current SARS-CoV-2 outbreak, which causes COVID-19, is particularly devastating for individuals with chronic medical conditions, in particular those with Down Syndrome (DS) who often exhibit a higher prevalence of respiratory tract infections, immune dysregulation and potential complications. The incidence of Alzheimer's disease (AD) is much higher in DS than in the general population, possibly increasing further the risk of COVID-19 infection and its complications. Here we provide a biological overview with regard to specific susceptibility of individuals with DS to SARS-CoV-2 infection as well as data from a recent survey on the prevalence of COVID-19 among them. We see an urgent need to protect people with DS, especially those with AD, from COVID-19 and future pandemics and focus on developing protective measures, which also include interventions by health systems worldwide for reducing the negative social effects of long-term isolation and increased periods of hospitalization.


Subject(s)
COVID-19/epidemiology , COVID-19/virology , Disease Susceptibility , Down Syndrome/epidemiology , Adolescent , Adult , Alzheimer Disease/complications , Alzheimer Disease/epidemiology , Alzheimer Disease/immunology , COVID-19/complications , COVID-19/prevention & control , COVID-19 Vaccines/administration & dosage , COVID-19 Vaccines/immunology , Comorbidity , Disease Susceptibility/immunology , Disease Susceptibility/virology , Down Syndrome/complications , Down Syndrome/immunology , Female , Hospitalization , Humans , Immune System/abnormalities , Incidence , Male , Pandemics/prevention & control , Prevalence , Risk Factors , Vaccination/methods
4.
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
5.
J Alzheimers Dis ; 84(4): 1447-1452, 2021.
Article in English | MEDLINE | ID: covidwho-1485013

ABSTRACT

Previous studies have identified dementia as a risk factor for death from coronavirus disease 2019 (COVID-19). However, it is unclear whether Alzheimer's disease (AD) is an independent risk factor for COVID-19 case fatality rate. In a retrospective cohort study, we identified 387,841 COVID-19 patients through TriNetX. After adjusting for demographics and comorbidities, we found that AD patients had higher odds of dying from COVID-19 compared to patients without AD (Odds Ratio: 1.20, 95%confidence interval: 1.09-1.32, p < 0.001). Interestingly, we did not observe increased mortality from COVID-19 among patients with vascular dementia. These data are relevant to the evolving COVID-19 pandemic.


Subject(s)
Alzheimer Disease , COVID-19 , Alzheimer Disease/complications , Alzheimer Disease/mortality , COVID-19/complications , COVID-19/mortality , Dementia, Vascular/complications , Humans , Retrospective Studies , Risk Factors
6.
Int J Mol Sci ; 22(15)2021 Jul 30.
Article in English | MEDLINE | ID: covidwho-1350316

ABSTRACT

Increasing evidence suggests that elderly people with dementia are vulnerable to the development of severe coronavirus disease 2019 (COVID-19). In Alzheimer's disease (AD), the major form of dementia, ß-amyloid (Aß) levels in the blood are increased; however, the impact of elevated Aß levels on the progression of COVID-19 remains largely unknown. Here, our findings demonstrate that Aß1-42, but not Aß1-40, bound to various viral proteins with a preferentially high affinity for the spike protein S1 subunit (S1) of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the viral receptor, angiotensin-converting enzyme 2 (ACE2). These bindings were mainly through the C-terminal residues of Aß1-42. Furthermore, Aß1-42 strengthened the binding of the S1 of SARS-CoV-2 to ACE2 and increased the viral entry and production of IL-6 in a SARS-CoV-2 pseudovirus infection model. Intriguingly, data from a surrogate mouse model with intravenous inoculation of Aß1-42 show that the clearance of Aß1-42 in the blood was dampened in the presence of the extracellular domain of the spike protein trimers of SARS-CoV-2, whose effects can be prevented by a novel anti-Aß antibody. In conclusion, these findings suggest that the binding of Aß1-42 to the S1 of SARS-CoV-2 and ACE2 may have a negative impact on the course and severity of SARS-CoV-2 infection. Further investigations are warranted to elucidate the underlying mechanisms and examine whether reducing the level of Aß1-42 in the blood is beneficial to the fight against COVID-19 and AD.


