Background: This paper offers an understanding of the lifeworld of a person with Parkinson's Disease derived from interpretative phenomenological analysis (IPA).
Aims: The paper has two main aims: firstly, to demonstrate how a focus on individual experience chimes with and can inform current ideas of a more personalised humanised form of healthcare for people living with Parkinson's disease; and secondly, to demonstrate how an IPA study can illuminate particularity whilst being able to make, albeit cautiously, more general knowledge claims that can inform wider caring practices.
Methods: It achieves these aims through the detailed description and interpretation of one person's experience of living with Parkinson's disease using the IPA approach.
Results: Three analytic themes point to how the various constituents of the lifeworld, such as embodiment, selfhood, temporality and relationality are made manifest. These enable the IPA researcher to make well-judged inferences, which can have value beyond the individual case.
Conclusions: A key feature of IPA is its commitment to an idiographic approach that recognises the value of understanding a situated experience from the perspective of a particular person or persons.
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http://dx.doi.org/10.1177/1744987118821396 | DOI Listing |
Sci Rep
December 2024
Department of Medical Microbiology, Radboudumc, Nijmegen, The Netherlands.
The aetiology of Alzheimer's disease (AD) and Parkinson's disease (PD) are unknown and tend to manifest at a late stage in life; even though these neurodegenerative diseases are caused by different affected proteins, they are both characterized by neuroinflammation. Links between bacterial and viral infection and AD/PD has been suggested in several studies, however, few have attempted to establish a link between fungal infection and AD/PD. In this study we adopted a nanopore-based sequencing approach to characterise the presence or absence of fungal genera in both human brain tissue and cerebrospinal fluid (CSF).
View Article and Find Full Text PDFNat Commun
December 2024
Department of Theory and Bio-Systems, Max Planck Institute of Colloids and Interfaces, 14476, Potsdam, Germany.
Neurodegeneration in Huntington's disease (HD) is accompanied by the aggregation of fragments of the mutant huntingtin protein, a biomarker of disease progression. A particular pathogenic role has been attributed to the aggregation-prone huntingtin exon 1 (HTTex1), generated by aberrant splicing or proteolysis, and containing the expanded polyglutamine (polyQ) segment. Unlike amyloid fibrils from Parkinson's and Alzheimer's diseases, the atomic-level structure of HTTex1 fibrils has remained unknown, limiting diagnostic and treatment efforts.
View Article and Find Full Text PDFNat Commun
December 2024
Weldon School of Biomedical Engineering, West Lafayette, Indiana, IN, USA.
Circuit-based biomarkers distinguishing the gradual progression of Lewy pathology across synucleinopathies remain unknown. Here, we show that seeding of α-synuclein preformed fibrils in mouse dorsal striatum and motor cortex leads to distinct prodromal-phase cortical dysfunction across months. Our findings reveal that while both seeding sites had increased cortical pathology and hyperexcitability, distinct differences in electrophysiological and cellular ensemble patterns were crucial in distinguishing pathology spread between the two seeding sites.
View Article and Find Full Text PDFNat Commun
December 2024
Center for Neurosciences, The Feinstein Institutes for Medical Research, Manhasset, NY, USA.
Isolated rapid eye movement sleep behavior disorder is a prodrome of α-synucleinopathies. Using positron emission tomography, we assessed changes in Parkinson's disease-related motor and cognitive metabolic networks and caudate/putamen dopaminergic input in a 4-year longitudinal imaging study of 13 male subjects with this disorder. We also correlated times to phenoconversion with baseline network expression in an independent validation sample.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Pathology, Molecular, and Cell-Based Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Introduction: Alzheimer's disease (AD), primary age-related tauopathy (PART), and chronic traumatic encephalopathy (CTE) all feature hyperphosphorylated tau (p-tau)-immunoreactive neurofibrillary degeneration, but differ in neuroanatomical distribution and progression of neurofibrillary degeneration and amyloid beta (Aβ) deposition.
Methods: We used Nanostring GeoMx Digital Spatial Profiling to compare the expression of 70 proteins in neurofibrillary tangle (NFT)-bearing and non-NFT-bearing neurons in hippocampal CA1, CA2, and CA4 subregions and entorhinal cortex of cases with autopsy-confirmed AD (n = 8), PART (n = 7), and CTE (n = 5).
Results: There were numerous subregion-specific differences related to Aβ processing, autophagy/proteostasis, inflammation, gliosis, oxidative stress, neuronal/synaptic integrity, and p-tau epitopes among these different disorders.
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