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  • 1.
    Hansson, Oskar
    et al.
    Lund University, Lund, Sweden; Skåne University Hospital, Lund, Sweden.
    Hall, Sara
    Lund University, Lund, Sweden; Skåne University Hospital, Lund, Sweden.
    Ohrfelt, Annika
    The Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
    Zetterberg, Henrik
    The Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
    Blennow, Kaj
    The Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
    Minthon, Lennart
    Lund University, Lund, Sweden.
    Nägga, Katarina
    Lund University, Lund, Sweden.
    Londos, Elisabet
    Lund University, Lund, Sweden.
    Varghese, Shiji
    United Arab Emirates University, Al Ain, United Arab Emirates.
    Majbour, Nour K
    United Arab Emirates University, Al Ain, United Arab Emirates.
    Al-Hayani, Abdulmonem
    King Abdulaziz University, Jeddah, Saudi Arabia.
    El-Agnaf, Omar Ma
    United Arab Emirates University, Al Ain, United Arab Emirates; King Abdulaziz University, Jeddah, Saudi Arabia.
    Levels of cerebrospinal fluid α-synuclein oligomers are increased in Parkinson's disease with dementia and dementia with Lewy bodies compared to Alzheimer's disease2014In: Alzheimer's Research & Therapy, E-ISSN 1758-9193, Alzheimer's research & therapy, ISSN 1758-9193, Vol. 6, no 3, article id 25Article in journal (Refereed)
    Abstract [en]

    INTRODUCTION: The objective was to study whether α-synuclein oligomers are altered in the cerebrospinal fluid (CSF) of patients with dementia, including Parkinson disease with dementia (PDD), dementia with Lewy bodies (DLB), and Alzheimer disease (AD), compared with age-matched controls.

    METHODS: In total, 247 CSF samples were assessed in this study, including 71 patients with DLB, 30 patients with PDD, 48 patients with AD, and 98 healthy age-matched controls. Both total and oligomeric α-synuclein levels were evaluated by using well-established immunoassays.

    RESULTS: The levels of α-synuclein oligomers in the CSF were increased in patients with PDD compared with the controls (P < 0.05), but not in patients with DLB compared with controls. Interestingly, the levels of α-synuclein oligomers in the CSF were also significantly higher in patients with PDD (P < 0.01) and DLB (P < 0.05) compared with patients with AD. The levels of CSF α-synuclein oligomers and the ratio of oligomeric/total-α-synuclein could distinguish DLB or PDD patients from AD patients, with areas under the curves (AUCs) of 0.64 and 0.75, respectively. In addition, total-α-synuclein alone could distinguish DLB or PDD patients from AD patients, with an AUC of 0.80.

    CONCLUSIONS: The levels of α-synuclein oligomers were increased in the CSF from α-synucleinopathy patients with dementia compared with AD cases.

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  • 2.
    Hansson, Oskar
    et al.
    Lund Univ, Sweden; Skane Univ Hosp, Sweden.
    Svensson, Martina
    Lund Univ, Sweden.
    Gustaysson, Anna-Marta
    Lund Univ, Sweden; Skane Univ Hosp, Sweden.
    Andersson, Emelie
    Lund Univ, Sweden.
    Yang, Yiyi
    Lund Univ, Sweden.
    Nägga, Katarina
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Local Health Care Services in Central Östergötland, Department of Acute Internal Medicine and Geriatrics. Lund Univ, Sweden.
    Hallmarker, Ulf
    Uppsala Univ, Sweden.
    James, Stefan
    Uppsala Univ, Sweden.
    Deierborg, Tomas
    Lund Univ, Sweden.
    Midlife physical activity is associated with lower incidence of vascular dementia but not Alzheimers disease2019In: Alzheimer's Research & Therapy, E-ISSN 1758-9193, ALZHEIMERS RESEARCH and THERAPY, Vol. 11, no 1, article id 87Article in journal (Refereed)
    Abstract [en]

    Background

    Physical activity might reduce the risk of developing dementia. However, it is still unclear whether the protective effect differs depending on the subtype of dementia. We aimed to investigate if midlife physical activity affects the development of vascular dementia (VaD) and Alzheimer’s disease (AD) differently in two large study populations with different designs.

    Methods

    Using a prospective observational design, we studied whether long-distance skiers of the Swedish Vasaloppet (n = 197,685) exhibited reduced incidence of VaD or AD compared to matched individuals from the general population (n = 197,684) during 21 years of follow-up (median 10, interquartile range (IQR) 5–15 years). Next, we studied the association between self-reported physical activity, stated twice 5 years apart, and incident VaD and AD in 20,639 participants in the Swedish population-based Malmo Diet and Cancer Study during 18 years of follow-up (median 15, IQR 14–17 years). Finally, we used a mouse model of AD and studied brain levels of amyloid-β, synaptic proteins, and cognitive function following 6 months of voluntary wheel running.

    Results

    Vasaloppet skiers (median age 36.0 years [IQR 29.0–46.0], 38% women) had lower incidence of all-cause dementia (adjusted hazard ratio (HR) 0.63, 95% CI 0.52–0.75) and VaD (adjusted HR 0.49, 95% CI 0.33–0.73), but not AD, compared to non-skiers. Further, faster skiers exhibited a reduced incidence of VaD (adjusted HR 0.38, 95% CI 0.16–0.95), but not AD or all-cause dementia compared to slower skiers. In the Malmo Diet and Cancer Study (median age 57.5 years [IQR 51.0–63.8], 60% women), higher physical activity was associated with reduced incidence of VaD (adjusted HR 0.65, 95% CI 0.49-0.87), but not AD nor all-cause dementia. These findings were also independent of APOE-ε4 genotype. In AD mice, voluntary running did not improve memory, amyloid-β, or synaptic proteins.

