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- Axenhus, Michael, et al.
(författare)
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Changes in dementia diagnoses in Sweden during the COVID-19 pandemic
- 2022
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Ingår i: BMC Geriatrics. - : BioMed Central. - 1471-2318. ; 22:1
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: The COVID-19 pandemic has caused large disruptions to healthcare systems. Refocus on COVID-19 related care might have contributed to indirect effects on other healthcare areas. Care focused on acute conditions have been negatively affected although research into the effects on chronic and care intensive patient groups such as patients with dementia diseases is lacking. In this study we evaluated dementia diagnosis trends in Sweden during 2015–2020 according to International Classification of Disease version 10 coding of common dementia diseases.Methods: Regional and national statistics in the form of International Classification of Disease version 10 coding, COVID-19 incidence, mortality data, and population census data were collected from the National Institute of Health and Welfare. Logistic regression analysis was performed to identify trends of dementia diagnosis during 2015–2020. Correlation test was performed between COVID-19 incidence, mortality rates, and dementia coding.Results: Dementia diagnosis incidence has been declining since 2015 and further decline was noted in many regions in Sweden during 2020. As COVID-19 incidence increased, fewer cases of dementia were diagnosed, a decrease that differentially impacted women and those who were advanced in age.Conclusions: Dementia diagnosis incidence in Sweden has been on a decline since 2015. The COVID-19 pandemic caused a further larger decline in dementia diagnosis incidence during 2020. COVID-19 incidence, but not mortality, was associated with decrease in dementia diagnosis incidence. There might be a large number of undiagnosed patients with dementia and healthcare reforms should be enacted to address this. Women and elderly are particularly vulnerable groups.
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| 2. |
- Axenhus, Michael
(författare)
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Characterization of proteins involved in disease progression in Alzheimer disease
- 2023
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Alzheimer disease (AD) is a neurodegenerative disease and severe neuronal loss is already taking place at the time of diagnosis. AD affects nearly 50 million people worldwide and the incidence is expected to rise significantly in the coming decades, making the disease a high priority healthcare concern. There are two main hallmarks of AD pathology, the intraneuronal tau tangles and the mostly extracellular amyloid plaques. Current treatment strategies for AD have tried targeting both tau and amyloid plaques although with limited success. However, since AD is a multifactorial disease with many risk factors, a multifaceted approach is necessary to tailor treatment. Further understanding of the pathogenesis of AD is required to enable the development of novel drugs and treatment strategies. In this thesis, we use proteomics, bioinformatics, and microscopy in an attempt to identify and characterize proteins which might influence AD progression and pathogenesis. We utilize the AD mouse model AppNL-F/NL-F, which is a knock-in mouse model that overproduces amyloid β leading to Aβ plaque pathology without artifacts associated with APP overexpression applied in previous AD mouse models. We also study AD brain and neuronal cultures obtained from the AppNL-F/NL-F mouse. In Paper I, we show that a combination of proteomics and bioinformatics can identify proteins involved in AD pathology in the AppNL-F/NL-F mice. Using immunofluorescence, we discovered that huntingtin, the pathogenic protein in Huntington disease, is abundant in the hippocampus of the AppNL-F/NL-F mouse at a presymptomatic stage. We furthermore localized the expression of huntingtin to pyramidal neuronal cells early in the mouse life span. In Paper II, we expand on our findings of huntingtin in the AppNL-F/NL-F mouse model by studying and characterizing the expression of huntingtin in the brain of AD patients and healthy controls. We found that huntingtin was increased in the frontal cortex and the hippocampus of AD patients. Huntingtin could be found in pyramidal neurons within both the frontal cortex and the hippocampus. The accumulation pattern of huntingtin in AD did not mimic the accumulation found in Huntington disease as there was no correlation between astrocytes and huntingtin in AD brain. Furthermore, using confocal microscopy we concluded that there was no association of tau protein and huntingtin in AD brain. In paper III, we investigated the localization of the protein DDX24, a protein identified via proteomics, in AD brain and neuronal cultures derived from the AppNL-F/NL-F mouse. DDX24 belongs to a family of proteins consisting of putative RNA helicases and is implicated in translation initiation, nuclear RNA splicing and ribosome assembly. We show that DDX24 accumulates in AD brain where it associates to areas important for memory formation. We also show that DDX24 is increased in the brain of AD patients compared to healthy controls. We found DDX24 to be increased in the brain and in the neuronal cells of the AppNL-F/NL-F mouse. Decreasing DDX24 levels increased APP levels in neuronal cells. DDX24 levels also appeared to be regulated by amyloid load or vice versa. In paper IV, we investigate neuritogenesis and neurogenesis in AD brain and in the AppNL-F/NL-F mouse model. We show that Ankyrin-3, a protein important for axonal development, is detectable in AD brain and in neurons derived from the AppNL-F/NL-F mouse. We also show that a known biomarker, doublecortin, is increased in embryonic and young mice brain derived from the AppNL-F/NL-F mouse when compared to controls. Overall, our studies use proteomics, bioinformatics, and microscopy to describe the presence of huntingtin, DDX24, Ankyrin-3 and doublecortin in the brain of AD patients and AppNL-F/NL-F mouse. These results can prove helpful in our future understanding of AD pathogenesis.
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| 3. |
- Axenhus, Michael, et al.
(författare)
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Comparative outcomes of uncemented and cemented stem revision in managing periprosthetic femoral fractures : a retrospective cohort study
- 2024
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Ingår i: Journal of Orthopaedics and Traumatology. - : Springer Nature. - 1590-9921 .- 1590-9999. ; 25:1
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Periprosthetic femoral fractures (PFFs) following hip arthroplasty, especially Vancouver B2 and B3 fractures, present a challenge due to the association with a loose femoral stem, necessitating either open reduction and internal fixation or stem revision. This study aims to compare outcomes between uncemented and cemented stem revisions in managing Vancouver B2 and B3 fractures, considering factors such as hip-related complications, reoperations, and clinical outcome.Methods: A retrospective cohort study was conducted at Danderyd Hospital, Sweden, from 2008 to 2022, encompassing operatively treated Vancouver B2 and B3 fractures. Patients were categorized into uncemented and cemented stem revision groups, with data collected on complications, revision surgeries, fracture healing times, and clinical outcomes.Results: A total of 241 patients were identified. Significant differences were observed between the two groups in patient demographics, with the cemented group comprising older patients and more females. Follow up ranged from 1 to 15 years. Average follow up time was 3.9 years for the cemented group and 5.5 years for the uncemented group. The cemented stems demonstrated lower rates of dislocation (8.9% versus 22.5%, P = 0.004) and stem loosening (0.6% versus 9.3%, P = 0.004) than the uncemented method. Moreover, the cemented group exhibited shorter fracture healing times (11.4 weeks versus 16.7 weeks, P = 0.034). There was no difference in clinical outcome between groups. Mortality was higher in the cemented group.Conclusions: This retrospective study indicates that cemented stem revision for Vancouver B2–3 fractures is correlated with lower dislocation and stem loosening rates, necessitating fewer reoperations and shorter fracture healing times compared with the uncemented approach. The cemented group had a notably higher mortality rate, urging caution in its clinical interpretation. Level of evidence III
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