Change search
Refine search result
1 - 7 of 7
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Rows per page
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sort
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
Select
The maximal number of hits you can export is 250. When you want to export more records please use the Create feeds function.
  • 1.
    Enache, Daniela
    et al.
    Department of Neurobiology, Care Sciences and Society, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden.
    Solomon, Alina
    Department of Neurobiology, Care Sciences and Society, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden, and Institute of Clinical Medicine/Neurology, University of Eastern Finland, Kuopio, Finland.
    Cavallin, Lena
    Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.
    Kåreholt, Ingemar
    Jönköping University, School of Health and Welfare, HHJ, Institute of Gerontology. Jönköping University, School of Health and Welfare, HHJ. ARN-J (Aging Research Network - Jönköping). Department of Neurobiology, Care Sciences and Society, Aging Research Center, Karolinska Institutet and Stockholm University, Stockholm, Sweden.
    Kramberger, Milica Gregoric
    Department of Neurobiology, Care Sciences and Society, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden, and Department of Neurology, University Medical Centre, Ljubljana, Slovenia.
    Aarsland, Dag
    Department of Neurobiology, Care Sciences and Society, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden, and Center for Age-Related Diseases, Psychiatric Clinic, Stavanger University Hospital, Stavanger, Norway.
    Kivipelto, Miia
    Department of Neurobiology, Care Sciences and Society, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden, and Institute of Clinical Medicine/Neurology, University of Eastern Finland, Kuopio, Finland.
    Eriksdotter, Maria
    Department of Geriatric Medicine, Memory Clinic, Karolinska University Hospital-Huddinge, Stockholm, Sweden.
    Winblad, Bengt
    Department of Neurobiology, Care Sciences and Society, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden.
    Jelic, Vesna
    Department of Geriatric Medicine, Memory Clinic, Karolinska University Hospital-Huddinge, Stockholm, Sweden.
    CAIDE Dementia Risk Score and biomarkers of neurodegeneration in memory clinic patients without dementia2016In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 42, p. 124-131Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to explore cross-sectional associations between Cardiovascular Risk Factors, Aging and Dementia Study (CAIDE) Dementia Risk Score and dementia-related cerebrospinal fluid and neuroimaging biomarkers in 724 patients without dementia from the Memory Clinic at Karolinska University Hospital, Huddinge, Sweden. We additionally evaluated the score's capacity to predict dementia. Two risk score versions were calculated: one including age, gender, obesity, hyperlipidemia, and hypertension; and one additionally including apolipoprotein E (APOE) ε4 carrier status. Cerebrospinal fluid was analyzed for amyloid β (Aβ), total tau, and phosphorylated tau. Visual assessments of medial temporal lobe atrophy (MTA), global cortical atrophy-frontal subscale, and Fazekas scale for white matter changes (WMC) were performed. Higher CAIDE Dementia Risk Score (version without APOE) was significantly associated with higher total tau, more severe MTA, WMC, and global cortical atrophy-frontal subscale. Higher CAIDE Dementia Risk Score (version with APOE) was associated with reduced Aβ, more severe MTA, and WMC. CAIDE Dementia Risk Score version with APOE seemed to predict dementia better in this memory clinic population with short follow-up than the version without APOE.

  • 2. Gatz, Margret
    et al.
    Frataglioni, L
    Johansson, Boo
    Berg, Stig
    Jönköping University, School of Health Science, HHJ, Institute of Gerontology. Jönköping University, School of Health Science, HHJ. Ageing - living conditions and health.
    Mortimer, J A
    Reynolds, Chandra A
    Fiske, M
    Pedersen, Nancy L
    Complete ascertainment of dementia in the Swedish Twin Registry: The Harmony Study2005In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 26, no 4, p. 439-447Article in journal (Refereed)
  • 3.
    Johansson, Carina S
    et al.
    Jönköping University, School of Health Science, HHJ, Dep. of Natural Science and Biomedicine.
    Stenström, M
    Hildebrand, C
    Target influence on aging of myelinated sensory nerve fibres1996In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 17, no 1, p. 61-66Article in journal (Refereed)
  • 4.
    Karlsson, Ida K.
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Bennet, A. M.
    Ploner, A.
    Andersson, T. M. -L
    Reynolds, C. A.
    Gatz, M.
    Pedersen, Nancy L.
    Apolipoprotein E ε4 genotype and the temporal relationship between depression and dementia2015In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 36, no 4, p. 1751-1756Article in journal (Refereed)
    Abstract [en]

