| 91. |
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| 92. |
- Jablonowski, Robert, et al.
(författare)
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The Authors Reply
- 2016
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Ingår i: JACC: Cardiovascular Imaging. - : Elsevier BV. - 1876-7591 .- 1936-878X. ; 9:8, s. 7-1016
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Tidskriftsartikel (refereegranskat)
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| 93. |
- Javanshiri, Keivan, et al.
(författare)
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Atherosclerosis, Hypertension, and Diabetes in Alzheimer's Disease, Vascular Dementia, and Mixed Dementia : Prevalence and Presentation
- 2018
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Ingår i: Journal of Alzheimer's Disease. - 1387-2877. ; 65:4, s. 1247-1258
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Tidskriftsartikel (refereegranskat)abstract
- Background: Alzheimer's disease (AD) is the most prevalent cause of dementia with vascular dementia (VaD) being second alongside with mixed AD and VaD, according to some. For some time, it has been proposed that cardiovascular disease (CaVD), hypertension, and diabetes mellitus (DM), which are known risk factors for VaD, also are associated with and contribute to the development of AD. Objective: The aim of this study was to investigate the prevalence of these proposed general risk factors, and to document presence of CaVD as evidenced from clinical records or from autopsy findings, further to correlate these with the diagnoses AD, VaD and mixed AD-VaD (MD), respectively. Methods: Autopsy reports at the Clinical Department of Pathology in Lund from 1992-2017 were analyzed. All cases with a complete autopsy report and a neuropathologically diagnosed dementia disorder (AD, VaD, or MD) were selected on the condition of a clinical diagnosis of dementia. Clinical data were retrieved through medical records and the Swedish National Diabetes Register (NDR). A total of 268 subjects were included. Results: In AD, there was less CaVD as significantly less organ/tissue findings (p < 0.05), significantly less hypertension (p < 0.001), and likewise significantly less DM (p = 0.0014) than in VaD, with the MD group results being set between these two in all aspects studied. Conclusion: AD and VaD exhibit such different profiles of organ and vascular damage as well as of hypertension and DM that they clearly point toward different pathogenic origin with low likelihood of shared risk factors.
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| 94. |
- Javanshiri, Keivan, et al.
(författare)
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Cardiac Alpha-Synuclein Is Present in Alpha-Synucleinopathies
- 2022
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Ingår i: Journal of Parkinson's Disease. - 1877-718X. ; 12:4, s. 1125-1131
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Tidskriftsartikel (refereegranskat)abstract
- Background: Alpha-synucleinopathies (AS) are characterized by pathologic aggregations of alpha-synuclein (α-syn) in the central nervous system, and comprise dementia with Lewy bodies, Parkinson's disease, and multiple system atrophy. Previous studies on AS have reported findings of α-syn pathology in the peripheral nervous system of multiple organs, including the heart.Objective: The aim of this study was to further investigate and confirm the presence of cardiac α-syn in AS compared to other major neurocognitive disorders in a neuropathologically confirmed cohort.Methods: All deceased patients with performed autopsy and with neuropathologically confirmed AS at the Clinical Department of Pathology in Lund 2010-May 2021 were evaluated for inclusion. Cases with insufficiently sampled cardiac tissue or only limited neuropathological investigation were excluded. An age-matched group of individuals with other neurodegenerative diseases, having no α-syn in the CNS, served as controls. In total, 68 AS and 32 control cases were included in the study. Immunohistochemistry for detection of cardiac α-syn aggregates was performed.Results: The AS group had a significantly higher prevalence of cardiac α-syn pathology (p≤0.001) than the control group, 82% and 0%, respectively.Conclusion: This study confirms the association between AS and the presence of cardiac α-syn in a neuropathologically confirmed cohort. This motivates further research on potential pathophysiological effects on cardiac function in AS patients.
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| 95. |
- Javanshiri, Keivan, et al.
(författare)
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Cardiovascular Disease, Diabetes Mellitus, and Hypertension in Lewy Body Disease: A Comparison with Other Dementia Disorders
- 2019
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Ingår i: Journal of Alzheimer's disease : JAD. - 1387-2877. ; 71:3, s. 851-859
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Tidskriftsartikel (refereegranskat)abstract
- Background: Research concerning the potential roles of cardiovascular disease (CaVD) and diabetes mellitus (DM) as risk factors for Lewy body disease (LBD) is limited. These disorders are, however, established risk factors for vascular dementia (VaD) and have been proposed as risk factors for Alzheimer’s disease (AD). Objective: The aim of this study was to investigate the prevalence of CaVD and DM in LBD and compare the results with previous findings in cases with AD, VaD, and mixed AD-VaD (MD). Methods: Autopsy reports at the Clinical Department of Pathology in Lund from 2001–2018 were analyzed. All cases with a complete neuropathological diagnosis of LBD were selected, not distinguishing between subjects with clinical Parkinson disease dementia and dementia with Lewy bodies, on the condition of a clinical diagnosis of dementia. Clinical data were retrieved through the patients’ medical records and the Swedish National Diabetes Register (NDR) and compared with those of the AD, VaD, and MD cases. Results: In LBD, there was less CaVD, significantly less DM (p = 0.002) and likewise significantly less hypertension (p < 0.001) than in VaD. The results of the LBD group were consistent with the results of the AD group. Conclusion Our findings of a low prevalence of CaVD and CaVD risk factors in LBD and in AD argue against the association between these risk factors and their contribution to the development of neurodegenerative diseases.
