Aim: To assess advanced cancer pain in older adults with dementia at the end-of-life.
Background: Self-report is the gold standard for pain assessment; however, people with Alzheimer's disease may lose the ability to report pain. Biochemical and neuropathological changes occur in Alzheimer's disease that impairs the affective, sensory, and motor pain processing regions of the brain. Because people with severe Alzheimer's disease may lose the ability to report their sensory and emotional response to pain verbally, external motor displays of pain, such as grimacing, have been suggested for use in people with Alzheimer's disease.
Design: Between groups cross sectional study.
Method: Retrospective chart audits of people with Alzheimer's disease in nine nursing homes in the US in 2009. Participants were nursing home residents (n = 48) with mild to very severe dementia, pain and cognitive measures were collected during the final 3 months of life. The primary outcome variable was the discomfort behaviour scale score (a measure of observed pain behaviour) and the main predictor variable was the cognitive performance scale score (a measure of Alzheimer's disease severity). Medication administration (opioid, non-narcotic, and psychotropic medications) recorded over the final 2 weeks of life was collected as a covariate of interest.
Results: Alzheimer's disease severity was negatively associated with pain behaviours. Post hoc procedures showed that this difference was due to the difference in pain behaviours between individuals with moderate and very severe Alzheimer's disease. Total amount of opioid analgesic, total number of doses of non-narcotic medications, and psychotropic medications administered over the last 2 weeks of life were not statistically significantly correlated with pain behaviour. An inverse correlation was found between cognitive ability (Cognitive Performance Scale score) and total amount of opioid medication indicating that individuals with severe Alzheimer's disease received less opioid.
Conclusion: Because people with worsening Alzheimer's disease have fewer pain behaviours, assessing pain using behavioural indicators can be a challenge. Improving methods to assess for pain in people with Alzheimer's disease is of critical public health importance. Moreover, future studies are urgently needed to further examine the sensory, emotional, and behavioural responses to pain in people with Alzheimer's disease.
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http://dx.doi.org/10.1111/j.1365-2648.2011.05929.x | DOI Listing |
Neurology
February 2025
Department of Neurology, Houston Methodist, TX, and Weill Cornell, New York, NY.
PLoS One
January 2025
Center for Innovation in Brain Science, University of Arizona Health Sciences, Tucson, Arizona, United States of America.
Translational validity of mouse models of Alzheimer's disease (AD) is variable. Because change in weight is a well-documented precursor of AD, we investigated whether diversity of human AD risk weight phenotypes was evident in a longitudinally characterized cohort of 1,196 female and male humanized APOE (hAPOE) mice, monitored up to 28 months of age which is equivalent to 81 human years. Autoregressive Hidden Markov Model (AHMM) incorporating age, sex, and APOE genotype was employed to identify emergent weight trajectories and phenotypes.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Yusuf Hamied Department of Chemistry, Centre for Misfolding Diseases, University of Cambridge, Cambridge CB2 1EW, United Kingdom.
The onset and development of Alzheimer's disease is linked to the accumulation of pathological aggregates formed from the normally monomeric amyloid-β peptide within the central nervous system. These Aβ aggregates are increasingly successfully targeted with clinical therapies at later stages of the disease, but the fundamental molecular steps in early stage disease that trigger the initial nucleation event leading to the conversion of monomeric Aβ peptide into pathological aggregates remain unknown. Here, we show that the Aβ peptide can form biomolecular condensates on lipid bilayers both in molecular assays and in living cells.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Institute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China.
Introduction: Alzheimer's disease (AD) patients with higher educational attainment (EA) often exhibit better cognitive function. However, the relationship among EA status, AD pathology, structural brain reserve, and cognitive decline requires further investigation.
Methods: We compared cognitive performance across different amyloid beta (Aβ) positron emission tomography (A ±) statuses and EA levels (High EA/Low EA).
Adv Sci (Weinh)
January 2025
Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, China.
Dietary high salt intake is increasingly recognized as a risk factor for cognitive decline and dementia, including Alzheimer's disease (AD). Recent studies have identified a population of disease-associated astrocytes (DAA)-like astrocytes closely linked to amyloid deposition and tau pathology in an AD mouse model. However, the presence and role of these astrocytes in high-salt diet (HSD) models remain unexplored.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!