Objectives: Detection of dementia is essential for improving the lives of patients but the extent of underdetection worldwide and its causes are not known. This study aimed to quantify the prevalence of undetected dementia and to examine its correlates.
Methods/setting/participants: A systematic search was conducted until October 2016 for studies reporting the proportion of undetected dementia and/or its determinants in either the community or in residential care settings worldwide. Random-effects models calculated the pooled rate of undetected dementia and subgroup analyses were conducted to identify determinants of the variation.
Primary And Secondary Outcome Measures: The outcome measures of interest were the prevalence and determinants of undetected dementia.
Results: 23 studies were eligible for inclusion in this review. The pooled rate of undetected dementia was 61.7% (95% CI 55.0% to 68.0%). The rate of underdetection was higher in China and India (vs Europe and North America), in the community setting (vs residential/nursing care), age of <70 years, male gender and diagnosis by general practitioner. However, it was lower in the studies using Mini-Mental State Examination (MMSE) diagnosis criteria.
Conclusions: The prevalence of undetected dementia is high globally. Wide variations in detecting dementia need to be urgently examined, particularly in populations with low socioeconomic status. Efforts are required to reduce diagnostic inequality and to improve early diagnosis in the community.
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http://dx.doi.org/10.1136/bmjopen-2016-011146 | DOI Listing |
Elife
December 2024
Science & Technology of Music and Sound Laboratory, IRCAM/CNRS/Sorbonne Université, Paris, France.
Metab Brain Dis
November 2024
Department of Virology and Biotechnology, ICMR-National Institute for Research in Tuberculosis, Chennai, 600031, India.
Acta Neuropathol
November 2024
Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK.
Mutations in ITM2B cause familial British, Danish, Chinese, and Korean dementias. In familial British dementia (FBD), a mutation in the stop codon of the ITM2B gene (also known as BRI2) causes a C-terminal cleavage fragment of the ITM2B/BRI2 protein to be extended by 11 amino acids. This fragment, termed amyloid-Bri (ABri), is highly insoluble and forms extracellular plaques in the brain.
View Article and Find Full Text PDFNeurobiol Aging
January 2025
Department of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA. Electronic address:
The hAβ-KI and APP-KI are two amyloid models that harbor mutations in the endogenous mouse App gene. Both hAβ-KI and APP-KI mice contain a humanized Aβ sequence, and APP-KI mice carry three additional familial AD mutations. We herein report that the Aβ levels and Aβ42/Aβ40 ratio in APP-KI homozygotes are dramatically higher than those in hAβ-KI homozygotes at 14 months of age.
View Article and Find Full Text PDFJ Am Geriatr Soc
October 2024
Department of Health Services, Policy, and Practice, Brown University School of Public Health, Providence, Rhode Island, USA.
Background: Accurate and timely diagnosis of dementia is necessary to allow affected individuals to make informed decisions and access appropriate resources. When dementia goes undetected until a hospitalization or nursing home stay, this could reflect delayed diagnosis or misdiagnosis, and may reflect underlying disparities in healthcare access.
Methods: In this retrospective cohort study, we used 2012-2020 Medicare claims and other administrative data to examine variation in setting of dementia diagnosis among fee-for-service Medicare beneficiaries with an initial claims-based dementia diagnosis in 2016.
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