Subject(s)
Amyloid beta-Peptides/metabolism , Angiotensin-Converting Enzyme 2/metabolism , Peptide Fragments/metabolism , SARS-CoV-2/enzymology , Spike Glycoprotein, Coronavirus/metabolism , A549 Cells , Alzheimer Disease/complications , Alzheimer Disease/metabolism , Amyloid beta-Peptides/chemistry , Animals , COVID-19/complications , COVID-19/metabolism , Chlorocebus aethiops , Humans , Interleukin-6/metabolism , Mice, Inbred C57BL , Mice, Transgenic , Peptide Fragments/chemistry , Protein Subunits/chemistry , Protein Subunits/metabolism , Spike Glycoprotein, Coronavirus/chemistry , Vero Cells , Virus Internalization
7.
Int J Mol Sci ; 22(15)2021 Jul 30.
Article in English | MEDLINE | ID: covidwho-1335101

ABSTRACT

Increasing evidence suggests that elderly people with dementia are vulnerable to the development of severe coronavirus disease 2019 (COVID-19). In Alzheimer's disease (AD), the major form of dementia, ß-amyloid (Aß) levels in the blood are increased; however, the impact of elevated Aß levels on the progression of COVID-19 remains largely unknown. Here, our findings demonstrate that Aß1-42, but not Aß1-40, bound to various viral proteins with a preferentially high affinity for the spike protein S1 subunit (S1) of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the viral receptor, angiotensin-converting enzyme 2 (ACE2). These bindings were mainly through the C-terminal residues of Aß1-42. Furthermore, Aß1-42 strengthened the binding of the S1 of SARS-CoV-2 to ACE2 and increased the viral entry and production of IL-6 in a SARS-CoV-2 pseudovirus infection model. Intriguingly, data from a surrogate mouse model with intravenous inoculation of Aß1-42 show that the clearance of Aß1-42 in the blood was dampened in the presence of the extracellular domain of the spike protein trimers of SARS-CoV-2, whose effects can be prevented by a novel anti-Aß antibody. In conclusion, these findings suggest that the binding of Aß1-42 to the S1 of SARS-CoV-2 and ACE2 may have a negative impact on the course and severity of SARS-CoV-2 infection. Further investigations are warranted to elucidate the underlying mechanisms and examine whether reducing the level of Aß1-42 in the blood is beneficial to the fight against COVID-19 and AD.


Subject(s)
Amyloid beta-Peptides/metabolism , Angiotensin-Converting Enzyme 2/metabolism , Peptide Fragments/metabolism , SARS-CoV-2/enzymology , Spike Glycoprotein, Coronavirus/metabolism , A549 Cells , Alzheimer Disease/complications , Alzheimer Disease/metabolism , Amyloid beta-Peptides/chemistry , Animals , COVID-19/complications , COVID-19/metabolism , Chlorocebus aethiops , Humans , Interleukin-6/metabolism , Mice, Inbred C57BL , Mice, Transgenic , Peptide Fragments/chemistry , Protein Subunits/chemistry , Protein Subunits/metabolism , Spike Glycoprotein, Coronavirus/chemistry , Vero Cells , Virus Internalization
8.
Aging (Albany NY) ; 13(11): 14552-14556, 2021 Jun 11.
Article in English | MEDLINE | ID: covidwho-1267005

ABSTRACT

SARS-CoV-2 more readily affects the elderly, especially as they present co-morbidities. In the COVID-19 pathogeny, ACE2 appears to be the key cell receptor for SARS-CoV-2 to infect humans. The level of ACE2 gene expression influences the susceptibility of contracting SARS-CoV-2. In circumstances in which the ACE2 level is low, the incidence of Covid-19 seems to be fewer. Two clinical patterns illustrate this observation, i. e., in infants and in Alzheimer's disease (AD). Very young children and AD patients get little COVID-19, in part probably due to decreased expression of ACE2. The determination of the nasal level of ACE2 gene expression could provide a useful scale to predict the susceptibility to contract the SARS-CoV-2 infection.


