African American/Black communities comprise 12.2% of the U.S. population, with a COVID-19 infection rate of more than 18% and marginal access to healthcare services. This scoping review synthesizes the emerging evidence on healthcare accessibility among older African American adult communities with dementia and COVID-19, as well as the resource requirements for this population during the pandemic. Searches of different databases for empirical studies and other sources on dementia and COVID-19 among older African American adults yielded 13 studies that met the following inclusion criteria: (a) focus on dementia and COVID-19, (b) sampled older African American adults, (c) investigated healthcare accessibility and resources, and (d) published between 2019 and 2022. Following the initial selection of the studies, eight were selected for relevance based on the Population, Concept, and Context (PCC) inclusion and exclusion criteria. Thematic analysis indicated that older African Americans with dementia and COVID-19 experienced longer delays in accessing timely healthcare, including transportation, intensive care units (ICUs), and mechanical ventilation. They also had reduced healthcare resources associated with a lack of health insurance, low financial resources, and an increased length of hospital stay, which further aggravated the negative effects of comorbid dementia and COVID-19 infections. Evidence showed that racial and age disparities affected older African American adults with dementia and COVID-19, resulting in lower healthcare access and marginal resources. This is consistent with historical and systemic inequities in meeting the healthcare needs of people of color in the United States, which was compounded for older African Americans during the COVID-19 pandemic.
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http://dx.doi.org/10.3390/ijerph20043494 | DOI Listing |
Background: The global outbreak of COVID-19, caused by the SARS-CoV-2 virus, has been linked to long-term neurological complications, including Alzheimer's disease (AD) among seniors. However, the precise genetic impact of COVID-19 on long-term AD development remains unclear.
Method: This study leveraged genome-wide association study (GWAS) data and genotype data to explore the genetic correlation between AD and various COVID-19 phenotypes across European ancestry (EA) and African ancestry (AA).
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December 2024
Institute of Neurosciences, L'Hospitalet de Llobregat, Barcelona, Spain.
Background: The increased vulnerability of Alzheimer's disease patients to severe SARS-CoV-2 infection raises crucial concerns, especially with the potential transition of the COVID-19 pandemic to an endemic state. Given the rising prevalence of Alzheimer's in an aging world-wide population, elucidating whether SARS-CoV-2 infection may induce or accelerate neurodegeneration becomes imperative.
Method: To investigate the neurodegenerative effects of SARS-CoV-2 infection, we generated brain organoids using human induced pluripotent stem lines from one non-demented control, one with sporadic Alzheimer's, and one with familial Alzheimer's.
Alzheimers Dement
December 2024
University of South Alabama, Mobile, AL, USA.
Background: Many survivors of lung injury, including those with bacterial pneumonia and COVID-19, suffer from incident dementia. Patients who have had pneumonia and other infections are at a higher risk for developing Alzheimer's disease and related dementias (ADRD) (Chu et al., BBI, 2022, Sipila et al.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
National Institutes of Health (NIH)/National Institute of Neurological Disorders and Stroke (NINDS), Bethesda, MD, USA.
Background: AD/ADRD diseases currently impact more than 6 million people in the US. Rare forms of AD/ADRD are caused directly and unambiguously by genetic mutations. However, most AD/ADRD burden is complex in etiology and thought to result from an interplay among multiple incompletely understood genetic, biochemical, lifestyle, environmental and psychosocial risk factors.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Neurosurgery, Clinical Neuroscience Research Center, Tulane University School of Medicine, New Orleans, LA, USA.
Background: SARS-CoV-2 causes a variety of neurological sequelae in COVID-19 survivors, including fatigue and cognitive dysfunction. Endothelial dysfunction is the unifying and central mechanism of COVID-19 illness and a major risk factor for vascular dementia (VaD). Endothelial dysfunction stems, in part, from an imbalance between nitric oxide (NO) generated by the endothelial nitric oxide synthase (eNOS) and reactive oxidant species produced by uncoupled-eNOS.
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