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  • Buchave, P, et al. (författare)
  • Cube Copying Test in Combination with rCBF or CSF Abeta(42)Predicts Development of Alzheimer's Disease.
  • 2008
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - Karger. - 1420-8008. ; 25:6, s. 544-552
  • Tidskriftsartikel (refereegranskat)abstract
    • Background/Aim: The aim was to identify subjects with incipient Alzheimer's disease (AD) among patients with mild cognitive impairment (MCI) using brief cognitive tests. Methods: A total of 147 MCI patients were followed for 4-6 years and the incidence of AD was 11.6%/year. At baseline, the cube copying test, clock drawing test, MMSE and measurements of regional cerebral blood flow (rCBF) and cerebrospinal fluid (CSF) beta-amyloid(1-42) (Abeta(42)) were performed. Results: The cube copying test, but not the clock drawing test, could predict AD among MCI patients with an area under the receiver operating characteristic curve of 0.64 (p < 0.01). The relative risk for future AD was increased in MCI subjects with impaired cube copying test (sex- and age-adjusted hazard ratio = 1.8, p < 0.05) and the incidence of AD was 18.2% in this subgroup. Combining the cube copying test with either rCBF or CSF Abeta(42) had additive effects on the risk assessment for future development of AD. MCI patients achieving high scores on both MMSE and cube copying test had a very low risk of developing AD (incidence of AD = 1.6%). Conclusion: In conclusion, combinations of the cube copying test with MMSE, rCBF and CSF Abeta(42) measurements can identify subgroups of MCI subjects with either substantially reduced or increased risk for future development of AD.
  • Damian, M., et al. (författare)
  • Single-Domain Amnestic Mild Cognitive Impairment Identified by Cluster Analysis Predicts Alzheimer's Disease in the European Prospective DESCRIPA Study
  • 2013
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - Karger. - 1420-8008. ; 36:1-2, s. 1-19
  • Tidskriftsartikel (refereegranskat)abstract
    • Background/Aims: To identify prodromal Alzheimer's disease (AD) subjects using a data-driven approach to determine cognitive profiles in mild cognitive impairment (MCI). Methods: A total of 881 MCI subjects were recruited from 20 memory clinics and followed for up to 5 years. Outcome measures included cognitive variables, conversion to AD, and biomarkers (e. g. CSF, and MRI markers). Two hierarchical cluster analyses (HCA) were performed to identify clusters of subjects with distinct cognitive profiles. The first HCA included all subjects with complete cognitive data, whereas the second one selected subjects with very mild MCI (MMSE >= 28). ANOVAs and ANCOVAs were computed to examine whether the clusters differed with regard to conversion to AD, and to AD-specific biomarkers. Results: The HCAs identified 4-cluster solutions that best reflected the sample structure. One cluster (aMCIsingle) had a significantly higher conversion rate (19%), compared to subjective cognitive impairment (SCI, p < 0.0001), and non-amnestic MCI (naMCI, p = 0.012). This cluster was the only one showing a significantly different biomarker profile (A beta(42), t-tau, APOE epsilon 4, and medial temporal atrophy), compared to SCI or naMCI. Conclusion: In subjects with mild MCI, the single-domain amnestic MCI profile was associated with the highest risk of conversion, even if memory impairment did not necessarily cross specific cut-off points. A cognitive profile characterized by isolated memory deficits may be sufficient to warrant applying prevention strategies in MCI, whether or not memory performance lies below specific z-scores. This is supported by our preliminary biomarker analyses. However, further analyses with bigger samples are needed to corroborate these findings. Copyright (C) 2013 S. Karger AG, Basel
  • Elbaz, Alexis, et al. (författare)
  • Independent and Joint Effects of the MAPT and SNCA Genes in Parkinson Disease
  • 2011
  • Ingår i: Annals of Neurology. - John Wiley and Sons Inc.. - 1531-8249. ; 69:5, s. 778-792
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: We studied the independent and joint effects of the genes encoding alpha-synuclein (SNCA) and microtubule-associated protein tau (MAPT) in Parkinson disease (PD) as part of a large meta-analysis of individual data from case-control studies participating in the Genetic Epidemiology of Parkinson's Disease (GEO-PD) consortium. Methods: Participants of Caucasian ancestry were genotyped for a total of 4 SNCA (rs2583988, rs181489, rs356219, rs11931074) and 2 MAPT (rs1052553, rs242557) single nucleotide polymorphism (SNPs). Individual and joint effects of SNCA and MAPT SNPs were investigated using fixed- and random-effects logistic regression models. Interactions were studied on both a multiplicative and an additive scale, and using a case-control and case-only approach. Results: Fifteen GEO-PD sites contributed a total of 5,302 cases and 