Background And Objectives: Many community dementia services such as home-visiting services and center-based activities were suspended during the coronavirus 2019 pandemic. This study investigated the efficacy of a caregiver-delivered cognitive stimulation therapy (CDCST) on people with dementia during the pandemic.
Research Design And Methods: This was a 2-arm randomized controlled trial involving 241 patient-caregiver dyads assigned to a 15-week CDCST or control group (usual care). We hypothesized that CDCST would facilitate significant improvements among people with dementia (cognition, behavioral/psychiatric symptoms, and quality of life) and their caregivers (caregiving appraisal, attitudes, and psychological well-being) at postintervention (T1) and at the 12-week follow-up (T2). Generalized estimating equations evaluated the study outcomes.
Results: A total of 230 dyads completed the study, with good program adherence (93%). Participants in the CDCST showed significant improvements in cognition (p < .001), behavioral and psychiatric symptoms (p =. 027), and quality of life (p =.001) at the 3-month follow-up period. Family caregivers had improved positive aspects of caregiving (p = .008; p = .049) and decreased negative attitudes toward people with dementia (p =. 013; p < .001) at both T1 and T2. There were nonsignificant changes in the caregivers' perceived burden, distress, and psychological well-being.
Discussion And Implications: Family caregivers could be trained to provide cognitive stimulation at home for people with dementia, which could benefit both parties. CDCST could manage to improve the cognition, neuropsychiatric symptoms, and quality of life of people with dementia, while also improving caregiving appraisal and negative attitudes among family caregivers.
Clinical Trial Registration Number: NCT03803592.
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http://dx.doi.org/10.1093/geront/gnad054 | DOI Listing |
J Aging Phys Act
January 2025
Bournemouth University Clinical Research Unit, Faculty of Health & Social Sciences, Bournemouth University, Poole, United Kingdom.
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View Article and Find Full Text PDFJAMA Netw Open
January 2025
Department of Health Policy and Management, Yale School of Public Health, New Haven, Connecticut.
Importance: Disparities in cognition, including dementia occurrence, persist between non-Hispanic Black (hereinafter, Black) and non-Hispanic White (hereinafter, White) older adults, and are possibly influenced by early educational differences stemming from structural racism. However, the association between school racial segregation and later-life cognition remains underexplored.
Objective: To investigate the association between childhood contextual exposure to school racial segregation and cognitive outcomes in later life.
Neuromolecular Med
December 2024
Key Laboratory of Physical Fitness and Exercise Rehabilitation of Hunan Province, College of Physical Education, Hunan Normal University, Changsha, 410012, China.
Alzheimer's disease (AD) is the most common neurodegenerative disorder. The neuropathology of AD appears in the hippocampus. The purpose of this work was to reveal key differentially expressed genes (DEGs) in the hippocampus of AD patients and healthy individuals.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Allen Institute for Brain Science, Seattle, WA, USA.
Background: Applying single-cell RNA sequencing (scRNA-seq) to the study of neurodegenerative disease has propelled the field towards a more refined cellular understanding of Alzheimer's disease (AD); however, directly linking protein pathology to transcriptomic changes has not been possible at scale. Recently, a high-throughput method was developed to generate high-quality scRNA-seq data while retaining cytoplasmic proteins. Tau is a cytoplasmic protein and when hyperphosphorylated is integrally involved in AD progression.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Laboratory for Neuropathology, KU Leuven, Leuven, Belgium.
Background: In 43-63% of symptomatic Alzheimer's disease (AD) patients, there is an observed accumulation of misfolded alpha-synuclein (αSyn). Two primary αSyn subtypes have been identified based on the underlying spreading pattern of this pathology: caudo-rostral and amygdala-predominant. Interactions between pathological TDP-43, Tau, and αSyn can aggravate their spread and aggregation.
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