Subject(s)
Angiotensin-Converting Enzyme 2/metabolism , COVID-19/etiology , SARS-CoV-2/metabolism , Alzheimer Disease/complications , Alzheimer Disease/metabolism , COVID-19/metabolism , Cerebrum/metabolism , Disease Susceptibility , Gene Expression , Humans , Infant , Nasal Mucosa/metabolism
9.
Alzheimer Dis Assoc Disord ; 36(1): 83-84, 2022.
Article in English | MEDLINE | ID: covidwho-1223417

ABSTRACT

Encephalopathy, delirium, and agitation are documented symptoms of coronavirus disease (COVID-19) infection, but research into the management of agitation in the setting of COVID-19 and pre-existing neuropsychiatric disease is ongoing. We present a 55-year-old male patient with early-onset Alzheimer disease and deteriorating mental and functional status who presented to our institution with agitation and persistent COVID-19 positivity on polymerase chain reaction testing. His agitation was improved through pharmacologic optimization including the avoidance of benzodiazepines and initiation of clonidine and prazosin, which temporally coincided with the resolution of his nearly 2-month long COVID-19 positivity.


Subject(s)
Alzheimer Disease , COVID-19 , Alzheimer Disease/complications , Alzheimer Disease/diagnosis , Benzodiazepines , COVID-19/complications , Humans , Male , Middle Aged , Psychomotor Agitation , SARS-CoV-2
10.
Transl Neurodegener ; 10(1): 15, 2021 04 30.
Article in English | MEDLINE | ID: covidwho-1215126

ABSTRACT

Alzheimer's disease (AD) has emerged as a key comorbidity of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). The morbidity and mortality of COVID-19 are elevated in AD due to multiple pathological changes in AD patients such as the excessive expression of viral receptor angiotensin converting enzyme 2 and pro-inflammatory molecules, various AD complications including diabetes, lifestyle alterations in AD, and drug-drug interactions. Meanwhile, COVID-19 has also been reported to cause various neurologic symptoms including cognitive impairment that may ultimately result in AD, probably through the invasion of SARS-CoV-2 into the central nervous system, COVID-19-induced inflammation, long-term hospitalization and delirium, and post-COVID-19 syndrome. In addition, the COVID-19 crisis also worsens behavioral symptoms in uninfected AD patients and poses new challenges for AD prevention. In this review, we first introduce the symptoms and pathogenesis of COVID-19 and AD. Next, we provide a comprehensive discussion on the aggravating effects of AD on COVID-19 and the underlying mechanisms from molecular to social levels. We also highlight the influence of COVID-19 on cognitive function, and propose possible routes of viral invasion into the brain and potential mechanisms underlying the COVID-19-induced cognitive impairment. Last, we summarize the negative impacts of COVID-19 pandemic on uninfected AD patients and dementia prevention.


Subject(s)
Alzheimer Disease/complications , COVID-19/complications , Pandemics , Aged , Aged, 80 and over , Alzheimer Disease/epidemiology , COVID-19/epidemiology , Comorbidity , Humans
11.
Geriatr Nurs ; 42(4): 787-791, 2021.
Article in English | MEDLINE | ID: covidwho-1213243

ABSTRACT

The COVID 19 pandemic has led to an increase in the number of patients in need of ventilation. Limitations in the number of respirators may cause an ethical problem for the medical and nursing staff in deciding who should be connected to the available respirators.  We conducted a cross-sectional survey among a convenience sample of 278 healthcare professionals at one medical center. They were asked to rank their preference in respirator allocation to three COVID-19 patients, one 80 years old with no cognitive illness, one 50 years old with Alzheimer's disease (AD), and one 80 years old with AD. Most respondents (75%) chose the 80-year-old AD patient as last preference, but were evenly divided on how to rank the other two patients. Medical staff have difficulty deciding whether age or cognitive status should be the deciding factor ventilator allocation. Determination of a set policy would help professionals with these decisions.


