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  • 1.
    Bloniecki, Victor
    et al.
    Department of Neurobiology, Caring Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institutet, Stockholm, Sweden; Department of Dermatology, Karolinska University Hospital, Solna, Sweden.
    Zetterberg, Henrik
    Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; UK Dementia Research Institute at UCL, London, UK; Department of Neurodegenerative Disease, UCL Institute of Neurology, London, UK.
    Aarsland, Dag
    Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK; Center for Age-Related Diseases, Stavanger University Hospital, Stavanger, Norway.
    Vannini, Patrizia
    Center for Alzheimer Research and Treatment, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
    Kvartsberg, Hlin
    Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
    Winblad, Bengt
    Department of Neurobiology, Caring Sciences and Society (NVS), Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden; Theme Aging, Karolinska University Hospital, Huddinge, Sweden.
    Blennow, Kaj
    Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
    Freund-Levi, yfi
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Neurobiology, Caring Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institutet, Stockholm, Sweden; Department of Psychiatry in Region Örebro County and School of Medical Sciences, Faculty of Medicine and Health, Örebro University, Örebro, Sweden; Department of Old Age Psychiatry, Psychology & Neuroscience, King's College London, London, UK.
    Are neuropsychiatric symptoms in dementia linked to CSF biomarkers of synaptic and axonal degeneration?2020Inngår i: Alzheimer's Research & Therapy, E-ISSN 1758-9193, Vol. 12, nr 1, artikkel-id 153Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: The underlying disease mechanism of neuropsychiatric symptoms (NPS) in dementia remains unclear. Cerebrospinal fluid (CSF) biomarkers for synaptic and axonal degeneration may provide novel neuropathological information for their occurrence. The aim was to investigate the relationship between NPS and CSF biomarkers for synaptic (neurogranin [Ng], growth-associated protein 43 [GAP-43]) and axonal (neurofilament light [NFL]) injury in patients with dementia.

    METHODS: A total of 151 patients (mean age ± SD, 73.5 ± 11.0, females n = 92 [61%]) were included, of which 64 had Alzheimer's disease (AD) (34 with high NPS, i.e., Neuropsychiatric Inventory (NPI) score > 10 and 30 with low levels of NPS) and 18 were diagnosed with vascular dementia (VaD), 27 with mixed dementia (MIX), 12 with mild cognitive impairment (MCI), and 30 with subjective cognitive impairment (SCI). NPS were primarily assessed using the NPI. CSF samples were analyzed using enzyme-linked immunosorbent assays (ELISAs) for T-tau, P-tau, Aβ1-42, Ng, NFL, and GAP-43.

    RESULTS: No significant differences were seen in the CSF levels of Ng, GAP-43, and NFL between AD patients with high vs low levels of NPS (but almost significantly decreased for Ng in AD patients < 70 years with high NPS, p = 0.06). No significant associations between NPS and CSF biomarkers were seen in AD patients. In VaD (n = 17), negative correlations were found between GAP-43, Ng, NFL, and NPS.

    CONCLUSION: Our results could suggest that low levels of Ng may be associated with higher severity of NPS early in the AD continuum (age < 70). Furthermore, our data may indicate a potential relationship between the presence of NPS and synaptic as well as axonal degeneration in the setting of VaD pathology.

