People living with advanced dementia risk being seen as someone without personhood in contemporary societies, an understanding that has been described and challenged for decades in dementia scholarly literature. Such perception can be characterised as forms of existential dehumanisation, which still asserts itself in dementia care practices, adversely affecting the ethical and caring aspects of such care. To challenge dehumanisation in dementia care, we must first learn to recognise what foster it in caring relations. Thus, the aim of our study is to identify existing perceptions of care recipients living with advanced dementia, which elicit dehumanising attitudes among formal caregivers. We conducted an integrative review based on Whittemore and Knafl's updated methodology. This allowed us to identify and analyse 26 articles incorporating both qualitative- and quantitative studies as well as theoretical- and grey literature all describing perceptions of care recipients living with dementia that lead to dehumanisation. Studying the darker sides in caring relations was to be beneficial in improving dementia care practices. Through an analytical process five themes that can sprout dehumanising attitudes in caring relations were identified, which include perceiving people living with advanced dementia as (1) absurd, (2) shadow, (3) perilous, (4) void, or (5) repugnant. We argue that these perceptions can be seen as unintentional and stem from a misled embodied perception, which caregivers should learn to recognise and consequently be able to resist through virtue ethics. Our study indicates that challenging dehumanisation is a practical matter of identifying and reacting in a timely way to ones misled embodied perceptions. We suggest the five themes offer a potential means to warn formal caregivers of impending dehumanising attitudes and help them to review how they ethically are thinking and perceiving the person living with advanced dementia.
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http://dx.doi.org/10.1177/09697330241277989 | DOI Listing |
Acta Neuropathol Commun
January 2025
Department of Physiology and Pharmacology, Sapienza University of Rome, 00185, Rome, Italy.
The generation of retinal models from human induced pluripotent stem cells holds significant potential for advancing our understanding of retinal development, neurodegeneration, and the in vitro modeling of neurodegenerative disorders. The retina, as an accessible part of the central nervous system, offers a unique window into these processes, making it invaluable for both study and early diagnosis. This study investigates the impact of the Frontotemporal Dementia-linked IVS 10 + 16 MAPT mutation on retinal development and function using 2D and 3D retinal models derived from human induced pluripotent stem cells.
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January 2025
Institute of Neuronal Cell Biology, Technical University Munich, Munich, Germany.
Our understanding of Alzheimer's disease (AD) has transformed from a purely neuronal perspective to one that acknowledges the involvement of glial cells. Despite remarkable progress in unraveling the biology of microglia, astrocytes and vascular elements, the exploration of oligodendrocytes in AD is still in its early stages. Contrary to the traditional notion of oligodendrocytes as passive bystanders in AD pathology, emerging evidence indicates their active participation in and reaction to amyloid and tau pathology.
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January 2025
Northwell Health, New Hyde Park, NY, USA.
Background: Oropharyngeal dysphagia (dysphagia) is a common (up to 86%) and devastating syndrome in hospitalized older adults with dementia.
Objective: To describe the perspectives of dysphagia management in hospitalized patients with dementia among hospital medicine providers (i.e.
Mol Biol Rep
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Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Raebareli Transit Campus, Bijnour-Sisendi Road, Sarojini Nagar, Lucknow, Uttar Pradesh, 226002, India.
Alzheimer's disease (AD) is a common neurodegenerative disease characterized by progressive memory loss and cognitive decline. The processes underlying the pathophysiology of AD are still not fully understood despite a great deal of research. Since mitochondrial dysfunction affects cellular energy metabolism, oxidative stress, and neuronal survival, it is becoming increasingly clear that it plays a major role in the development of AD.
View Article and Find Full Text PDFJ Biol Chem
January 2025
UK Dementia Research Institute at the University of Cambridge, Department of Clinical Neurosciences, Hills Road, Cambridge, CB2 0AH, United Kingdom. Electronic address:
The assembly of tau into filaments defines tauopathies, a group of neurodegenerative diseases including Alzheimer's disease (AD), Pick's disease (PiD), corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP). The seeded aggregation of tau has been modelled in cell culture using pro-aggregant modifications such as truncation of N- and C-termini and point-mutations within the microtubule-binding repeat domain. This limits the applicability of research findings to sporadic disease, where aggregates contain wild-type, full-length tau.
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