Subject(s)
Alzheimer Disease/complications , COVID-19/therapy , Health Care Rationing/methods , Personnel, Hospital/psychology , Ventilators, Mechanical , Aged, 80 and over , COVID-19/epidemiology , Choice Behavior , Cross-Sectional Studies , Humans , Pandemics , SARS-CoV-2
12.
Alzheimer Dis Assoc Disord ; 35(2): 172-177, 2021.
Article in English | MEDLINE | ID: covidwho-1201049

ABSTRACT

In March 2020, the novel coronavirus (COVID-19) became a global pandemic that would cause most in-person visits for clinical studies to be put on pause. Coupled with protective stay at home guidelines, clinical research at the Icahn School of Medicine at Mount Sinai Alzheimer's Disease Research Center (ISMMS ADRC) needed to quickly adapt to remain operational and maintain our cohort of research participants. Data collected by the ISMMS ADRC as well as from other National Institute on Aging (NIA) Alzheimer Disease centers, follows the guidance of the National Alzheimer Coordinating Center (NACC). However, at the start of this pandemic, NACC had no alternative data collection mechanisms that could accommodate these safety guidelines. To stay in touch with our cohort and to ensure continued data collection under different stages of quarantine, the ISMMS ADRC redeployed their work force to continue their observational study via telehealth assessment. On the basis of this experience and that of other centers, NACC was able to create a data collection process to accommodate remote assessment in mid-August. Here we review our experience in filling the gap during this period of isolation and describe the adaptations for clinical research, which informed the national dialog for conducting dementia research in the age of COVID-19 and beyond.


Subject(s)
Alzheimer Disease/epidemiology , COVID-19/diagnosis , Data Collection , SARS-CoV-2/pathogenicity , Alzheimer Disease/complications , COVID-19/complications , COVID-19/virology , Dementia/complications , Humans
13.
Alzheimers Dement ; 17(11): 1818-1831, 2021 11.
Article in English | MEDLINE | ID: covidwho-1195110

ABSTRACT

INTRODUCTION: Dementia has been associated with COVID-19 prevalence, but whether this reflects higher infection, older age of patients, or disease severity remains unclear. METHODS: We investigated a cohort of 12,863 UK Biobank community-dwelling individuals > 65 years old (1814 individuals ≥ 80 years old) tested for COVID-19. Individuals were stratified by age to account for age as a confounder. Risk factors were analyzed for COVID-19-positive diagnosis, hospitalization, and death. RESULTS: All-cause dementia, Alzheimer's disease (AD), and Parkinson's disease (PD) were associated with COVID-19-positive diagnosis, and all-cause dementia and AD remained associated in individuals ≥ 80 years old. All-cause dementia, AD, or PD were not risk factors for overall hospitalization, but increased the risk of hospitalization of COVID-19 patients. All-cause dementia and AD increased the risk of COVID-19-related death, and all-cause dementia was uniquely associated with increased death in ≥ 80-year-old patients. DISCUSSION: All-cause dementia and AD are age-independent risk factors for disease severity and death in COVID-19.


Subject(s)
COVID-19/mortality , Dementia/epidemiology , Age Factors , Aged , Aged, 80 and over , Alzheimer Disease/complications , Alzheimer Disease/epidemiology , COVID-19/complications , Comorbidity , Dementia/complications , Female , Hospitalization , Humans , Independent Living , Inpatients , Male , Parkinson Disease/complications , Parkinson Disease/epidemiology , Prevalence , Prospective Studies , Risk Factors , Severity of Illness Index , United Kingdom/epidemiology
14.
J Alzheimers Dis ; 78(2): 479-503, 2020.
Article in English | MEDLINE | ID: covidwho-1080922