4,161 controls. All 4 SNCA SNPs and the MAPT H1-haplotype-defining SNP (rs1052553) displayed a highly significant marginal association with PD at the significance level adjusted for multiple comparisons. For SNCA, the strongest associations were observed for SNPs located at the 30 end of the gene. There was no evidence of statistical interaction between any of the 4 SNCA SNPs and rs1052553 or rs242557, neither on the multiplicative nor on the additive scale. Interpretation: This study confirms the association between PD and both SNCA SNPs and the H1 MAPT haplotype. It shows, based on a variety of approaches, that the joint action of variants in these 2 loci is consistent with independent effects of the genes without additional interacting effects. ANN NEUROL 2011; 69: 778-792
  • Englund, Hillevi, et al. (författare)
  • Increase in beta-Amyloid Levels in Cerebrospinal Fluid of Children with Down Syndrome
  • 2007
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - 1420-8008 .- 1421-9824. ; 24:5, s. 369-374
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Individuals with Down syndrome (DS) invariably develop Alzheimer's disease (AD) during their life span. It is therefore of importance to study young DS patients when trying to elucidate early events in AD pathogenesis. Aim: To investigate how levels of different amyloid-<img src="http://content.karger.com/ProdukteDB/Showpic.asp?filename=/images/entity/beta.gif" /> (A<img src="http://content.karger.com/ProdukteDB/Showpic.asp?filename=/images/entity/beta.gif" />) peptides, as well as tau and phosphorylated tau, in cerebrospinal fluid (CSF) from children with DS change over time. The first CSF sample was taken at 8 months and the following two samples at 20-40 and 54 months of age. Results: Individual levels of the A<img src="http://content.karger.com/ProdukteDB/Showpic.asp?filename=/images/entity/beta.gif" /> peptides, as well as total A<img src="http://content.karger.com/ProdukteDB/Showpic.asp?filename=/images/entity/beta.gif" /> levels in CSF increased over time when measured with Western blot. Tau in CSF decreased whereas there was no change in levels of phosphorylated tau over time. Conclusion: The increasing levels of A<img src="http://content.karger.com/ProdukteDB/Showpic.asp?filename=/images/entity/beta.gif" /> in CSF during early childhood of DS patients observed in this study are probably due to the trisomy of the A<img src="http://content.karger.com/ProdukteDB/Showpic.asp?filename=/images/entity/beta.gif" /> precursor APP, which leads to an overproduction of A<img src="http://content.karger.com/ProdukteDB/Showpic.asp?filename=/images/entity/beta.gif" />. Despite the increased CSF concentrations of A<img src="http://content.karger.com/ProdukteDB/Showpic.asp?filename=/images/entity/beta.gif" />, there were no signs of an AD-indicating tau pattern in CSF, since the levels of total tau decreased and phosphorylated tau remained unchanged. This observation further strengthens the theory of A<img src="http://content.karger.com/ProdukteDB/Showpic.asp?filename=/images/entity/beta.gif" /> pathology preceding tau pathology in AD.
  • Freund-Levi, Yvonne, et al. (författare)
  • Effects of omega-3 fatty acids on inflammatory markers in cerebrospinal fluid and plasma in Alzheimer's disease : the OmegAD study
  • 2009
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - S. Karger. - 1420-8008. ; 27:5, s. 481-490
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: omega-3 fatty acids (omega-3 FAs) found in dietary fish or fish oils are anti-inflammatory agents that may influence Alzheimer's disease (AD).OBJECTIVE: To study the effects of dietary omega-3 FA supplementation on inflammatory markers in cerebrospinal fluid (CSF) and plasma from patients with mild to moderate AD.METHODS: Thirty-five patients (70.3 +/- 8.2 years) were randomized to a daily intake of 2.3 g omega-3 FAs or placebo for 6 months. The inflammatory markers interleukin (IL)-6, tumour necrosis factor-alpha and soluble interleukin-1 receptor type II (sIL-1RII) were analysed in CSF and plasma at baseline and at 6 months. The AD markers tau-protein, hyperphosphorylated tau-protein and beta-amyloid (Abeta(1-42)) were assessed in CSF. High-sensitivity C-reactive protein was assessed in plasma. A possible relation to the APOE genotype was investigated.RESULTS: There was no significant treatment effect of omega-3 FAs on inflammatory and AD biomarkers in CSF or on inflammatory markers in plasma, nor was there any relation with APOE. A significant correlation was observed at baseline between sIL-1RII and Abeta(1-42) levels in CSF.CONCLUSIONS: Treatment of AD patients with omega-3 FAs for 6 months did not influence inflammatory or biomarkers in CSF or plasma. The correlation between sIL-1RII and Abeta(1-42) may reflect the reciprocal interactions between IL-1 and Abeta peptides.
  • Gisslén, Magnus, 1962-, et al. (författare)
  • Amyloid and tau cerebrospinal fluid biomarkers in HIV infection.
