Purpose: Fatigue is a common symptom of multiple sclerosis (MS) and can adversely affect all aspect of quality of life. The etiology of fatigue remains unclear, and its treatments are suboptimal. Characterizing the phenotypes of fatigued persons with MS may help advance research on fatigue's etiology and identify ways to personalize fatigue interventions to improve quality of life. The purpose of this study was to identify fatigue phenotypes; examine phenotype stability overtime; and characterize phenotypes by health and function, social and environmental determinants, psychosocial factors, and engagement in healthy behaviors.
Methods: We conducted a longitudinal study over a 3-month period with 289 fatigued participants with MS. To identify fatigue phenotypes and determine transition probabilities, we used latent profile and transition analyses with valid self-report measures of mental and physical fatigue severity, the mental and physical impact of fatigue, depression, anxiety, and sleep quality. We used ANOVAs and effect sizes to characterize differences among phenotypes.
Results: The best fitting model included six subgroups of participants: Mild Phenotype, Mild-to-Moderate Phenotype, Moderate-to-Severe Phenotype, Severe Phenotype, Fatigue-dominant Phenotype, and Mental Health-dominant Phenotype. The transition analysis indicated that phenotypic membership was highly stable. Variables with a large eta squared effect size included environmental barriers, self-efficacy, and fatigue catastrophizing.
Conclusion: These results indicate that the magnitude of fatigue experienced may be more important to consider than the type of fatigue when characterizing fatigue phenotypes. Future research should explore whether tailoring interventions to environmental barriers, self-efficacy, and fatigue catastrophizing reduce the likelihood of transitioning to a more severe phenotype.
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http://dx.doi.org/10.1007/s11136-022-03204-0 | DOI Listing |
Sci Rep
January 2025
Opensci, LLC, Tucson, AZ, 85750, USA.
The transition to menopause is associated with disappearance of menstrual cycle symptoms and emergence of vasomotor symptoms. Although menopausal women report a variety of additional symptoms, it remains unclear which emerge prior to menopause, which occur in predictable clusters, how clusters change across the menopausal transition, or if distinct phenotypes are present within each life stage. We present an analysis of symptoms in premenopausal to menopausal women using the MenoLife app, which includes 4789 individuals (23% premenopausal, 29% perimenopausal, 48% menopausal) and 147,501 symptom logs (19% premenopausal, 39% perimenopausal, 42% menopausal).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Background: Clinicopathological studies of Alzheimer's disease (AD) have demonstrated that synaptic or neuronal loss and clinical cognitive decline do not reliably correlate with fibrillar amyloid burden. We created a transgenic mouse model overexpressing Dutch (E693Q) mutant human amyloid precursor protein (APP) driven by the pan-neuronal Thy1 promoter. Accumulation of APP carboxyl-terminal fragments was observed in the brains of these mice, which develop an impaired learning phenotype directly proportional to brain oAβ levels.
View Article and Find Full Text PDFImmunohematology
December 2024
International Blood Group Reference Laboratory, NHS Blood and Transplant, Bristol, UK.
A previously healthy 32-year-old male patient was admitted to hospital with malaise, dyspnea, anemia, thrombocytopenia, and leukopenia. Anemia and thrombocytopenia worsened during the third week. Considering the possible need for transfusion, routine ABO and D typing and an antibody detection test were performed.
View Article and Find Full Text PDFFront Oncol
December 2024
Clinic for Gastroenterology and Gastrointestinal Oncology, University Medical Center Göttingen (UMG), Göttingen, Germany.
Pancreatic ductal adenocarcinoma (PDAC) is characterized by its poor prognosis. Traditional Japanese herbal medicine (Kampo), such as Juzentaihoto (a standardized combination of 10 herbal extracts), has shown immune modulatory effects, modulation of microcirculation, and amelioration of fatigue. It is administered to patients to prevent deterioration of cachexia and counteract side effects of chemotherapy.
View Article and Find Full Text PDFFront Physiol
December 2024
Institute of Biochemistry and Cell Biology, National Research Council (CNR), Monterotondo (RM), Italy.
Duchenne muscular dystrophy (DMD) is caused by mutations in the gene encoding dystrophin, a subsarcolemmal protein whose absence results in increased susceptibility of the muscle fiber membrane to contraction-induced injury. This results in increased calcium influx, oxidative stress, and mitochondrial dysfunction, leading to chronic inflammation, myofiber degeneration, and reduced muscle regenerative capacity. Fast glycolytic muscle fibers have been shown to be more vulnerable to mechanical stress than slow oxidative fibers in both DMD patients and DMD mouse models.
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