ABSTRACT

Alzheimer's and Parkinson's diseases (AD, PD) have a pediatric and young adult onset in Metropolitan Mexico City (MMC). The SARS-CoV-2 neurotropic RNA virus is triggering neurological complications and deep concern regarding acceleration of neuroinflammatory and neurodegenerative processes already in progress. This review, based on our MMC experience, will discuss two major issues: 1) why residents chronically exposed to air pollution are likely to be more susceptible to SARS-CoV-2 systemic and brain effects and 2) why young people with AD and PD already in progress will accelerate neurodegenerative processes. Secondary mental consequences of social distancing and isolation, fear, financial insecurity, violence, poor health support, and lack of understanding of the complex crisis are expected in MMC residents infected or free of SARS-CoV-2. MMC residents with pre-SARS-CoV-2 accumulation of misfolded proteins diagnostic of AD and PD and metal-rich, magnetic nanoparticles damaging key neural organelles are an ideal host for neurotropic SARS-CoV-2 RNA virus invading the body through the same portals damaged by nanoparticles: nasal olfactory epithelium, the gastrointestinal tract, and the alveolar-capillary portal. We urgently need MMC multicenter retrospective-prospective neurological and psychiatric population follow-up and intervention strategies in place in case of acceleration of neurodegenerative processes, increased risk of suicide, and mental disease worsening. Identification of vulnerable populations and continuous effort to lower air pollution ought to be critical steps.


Subject(s)
Alzheimer Disease/complications , Brain Diseases/etiology , Coronavirus Infections/complications , Environmental Pollutants/adverse effects , Nanoparticles/adverse effects , Parkinson Disease/complications , Pneumonia, Viral/complications , Adult , Air Pollution/adverse effects , Alzheimer Disease/physiopathology , COVID-19 , Disease Progression , Humans , Middle Aged , Pandemics , Parkinson Disease/physiopathology , Suicide/statistics & numerical data , Urban Population
15.
Alzheimers Dement ; 17(8): 1297-1306, 2021 08.
Article in English | MEDLINE | ID: covidwho-1070694

ABSTRACT

INTRODUCTION: At present, there is limited data on the risks, disparity, and outcomes for COVID-19 in patients with dementia in the United States. METHODS: This is a retrospective case-control analysis of patient electronic health records (EHRs) of 61.9 million adult and senior patients (age ≥ 18 years) in the United States up to August 21, 2020. RESULTS: Patients with dementia were at increased risk for COVID-19 compared to patients without dementia (adjusted odds ratio [AOR]: 2.00 [95% confidence interval (CI), 1.94-2.06], P < .001), with the strongest effect for vascular dementia (AOR: 3.17 [95% CI, 2.97-3.37], P < .001), followed by presenile dementia (AOR: 2.62 [95% CI, 2.28-3.00], P < .001), Alzheimer's disease (AOR: 1.86 [95% CI, 1.77-1.96], P < .001), senile dementia (AOR: 1.99 [95% CI, 1.86-2.13], P < .001) and post-traumatic dementia (AOR: 1.67 [95% CI, 1.51-1.86] P < .001). Blacks with dementia had higher risk of COVID-19 than Whites (AOR: 2.86 [95% CI, 2.67-3.06], P < .001). The 6-month mortality and hospitalization risks in patients with dementia and COVID-19 were 20.99% and 59.26%, respectively. DISCUSSION: These findings highlight the need to protect patients with dementia as part of the strategy to control the COVID-19 pandemic.


Subject(s)
COVID-19/complications , Dementia/complications , Adolescent , Adult , Aged , Aged, 80 and over , Alzheimer Disease/complications , Alzheimer Disease/epidemiology , Brain Injuries, Traumatic/complications , Brain Injuries, Traumatic/epidemiology , COVID-19/epidemiology , Case-Control Studies , Dementia/epidemiology , Dementia, Vascular/complications , Dementia, Vascular/epidemiology , Demography , Electronic Health Records , Female , Healthcare Disparities , Hospitalization/statistics & numerical data , Humans , Male , Middle Aged , Retrospective Studies , Treatment Outcome , United States/epidemiology , Young Adult
16.
Int J Mol Sci ; 22(4)2021 Feb 08.
Article in English | MEDLINE | ID: covidwho-1069829