    Conclusions

    Our results indicate that physical activity in midlife is associated with lower incidence of VaD. Using three different study designs, we found no significant association between physical activity and subsequent development of AD.

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  • 3.
    Nägga, Katarina
    et al.
    Lund University, Malmö, Sweden.
    Wattmo, Carina
    Lund University, Malmö, Sweden.
    Zhang, Yi
    Karolinska University Hospital, Stockholm, Sweden.
    Wahlund, Lars-Olof
    Karolinska University Hospital, Stockholm, Sweden.
    Palmqvist, Sebastian
    Lund University, Malmö, Sweden; Skåne University Hospital, Lund, Sweden.
    Cerebral inflammation is an underlying mechanism of early death in Alzheimer's disease: a 13-year cause-specific multivariate mortality study2014In: Alzheimer's Research & Therapy, E-ISSN 1758-9193, Alzheimer's research & therapy, ISSN 1758-9193, Vol. 6, no 4, article id 41Article in journal (Refereed)
    Abstract [en]

    INTRODUCTION: Although Alzheimer's disease (AD) is associated with early death, its life expectancy differs greatly between patients. A better understanding of this heterogeneity may reveal important disease mechanisms underlying the malignancy of AD. The aim of this study was to examine the relation between AD pathologies and early death in AD caused by dementia.

    METHODS: At a memory clinic, 247 referred consecutive patients with AD were monitored during 12.6 ± 1.6 years. Multivariate Cox regression analyses were performed with baseline measures of amyloid beta (Aβ) pathology (APOE genotype, cerebrospinal fluid (CSF) Aβ42) tau pathology (CSF phosphorylated tau and total tau), cerebrovascular pathology (white-matter lesions and CSF/serum albumin ratio), neuroinflammatory pathology (CSF soluble vascular cell adhesion molecule-1, sVCAM-1), frontal, temporal, and central brain atrophies, global cognition, sex, and age. Comorbidities and medications also were analyzed. All continuous variables were transformed to z scores to compare hazard ratios (HRs) and 95% confidence intervals (CIs).

    RESULTS: At follow-up, 89% of the patients had died. The mean survival time was 6.4 ± 3.0 years. The AD pathology that independently predicted an early death caused by dementia was cerebral inflammation (sVCAM-1; HR, 1.32; 95% CI, 1.07-1.64). Other independent predictors were lower global cognition (HR, 0.51; 95% CI, 0.43-0.61), frontal atrophy (HR, 1.38; 95% CI, 1.12-1.70), and medial temporal atrophy (HR, 1.23; 95% CI, 1.02-1.49). When examining death caused by dementia and related causes (vascular diseases and infections), age (HR, 1.23; 95% CI, 1.04-1.46) and cerebrovascular pathology (white-matter lesions: HR, 1.17; 95% CI, 1.01-1.36; and CSF/serum albumin ratio: HR, 1.16; 95% CI, 1.001-1.34) were also significant risk factors in addition to the previous variables. No comorbidity or medication was significant in the specific-cause models.

    CONCLUSIONS: This is the first study to link neuroinflammation independently to early death in AD and, hence, a rapidly progressing disease. Frontal and medial temporal atrophies and low cognition were also significant predictors. These are probably downstream biomarkers that reflect neuronal degeneration and late-stage disease. Our results suggest that inflammation, and not amyloid or tau pathology, is an independent underlying mechanism in the malignancy of AD.

  • 4.
    Wennström, Malin
    et al.
    Lund University, Malmö, Sweden.
    Hall, Sara
    Lund University, Malmö, Sweden.
    Nägga, Katarina
    Lund University, Malmö, Sweden.
    Londos, Elisabet
    Lund University, Malmö, Sweden.
    Minthon, Lennart
    Lund University, Malmö, Sweden.
    Hansson, Oskar
    Lund University, Malmö, Sweden.
    Cerebrospinal fluid levels of IL-6 are decreased and correlate with cognitive status in DLB patients2015In: Alzheimer's Research & Therapy, E-ISSN 1758-9193, Alzheimer's research & therapy, ISSN 1758-9193, Vol. 7, no 1, article id 63Article in journal (Refereed)
    Abstract [en]

    INTRODUCTION: Inflammatory processes have previously been shown to influence cognition and progression of dementia. An involvement of interleukin (IL)-6 has in particular been suggested as altered levels of IL-6 in cerebrospinal fluid (CSF) have been found in patients with Alzheimer's disease (AD). Also, an association between cognitive decline and levels of IL-6 in CSF have been reported. The aim of the present study was to investigate whether patients clinically diagnosed with dementia with Lewy bodies (DLB) display altered CSF IL-6 levels in comparison with patients with AD and control subjects without dementia and whether the IL-6 levels are correlated with cognitive status and biomarkers for AD and synucleinopathy.

    METHODS: To analyse CSF of patients with AD (n = 45), patients with DLB (n = 29) and control subjects without dementia (n = 36), we used immunoassays to measure levels of IL-6 (multiplex electrochemiluminescence); AD markers phosphorylated tau, total tau and amyloid-β1-42 (enzyme-linked immunosorbent assay [ELISA]); and α-synuclein (ELISA). Cognitive status was evaluated using the Mini Mental State Examination (MMSE).

    RESULTS: Our analysis showed significantly lower levels of IL-6 in CSF from patients with DLB than in CSF from patients with AD and control subjects without dementia. The IL-6 levels were also negatively correlated with MMSE and positively correlated with α-synuclein CSF levels.

    CONCLUSIONS: Our findings support previous studies by demonstrating a link between inflammatory processes and dementia progression and further strengthen the hypothesis that IL-6 is involved in dementia pathology and cognitive decline.

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