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| 96. |
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| 97. |
- Javanshiri, Keivan, et al.
(författare)
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Sudden cardiac death in synucleinopathies
- 2023
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Ingår i: Journal of Neuropathology and Experimental Neurology. - : Oxford University Press (OUP). - 1554-6578 .- 0022-3069. ; 82:3, s. 242-249
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Tidskriftsartikel (refereegranskat)abstract
- The purpose of this study was to investigate the cause of death in subjects with α-synucleinopathies (ASs) and the confirmed presence of cardiac α-synuclein (α-syn), compared to non-AS disorders in a neuropathologically confirmed cohort. In total, 78 neuropathologically confirmed AS cases positive for cardiac α-syn were included in the study. Individuals with other neurocognitive diseases, having no α-syn in the brainstem or above, nor in cardiac nerves, served as controls (n = 53). Data regarding the cause of death, cardiac α-syn, pathological cardiac findings, and cardio- and cerebrovascular disease were assembled from autopsy reports and medical records. In the AS group, there was a significantly higher prevalence of sudden cardiac death ([SCD]; n = 40, 51.3%) compared to the control group (n = 12, 22.6%, p
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| 98. |
- Järnum, Hanna, et al.
(författare)
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Diffusion and perfusion MRI of the brain in comatose patients treated with mild hypothermia after cardiac arrest: A prospective observational study.
- 2009
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Ingår i: Resuscitation. - : Elsevier BV. - 1873-1570 .- 0300-9572. ; 80, s. 425-430
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Outcome for resuscitated cardiac arrest (CA) patients is poor. The 1-year survival rate with favourable neurological outcome (CPC 1-2) after out-of-hospital CA is reported to be 4%. Among resuscitated patients treated within an ICU, approximately 50% regain consciousness, whereas the other 50% remain comatose before they die. Induced hypothermia significantly improves the neurological outcome and survival in patients with primary CA who remain comatose after return of spontaneous circulation. AIM: To evaluate magnetic resonance imaging (MRI) changes in resuscitated CA patients remaining in coma after treatment with hypothermia. METHODS: This prospective, observational study comprised 20 resuscitated CA patients who remained in coma 3 days after being treated with mild hypothermia (32-34 degrees C during 24h). Diffusion and perfusion MRI of the entire brain was performed approximately 5 days after CA. Autopsy was done on two patients. RESULTS: The largest number of diffusion changes on MRI was found in the 16 patients who died. The parietal lobe showed the largest difference in number of acute ischaemic MRI lesions in deceased compared with surviving patients. Perfusion changes, >/=+/-2 SD compared with healthy volunteers from a previously published cerebral perfusion study, were found in seven out of eight patients. The autopsies showed lesions corresponding to the pathologic changes seen on MRI. CONCLUSION: Diffusion and perfusion MRI are potentially helpful tools for the evaluation of ischaemic brain damage in resuscitated comatose patients treated with hypothermia after CA.
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| 99. |
- Karlsson, Christine, et al.
(författare)
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Genetic intratumour heterogeneity in high-grade brain tumours is associated with telomere-dependent mitotic instability.
- 2007
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Ingår i: Neuropathology & Applied Neurobiology. - : Wiley. - 1365-2990 .- 0305-1846. ; 33:4, s. 440-454
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Tidskriftsartikel (refereegranskat)abstract
- Glioblastoma multiforme (GBM) and other high-grade brain tumours are typically characterized by complex chromosome abnormalities and extensive intratumour cytogenetic heterogeneity. The mechanisms behind this diversity have been little explored. In this study, we analysed the pattern of chromosome segregation at mitosis in 20 brain tumours. We found an abnormal segregation of chromatids at mitosis through anaphase bridging (10-25% of anaphase cells) in all 10 GBMs. Anaphase bridging was also found in two medulloblastomas (7-15%), one anaplastic astrocytoma (17%) and one oligodendroglioma (6%). These tumours showed a relatively high degree of cytogenetic complexity and heterogeneity. In contrast, cell division abnormalities were not found in low-grade brain tumours with less complex karyotypes, including two pilocytic astrocytomas and two ependymomas. Further analysis of two GBMs by fluorescence in situ hybridization with telomeric repeat probes revealed excessive shortening of TTAGGG repeats, indicating dysfunctional protection of chromosome ends. In xenografts established from these GBMs, there was a gradual reduction in cytogenetic heterogeneity through successive passages as the proportion of abnormally short telomeres was reduced and the frequency of anaphase bridges decreased from >25% to 0. However, bridging could be reintroduced in late-passage xenograft cells by pharmacological induction of telomere shortening, using a small-molecule telomerase inhibitor. Telomere-dependent abnormal segregation of chromosomes at mitosis is thus a common phenomenon in high-grade brain tumours and may be one important factor behind cytogenetic intratumour diversity in GBM.
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| 100. |
- Kongstad, Poul, et al.
(författare)
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Mechanical compressions and autopsy findings
- 2005
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Ingår i: Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. - 1757-7241. ; 13:2, s. 87-88
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Tidskriftsartikel (refereegranskat)
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