ABSTRACT

Alzheimer's disease is a chronic neurodegenerative disorder and represents the main cause of dementia globally. Currently, the world is suffering from the coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a virus that uses angiotensin-converting enzyme 2 (ACE2) as a receptor to enter the host cells. In COVID-19, neurological manifestations have been reported to occur. The present study demonstrates that the protein expression level of ACE2 is upregulated in the brain of patients with Alzheimer's disease. The increased ACE2 expression is not age-dependent, suggesting the direct relationship between Alzheimer's disease and ACE2 expression. Oxidative stress has been implicated in the pathogenesis of Alzheimer's disease, and brains with the disease examined in this study also exhibited higher carbonylated proteins, as well as an increased thiol oxidation state of peroxiredoxin 6 (Prx6). A moderate positive correlation was found between the increased ACE2 protein expression and oxidative stress in brains with Alzheimer's disease. In summary, the present study reveals the relationships between Alzheimer's disease and ACE2, the receptor for SARS-CoV-2. These results suggest the importance of carefully monitoring patients with both Alzheimer's disease and COVID-19 in order to identify higher viral loads in the brain and long-term adverse neurological consequences.


Subject(s)
Alzheimer Disease/metabolism , Angiotensin-Converting Enzyme 2/metabolism , COVID-19/epidemiology , COVID-19/metabolism , Hippocampus/metabolism , Pandemics , Receptors, Virus/metabolism , SARS-CoV-2/metabolism , Up-Regulation , Alzheimer Disease/complications , Alzheimer Disease/pathology , Amyloid beta-Peptides/metabolism , Autopsy , COVID-19/complications , COVID-19/virology , Hippocampus/pathology , Humans , Oxidation-Reduction , Oxidative Stress , Peroxiredoxin VI/metabolism , Plaque, Amyloid/metabolism , Protein Carbonylation , Severity of Illness Index , Virus Internalization
17.
Clin Interv Aging ; 15: 2407-2414, 2020.
Article in English | MEDLINE | ID: covidwho-1034928

ABSTRACT

PURPOSE: The current study aimed 1) to assess laypersons' priority-setting preferences for allocating ventilators to COVID-19 patients with and without AD while differentiating between a young and an old person with the disease, and 2) to examine the factors associated with these preferences. METHODS: A cross-sectional online survey was conducted among a sample of 309 Israeli Jewish persons aged 40 and above. RESULTS: Overall, almost three quarters (71%) of the participants chose the 80-year-old patient with a diagnosis of AD to be the last to be provided with a ventilator. The preferences of the remaining quarter were divided between the 80-year-old person who was cognitively intact and the 55-year-old person with AD. Education and subjective knowledge about AD were significantly associated with participants' preferences. CONCLUSION: Our results suggest that cognitive status might not be a strong discriminating factor for laypersons' preferences for allocating ventilators during the COVID-19 pandemic.


Subject(s)
Alzheimer Disease/complications , COVID-19/therapy , Aged, 80 and over , Female , Humans , Male , Middle Aged , SARS-CoV-2 , Ventilators, Mechanical
18.
Med Hypotheses ; 147: 110479, 2021 Feb.
Article in English | MEDLINE | ID: covidwho-1009752

ABSTRACT

The association of the coronavirus disease 2019 (COVID-19) with significant neurological and neuropsychiatric complications has been increasingly reported, both during the acute illness and in its aftermath. However, due to the short duration of patient follow up until now, it is not clear whether this infection will be associated with longer-term neurological and/or neuropsychiatric sequelae. In particular, the question of whether COVID-19 will be associated with an increased risk and rate of future dementia remains open and subject to speculation. During the course of the COVID-19 pandemic, an increasing number of patients have reported sudden anosmia or other olfactory dysfunction as concurrent symptoms. The possibility that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may reach the brain via the olfactory nerve or an upper nasal trancribrial route is an interesting working hypothesis. Among the identified genetic risk factors for Late-onset Alzheimer's disease (LOAD), Apo E4 is one of the strongest and most frequent. People carrying one or two copies of the e4 allele of Apo E4 have significant odor recognition deficits in comparison to those not carrying this haplotype. The hypothesis invoked in this paper is that anosmia/olfactory dysfunctions induced by SARS-CoV-2 may cause an increased a risk of future neurodegenerative dementia in ApoE4 carriers, and that this risk would be higher than in Apo E4 carriers affected by anosmia not induced by SARS-CoV-2. This would be associated with virus-induced chronic modifications in the central nervous system. It is proposed that COVID-19 patients with anosmia and no other serious symptoms should be followed up as part of specifically designed and approved studies in order to identify the early stages of dementia (especially LOAD and Dementia with Lewy Bodies), thereby improving our knowledge of the mechanisms involved in pre-cognitive stages of neurodegenerative dementia and making best use of any available therapies. This latter opportunity is unique and should not be lost.