  • 2009
  • Ingår i: BMC neurology. - 1471-2377. ; 9:1
  • Tidskriftsartikel (refereegranskat)abstract
    • ABSTRACT: BACKGROUND: Because of the emerging intersections of HIV infection and Alzheimer's disease, we examined cerebrospinal fluid (CSF) biomarkers related of amyloid and tau metabolism in HIV-infected patients. METHODS: In this cross-sectional study we measured soluble amyloid precursor proteins alpha and beta (sAPPalpha and sAPPbeta), amyloid beta fragment 1-42 (Abeta1-42), and total and hyperphosphorylated tau (t-tau and p-tau) in CSF of 86 HIV-infected (HIV+) subjects, including 21 with AIDS dementia complex (ADC), 25 with central nervous system (CNS) opportunistic infections and 40 without neurological symptoms and signs. We also measured these CSF biomarkers in 64 uninfected (HIV-) subjects, including 21 with Alzheimer's disease, and both younger and older controls without neurological disease. RESULTS: CSF sAPPalpha and sAPPbeta concentrations were highly correlated and reduced in patients with ADC and opportunistic infections compared to the other groups. The opportunistic infection group but not the ADC patients had lower CSF Abeta1-42 in comparison to the other HIV+ subjects. CSF t-tau levels were high in some ADC patients, but did not differ significantly from the HIV+ neuroasymptomatic group, while CSF p-tau was not increased in any of the HIV+ groups. Together, CSF amyloid and tau markers segregated the ADC patients from both HIV+ and HIV- neuroasymptomatics and from Alzheimer's disease patients, but not from those with opportunistic infections. CONCLUSIONS: Parallel reductions of CSF sAPPalpha and sAPPbeta in ADC and CNS opportunistic infections suggest an effect of CNS immune activation or inflammation on neuronal amyloid synthesis or processing. Elevation of CSF t-tau in some ADC and CNS infection patients without concomitant increase in p-tau indicates neural injury without preferential accumulation of hyperphosphorylated tau as found in Alzheimer's disease. These biomarker changes define pathogenetic pathways to brain injury in ADC that differ from those of Alzheimer's disease.
  • Gustafson, Deborah, 1966-, et al. (författare)
  • Body Mass Index, Cognition, Disability, APOE Genotype, and Mortality: The "Treviso Longeva" Study
  • 2012
  • Ingår i: American Journal of Geriatric Psychiatry. - 1064-7481. ; 20:7, s. 594-602
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives: The concurrent contributions of dynamic, interrelated late-life parameters, such as bodymass index (BMI), cognition, and physical functioning on mortality in the elderly are unclear, as is the influence of APOE genotype. We explored these measures in relation to 7-year mortality in long-lived Italian elderly. Design: A representative, age-stratified, population sample. Setting: The Treviso Longeva (TRELONG) Study, in Treviso, Italy. Participants: Three hundred eleven men and 357 women, aged 70 years and older (mean age 84 +/- 8 years). Measurements: Seven-year mortality, BMI, Mini-Mental State Examination (MMSE) score, Activities of Daily Living (ADL), APOE genotype, and a variety of clinical and survey data. Results: In separate age-and sex-adjusted analyses, BMI <18.5 kg/m(2), MMSE <= 24, and ADL <6, were associated with greater 7-year mortality among adults aged 70 years and older. In a multivariate model including all factors, MMSE <= 24, and ADL <6 were associated with greater mortality; BMI >= 30 kg/m(2) was protective. There were no interactions between BMI, MMSE, or ADL. When excluding those dying within 3 years of baseline, only an MMSE <= 24 was related to mortality. APOE epsilon 4 was not related to mortality. Conclusion: Higher MMSE score, higher ADL score, and higher BMI, independent of age, sex, and other factors, are markers for longer life among northern Italian adults aged 70 years or older. Global cognition, BMI, and physical functioning, assessed by short, simple tests are profound indicators of death within less than a decade. (Am J Geriatr Psychiatry 2012; 20:594-602)
  • Hansson, Oskar, et al. (författare)
  • Prediction of Alzheimer's Disease Using the CSF Abeta42/Abeta40 Ratio in Patients with Mild Cognitive Impairment.
  • 2007
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - Karger. - 1420-8008. ; 23:5, s. 316-320
  • Tidskriftsartikel (refereegranskat)abstract
    • Evidence supports an important role for beta-amyloid (A beta) in the pathogenesis of Alzheimer's disease ( AD). Here, we investigate baseline levels of the 40- and 42-amino-acid-long A beta peptides (A beta 40 and A beta 42) in cerebrospinal fluid (CSF) from a cohort of patients with mild cognitive impairment (MCI, n = 137) in relation to the final diagnosis after 4 - 6 years of follow-up time. CSF A beta 42 concentration at baseline and the A beta 42/A beta 40 ratio were significantly decreased in the MCI patients who developed AD as compared to cognitively stable MCI patients and MCI patients who developed other forms of dementia ( p < 0.001). The baseline levels of A beta 40 were similar in all MCI groups but correlated with change in Mini Mental State Examination scores in converters to AD. The A beta 42/A beta 40 ratio was superior to A beta 42 concentration with regard to identifying incipient AD in MCI ( p < 0.05). In conclusion, the data provide further support for the view that amyloid precursor protein metabolism is disturbed in early sporadic AD and points to the usefulness of the A beta 42/ A beta 40 ratio as a predictive biomarker for AD.
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