    To investigate how apolipoprotein E (. APOE) affects the temporal relationship between depression and dementia, we conducted a nested case-control study with longitudinal depression and dementia evaluations from several population studies by using 804 dementia cases and 1600 matched controls, totaling 1519 unique individuals. Depression within 10 years of onset of dementia was strongly associated with dementia diagnosis regardless of APOE status (incidence rate ratio [IRR] 5.25, 95% confidence interval [95% CI] 3.32-8.31 for ε4 carriers, IRR 4.40, 95%CI 3.23-5.99 for noncarriers). However, we found a significant interaction between depression more than 10 years before the onset of dementia and APOE (. p= 0.01), with depression more distal to dementia being a risk factor only in ε4 carriers (IRR 3.39, 95% CI 1.69-6.78 for carriers, IRR 1.01, 95% CI 0.60-1.70 for noncarriers). Thus, depression with onset close in time to dementia onset is associated with disease irrespective of APOE genotype, whereas depression more distal to dementia onset is a risk factor only in ε4-carriers. This is the first study to show the interaction between APOE and depression to be dependent on timing of depression onset.

  • 5.
    Reynolds, Chandra A.
    et al.
    Department of Psychology, University of California, Riverside, CA, USA.
    Zavala, Catalina
    Department of Psychology, University of California, Riverside, CA, USA.
    Gatz, Margaret
    Department of Psychology, University of Southern California, USA.
    Vie, Loryana
    Department of Psychology, University of California, Riverside, CA, USA.
    Johansson, Boo
    Department of Psychology, University of Gothenburg, Sweden.
    Malmberg, Bo
    Jönköping University, School of Health and Welfare, HHJ, Institute of Gerontology. Jönköping University, School of Health and Welfare, HHJ. Ageing - living conditions and health.
    Ingelsson, Erik
    Department of Medical Epidemiology and Biostatistics Karolinska Institutet, Sweden.
    Prince, Jonathan A.
    Department of Medical Epidemiology and Biostatistics Karolinska Institutet, Sweden.
    Pedersen, Nancy L.
    Department of Medical Epidemiology and Biostatistics Karolinska Institutet, Sweden.
    Sortilin receptor 1 predicts longitudinal cognitive change2013In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 34, no 6, p. 1710.e11-1710.e18Article in journal (Refereed)
    Abstract [en]

    The gene encoding sortilin receptor 1 (SORL1) has been associated with Alzheimer's disease risk. We examined 15 SORL1 variants and single nucleotide polymorphism (SNP) set risk scores in relation to longitudinal verbal, spatial, memory, and perceptual speed performance, testing for age trends and sex-specific effects. Altogether, 1609 individuals from 3 population-based Swedish twin studies were assessed up to 5 times across 16 years. Controlling for apolipoprotein E genotype (APOE), multiple simple and sex-moderated associations were observed for spatial, episodic memory, and verbal trajectories (p = 1.25E-03 to p = 4.83E-02). Five variants (rs11600875, rs753780, rs7105365, rs11820794, rs2070045) were associated across domains. Notably, in those homozygous for the rs2070045 risk allele, men demonstrated initially favorable performance but accelerating declines, and women showed overall lower performance. SNP set risk scores predicted spatial (Card Rotations, p = 5.92E-03) and episodic memory trajectories (Thurstone Picture Memory, p = 3.34E-02), where higher risk scores benefited men's versus women's performance up to age 75 but with accelerating declines. SORL1 is associated with cognitive aging, and might contribute differentially to change in men and women.