Subject(s)
Alzheimer Disease/genetics , Anosmia/complications , Apolipoprotein E4/genetics , COVID-19/complications , Dementia/genetics , Olfaction Disorders/complications , Alzheimer Disease/complications , Dementia/complications , Humans , Inflammation , Models, Theoretical , Prevalence , Risk , Smell
19.
J Alzheimers Dis ; 78(2): 537-541, 2020.
Article in English | MEDLINE | ID: covidwho-1000042

ABSTRACT

We aimed to evaluate the frequency and mortality of COVID-19 in patients with Alzheimer's disease (AD) and frontotemporal dementia (FTD). We conducted an observational case series. We enrolled 204 patients, 15.2% of whom were diagnosed with COVID-19, and 41.9% of patients with the infection died. Patients with AD were older than patients with FTD (80.36±8.77 versus 72.00±8.35 years old) and had a higher prevalence of arterial hypertension (55.8% versus 26.3%). COVID-19 occurred in 7.3% of patients living at home, but 72.0% of those living at care homes. Living in care facilities and diagnosis of AD were independently associated with a higher probability of death. We found that living in care homes is the most relevant factor for an increased risk of COVID-19 infection and death, with AD patients exhibiting a higher risk than those with FTD.


Subject(s)
Alzheimer Disease/complications , Alzheimer Disease/mortality , Coronavirus Infections/complications , Coronavirus Infections/mortality , Frontotemporal Dementia/complications , Frontotemporal Dementia/mortality , Pneumonia, Viral/complications , Pneumonia, Viral/mortality , Age Factors , Aged , Aged, 80 and over , COVID-19 , Female , Humans , Hypertension/complications , Independent Living , Male , Nursing Homes , Pandemics , Prevalence , Risk Factors
20.
J Alzheimers Dis ; 78(4): 1775-1782, 2020.
Article in English | MEDLINE | ID: covidwho-963307

ABSTRACT

BACKGROUND: The emergence of the coronavirus disease 2019 (COVID-19) has brought large challenges to dementia patients. We reviewed the existing literature on COVID-19 to assess the incidence and mortality of dementia comorbidities in COVID-19 patients. OBJECTIVE: To investigate the impact of pre-existing dementia comorbidities on COVID-19. METHODS: We searched the PubMed, Embase, and Web of Science databases for patients with preexisting dementia who were diagnosed with COVID-19. The statistical data on the prevalence and mortality of dementia comorbidities were examined. A fixed-or random-effect model was used to calculate the overall pooled risk estimates. Forest plots were generated to show the summarized results. RESULTS: A total of 265 articles were retrieved from the three databases. After removing duplicates and performing two screenings, 10 articles were selected for meta-analysis, including 119,218 participants. Overall, the meta-analysis of the 10 studies showed that the incidence of dementia in COVID-19 patients was (R: 9%, [95% CI: 6% to 13%]). Moreover, the meta-analysis of 9 studies showed that the mortality rate of individuals with dementia after being infected with COVID-19 was higher than that of individuals with no dementia (OR: 5.17 [95% CI: 2.31 to 11.59]). Substantial heterogeneity was observed in this meta-analysis. Significant publication bias was also found. CONCLUSION: Emerging literature shows that dementia comorbidities are a high risk factor for the prevalence and mortality of COVID-19. Our results should have an impact on preventive interventions and encourage more targeted approaches to prioritize older people with specific risk factors, such as dementia.


Subject(s)
COVID-19/complications , COVID-19/therapy , Dementia/complications , Aged , Aged, 80 and over , Alzheimer Disease/complications , Alzheimer Disease/epidemiology , Alzheimer Disease/mortality , COVID-19/epidemiology , COVID-19/mortality , Dementia/epidemiology , Dementia/mortality , Female , Humans , Incidence , Male , Middle Aged , Prevalence , Treatment Outcome
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