  • 2.
    Bos, Isabelle
    et al.
    Department of Psychiatry and Neuropsychology, School of Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands.
    Verhey, Frans R.
    Department of Psychiatry and Neuropsychology, School of Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands.
    Ramakers, Inez H. G. B.
    Department of Psychiatry and Neuropsychology, School of Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands.
    Jacobs, Heidi I. L.
    Department of Psychiatry and Neuropsychology, School of Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands.
    Soininen, Hilkka
    Institute of Clinical Medicine, Neurology, University of Eastern Finland, Kuopio, Finland; Neurocenter & Department of Neurology, Kuopio University Hospital, Kuopio, Finland.
    Freund-Levi, Yvonne
    Department of Neurobiology, Caring Sciences and Society (NVS), Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Hampel, Harald
    AXA Research Fund and UPMC Chair, Sorbonne Universités, Université Pierre et Marie Curie (UPMC), Paris, France; Institut du cerveau et de la moelle (ICM), Hôpital Pitié-Salpêtrière, Paris, France.
    Tsolaki, Magda
    Aristotle University of Thessaloniki, Memory and Dementia Center, 3rd Department of Neurology, “G Papanicolau” General Hospital, Thessaloniki, Greece.
    Wallin, Åsa K.
    Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University, Lund, Sweden.
    van Buchem, Mark A.
    Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands.
    Oleksik, Ania
    Department of Gerontology and Geriatrics, Leiden University Medical Center, Leiden, The Netherlands.
    Verbeek, Marcel M.
    Departments of Neurology and Laboratory Medicine, Donders Institute for Brain, Cognition and Behaviour, Radboud Alzheimer Center, Radboud University Medical Center, Nijmegen, The Netherlands.
    Olde Rikkert, Marcel
    Radboudumc Alzheimer Centre, Department of Geriatric Medicine, Radboud University Medical Center, Nijmegen, The Netherlands.
    van der Flier, Wiesje M.
    Department of Neurology, Alzheimer Centre, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, Netherlands.
    Scheltens, Philip
    Department of Neurology, Alzheimer Centre, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, Netherlands.
    Aalten, Pauline
    Department of Psychiatry and Neuropsychology, School of Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands.
    Visser, Pieter Jelle
    Department of Psychiatry and Neuropsychology, School of Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands; Department of Neurology, Alzheimer Centre, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, Netherlands.
    Vos, Stephanie J. B.
    Department of Psychiatry and Neuropsychology, School of Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands.
    Cerebrovascular and amyloid pathology in predementia stages: the relationship with neurodegeneration and cognitive decline2017Inngår i: Alzheimer's Research & Therapy, E-ISSN 1758-9193, Vol. 9, nr 1, artikkel-id 101Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Cerebrovascular disease (CVD) and amyloid-β (Aβ) often coexist, but their influence on neurodegeneration and cognition in predementia stages remains unclear. We investigated the association between CVD and Aβ on neurodegenerative markers and cognition in patients without dementia.

    METHODS: We included 271 memory clinic patients with subjective or objective cognitive deficits but without dementia from the BioBank Alzheimer Center Limburg cohort (n = 99) and the LeARN (n = 50) and DESCRIPA (n = 122) multicenter studies. CSF Aβ1-42 and white matter hyperintensities (WMH) on magnetic resonance imaging (MRI) scans were used as measures of Aβ and CVD, respectively. Individuals were classified into four groups based on the presence (+) or absence (-) of Aβ and WMH. We investigated differences in phosphorylated tau, total tau (t-tau), and medial temporal lobe atrophy (MTA) between groups using general linear models. We examined cognitive decline and progression to dementia using linear mixed models and Cox proportional hazards models. All analyses were adjusted for study and demographics.

    RESULTS: MTA and t-tau were elevated in the Aβ - WMH+, Aβ + WMH-, and Aβ + WMH+ groups. MTA was most severe in the Aβ + WMH+ group compared with the groups with a single pathology. Both WMH and Aβ were associated with cognitive decline, but having both pathologies simultaneously was not associated with faster decline.

    CONCLUSIONS: In the present study, we found an additive association of Aβ and CVD pathology with baseline MTA but not with cognitive decline. Because our findings may have implications for diagnosis and prognosis of memory clinic patients and for future scientific research, they should be validated in a larger sample with longer follow-up.

  • 3.
    Bos, Isabelle
    et al.
    Department of Psychiatry and Neuropsychology, School of Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands.
    Verhey, Frans R
    Department of Psychiatry and Neuropsychology, School of Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands.
    Ramakers, Inez H G B
    Department of Psychiatry and Neuropsychology, School of Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands.
    Jacobs, Heidi I L
    Department of Psychiatry and Neuropsychology, School of Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands.
    Soininen, Hilkka
    Institute of Clinical Medicine, Neurology, University of Eastern Finland, Kuopio, Finland; Neurocenter and Department of Neurology, Kuopio University Hospital, Kuopio, Finland.
    Freund-Levi, Yvonne
    Department of Neurobiology, Caring Sciences and Society (NVS), Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Hampel, Harald
    Institut du cerveau et de la moelle (ICM), Hôpital Pitié-Salpêtrière, Paris, France; AXA Research Fund and UPMC Chair Sorbonne Universités, Université Pierre et Marie Curie (UPMC), Paris, France.
    Tsolaki, Magda
    Memory and Dementia Center, 3rd Department of Neurology, Aristotle University of Thessaloniki, G Papanicolau, General Hospital, Thessaloniki, Greece.
    Wallin, Åsa K
    Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University, Lund, Sweden.
    van Buchem, Mark A
    Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands.
    Oleksik, Ania
    Department of Gerontology and Geriatrics, Leiden University Medical Center, Leiden, The Netherlands.
    Verbeek, Marcel M
    Departments of Neurology and Laboratory Medicine, Donders Institute for Brain, Cognition and Behaviour, Radboud Alzheimer Center, Radboud University Medical Center, Nijmegen, The Netherlands.
    Rikkert, Marcel Olde
    Radboudumc Alzheimer Centre, Department of Geriatric Medicine, Radboud University Medical Center, Nijmegen, The Netherlands.
    van der Flier, Wiesje M
    Department of Neurology, Alzheimer Centre, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, Netherlands.
    Scheltens, Philip
    Department of Neurology, Alzheimer Centre, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, Netherlands.
    Aalten, Pauline
    Department of Psychiatry and Neuropsychology, School of Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands.
    Visser, Pieter Jelle
    Department of Psychiatry and Neuropsychology, School of Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands; Department of Neurology, Alzheimer Centre, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, Netherlands.
    Vos, Stephanie J B
    Department of Psychiatry and Neuropsychology, School of Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands.
    Correction to: Cerebrovascular and amyloid pathology in predementia stages2018Inngår i: Alzheimer's Research & Therapy, E-ISSN 1758-9193, Vol. 10, nr 56Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Upon publication of this article [1], it was noticed that there were some inconsistencies in Tables 1, 2 and 3. Some of the superscript letters were incorrectly assigned. Please see below the correct tables.

  • 4.
    Wu, Jie
    et al.
    Institute of Neurology, Huashan Hospital, Fudan University, Shanghai, China; National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China; National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
    Xiao, Zhenxu
    Institute of Neurology, Huashan Hospital, Fudan University, Shanghai, China; National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China; National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
    Wang, Mengjing
    National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China; Departemnt of Nephrology, National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China.
    Wu, Wanqing
    Institute of Neurology, Huashan Hospital, Fudan University, Shanghai, China; National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China; National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
    Ma, Xiaoxi
    Institute of Neurology, Huashan Hospital, Fudan University, Shanghai, China; National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China; National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
    Liang, Xiaoniu
    Institute of Neurology, Huashan Hospital, Fudan University, Shanghai, China; National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China; National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
    Zheng, Li
    Institute of Neurology, Huashan Hospital, Fudan University, Shanghai, China; National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China; National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
    Ding, Saineng
    Institute of Neurology, Huashan Hospital, Fudan University, Shanghai, China; National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China; National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
    Luo, Jianfeng
    Department of Biostatistics, School of Public Health, Fudan University, Shanghai, China.
    Cao, Yang
    Örebro universitet, Institutionen för medicinska vetenskaper. Clinical Epidemiology and Biostatistics, School of Medical Sciences, Örebro University, Örebro, Sweden.
    Hong, Zhen
    Institute of Neurology, Huashan Hospital, Fudan University, Shanghai, China; National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China; National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
    Chen, Jing
    National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China; Departemnt of Nephrology, National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China.
    Zhao, Qianhua
    Institute of Neurology, Huashan Hospital, Fudan University, Shanghai, China; National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China; National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China; MOE Frontiers Center for Brain Science, Fudan University, Shanghai, China.
    Ding, Ding
    Institute of Neurology, Huashan Hospital, Fudan University, Shanghai, China; National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China; National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
    The impact of kidney function on plasma neurofilament light and phospho-tau 181 in a community-based cohort: the Shanghai Aging Study2024Inngår i: Alzheimer's Research & Therapy, E-ISSN 1758-9193, Vol. 16, nr 1, artikkel-id 32Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: The blood-based biomarkers are approaching the clinical practice of Alzheimer's disease (AD). Chronic kidney disease (CKD) has a potential confounding effect on peripheral protein levels. It is essential to characterize the impact of renal function on AD markers.

    METHODS: Plasma phospho-tau181 (P-tau181), and neurofilament light (NfL) were assayed via the Simoa HD-X platform in 1189 dementia-free participants from the Shanghai Aging Study (SAS). The estimated glomerular filter rate (eGFR) was calculated. The association between renal function and blood NfL, P-tau181 was analyzed. An analysis of interactions between various demographic and comorbid factors and eGFR was conducted.

    RESULTS: The eGFR levels were negatively associated with plasma concentrations of NfL and P-tau181 (B = - 0.19, 95% CI - 0.224 to - 0.156, P < 0.001; B = - 0.009, 95% CI - 0.013 to -0.005, P < 0.001, respectively). After adjusting for demographic characteristics and comorbid diseases, eGFR remained significantly correlated with plasma NfL (B = - 0.010, 95% CI - 0.133 to - 0.068, P < 0.001), but not with P-tau181 (B = - 0.003, 95% CI - 0.007 to 0.001, P = 0.194). A significant interaction between age and eGFR was found for plasma NfL (Pinteraction < 0.001). In participants ≥ 70 years and with eGFR < 60 ml/min/1.73 m2, the correlation between eGFR and plasma NfL was significantly remarkable (B = - 0.790, 95% CI - 1.026 to - 0,554, P < 0.001).

    CONCLUSIONS: Considering renal function and age is crucial when interpreting AD biomarkers in the general aging population.

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