  • 6.
    Smailovic, Una
    et al.
    Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden.
    Koenig, Thomas
    Translational Research Center, University Hospital of Psychiatry, University of Bern, Bern, Switzerland.
    Kåreholt, Ingemar
    Jönköping University, School of Health and Welfare, HHJ, Institute of Gerontology. Jönköping University, School of Health and Welfare, HHJ. ARN-J (Aging Research Network - Jönköping). Aging Research Centre, Karolinska Institutet and Stockholm University, Stockholm, Sweden.
    Andersson, Thomas
    Department of Clinical Neurophysiology, Karolinska University Hospital, Huddinge, Sweden.
    Kramberger, Milica Gregoric
    Department of Neurology, University Medical Centre, Ljubljana, Slovenia.
    Winblad, Bengt
    Alzheimer Research Center, Division of Neurogeriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden.
    Jelic, Vesna
    Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden.
    Quantitative EEG power and synchronization correlate with Alzheimer's disease CSF biomarkers.2018In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 63, p. 88-95Article in journal (Refereed)
    Abstract [en]

    Synaptic dysfunction is the best anatomical correlate of early cognitive impairment in Alzheimer's disease (AD). Electroencephalography (EEG) directly reflects brain electrical activity at the level of synapses. The aim of the present study was to investigate correlations of quantitative EEG measures, global field power (GFP) and global field synchronization (GFS), with conventional cerebrospinal fluid (CSF) biomarkers of neurodegeneration in patients diagnosed with subjective cognitive decline (n = 210), mild cognitive impairment (n = 230), and AD (n = 197). Decreased CSF amyloid β42 significantly correlated with increased theta and delta GFP, whereas increased p- and t-tau with decreased alpha and beta GFP. Decreased CSF amyloid β42 and increased p- and t-tau were significantly associated with decreased GFS alpha and beta. Subanalysis of the separate diagnostic groups demonstrated significant correlations between CSF biomarkers and generalized power and synchronization already in the subjective cognitive decline and mild cognitive impairment group. These results provide evidence that quantitative EEG measures are associated and possibly sensitive to distinct AD-like CSF biomarker profiles in cognitively impaired patients and are therefore promising early noninvasive markers of AD.

  • 7.
    Vuorinen, Miika
    et al.
    University of Eastern Finland.
    Kåreholt, Ingemar
    Jönköping University, School of Health and Welfare, HHJ. Ageing - living conditions and health. Jönköping University, School of Health and Welfare, HHJ, Institute of Gerontology.
    Julkunen, Valtteri
    University of Eastern Finland.
    Spulber, Gabriela
    University of Eastern Finland.
    Niskanen, Eini
    University of Eastern Finland.
    Paajanen, Teemu
    University of Eastern Finland.
    Soininen, Hilkka
    University of Eastern Finland.
    Kivipelto, Miia
    University of Eastern Finland.
    Solomon, Alina
    University of Eastern Finland.
    Changes in vascular factors 28 years from midlife and late-life cortical thickness2013In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 34, no 1, p. 100-109Article in journal (Refereed)
    Abstract [en]

    We assessed midlife blood pressure (BP), body mass index, total cholesterol, and their changes over time in relation to cortical thickness on magnetic resonance imaging 28 years later in 63 elderly at risk of dementia. Participants in the population-based Cardiovascular Risk Factors, Aging, and Dementia study were first examined at midlife. A first follow-up was conducted after 21 years, and a second follow-up after an additional 7 years. Magnetic resonance images from the second follow-up were analyzed using algorithms developed at McGill University, Montreal, Canada. Midlife hypertension was related to thinner cortex in several brain areas, including insular, frontal, and temporal cortices. In elderly with thinner insular cortex, there was a continuous decline in systolic BP and an increase in pulse pressure after midlife, while in elderly with thicker insular cortex the decline in systolic BP started at older ages, paralleled by a decline in pulse pressure. No associations were found between body mass index, cholesterol, or apolipoprotein E ε4 allele and cortical thickness in this group of elderly at risk individuals.

1 - 7 of 7
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf