Introduction: Dementia is a growing health and social concern for all Australians. Whilst the prevalence of dementia amongst Australia's indigenous people is unclear, there is some evidence that dementia rates are five times that of the general Australian population. To date no studies have examined dementia knowledge levels in indigenous communities.
Purpose Of The Study: This paper aims to explore indigenous Australians' understanding, knowledge and misconceptions of dementia.
Design And Methods: Hundered and seventy-four indigenous adults participated in a cross-sectional survey using a modified version of the Alzheimer's Disease Knowledge Test (ADK). The survey included demographic information, two open-ended questions and 20 multiple choice questions. Each ADK item was examined to identify responses that revealed commonly held correct beliefs, knowledge gaps and misconceptions.
Results: The overall level of understanding of dementia was poor. Younger participants were significantly more likely to have no knowledge of Alzheimer's Disease, whereas the other age groups were most likely to have at least some knowledge. It was also revealed that there are common misconceptions about Alzheimer's Disease held by both indigenous and non-indigenous communities.
Implications: Culturally appropriate awareness campaigns and targeted educational interventions need to be implemented to improve the general level of understanding of dementia in indigenous communities.
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http://dx.doi.org/10.1002/gps.2578 | DOI Listing |
J Neuroinflammation
January 2025
Stark Neurosciences Research Institute, Department of Neurology, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Over recent years, the retina has been increasingly investigated as a potential biomarker for dementia. A number of studies have looked at the effect of Alzheimer's disease (AD) pathology on the retina and the associations of AD with visual deficits. However, while OCT-A has been explored as a biomarker of cerebral small vessel disease (cSVD), studies identifying the specific retinal changes and mechanisms associated with cSVD are lacking.
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Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, MD, 20815, USA.
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View Article and Find Full Text PDFJ Neuroinflammation
January 2025
Department of Translational Neuroscience, Barrow Neurological Institute, Phoenix, AZ, 85013, USA.
The ApoE ε4 allele (APOEε4) is a major genetic risk factor for sporadic Alzheimer's disease (AD) and is linked to demyelination and cognitive decline. However, its effects on the lipid transporters apolipoprotein E (ApoE) and fatty acid-binding protein 7 (Fabp7), which are crucial for the maintenance of myelin in white matter (WM) during the progression of AD remain underexplored. To evaluate the effects of APOEε4 on ApoE, Fabp7 and myelin in the WM of the frontal cortex (FC), we examined individuals carrying one ε4 allele that came to autopsy with a premortem clinical diagnosis of no cognitive impairment (NCI), mild cognitive impairment (MCI) and mild to moderate AD compared with non-carrier counterparts.
View Article and Find Full Text PDFPrevious studies have suggested that systemic viral infections may increase risks of dementia. Whether this holds true for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus infections is unknown. Determining this is important for anticipating the potential future incidence of dementia.
View Article and Find Full Text PDFNat Med
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Department of Neurology & Neurological Sciences, Stanford Movement Disorders Center, Stanford University, Stanford, CA, USA.
Cerebral accumulation of alpha-synuclein (αSyn) aggregates is the hallmark event in a group of neurodegenerative diseases-collectively called synucleinopathies-which include Parkinson's disease, dementia with Lewy bodies and multiple system atrophy. Currently, these are diagnosed by their clinical symptoms and definitively confirmed postmortem by the presence of αSyn deposits in the brain. Here, we summarize the drawbacks of the current clinical definition of synucleinopathies and outline the rationale for moving toward an earlier, biology-anchored definition of these disorders, with or without the presence of clinical symptoms.
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