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Sökning: LAR1:gu > Lunds universitet > Minthon Lennart 1951

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1.
  • Andersson, Malin E, 1978-, et al. (författare)
  • Kinesin gene variability may affect tau phosphorylation in early Alzheimer's disease.
  • 2007
  • Ingår i: International journal of molecular medicine. - 1107-3756. ; 20:2, s. 233-9
  • Tidskriftsartikel (refereegranskat)abstract
    • Kinesin is a microtubule-associated motor protein that transports Alzheimer-associated amyloid precursor protein (APP) in neurons. In animal models, impaired kinesin-mediated APP transport seems to enhance formation of the neurotoxic 42 amino acid fragment of beta-amyloid (A beta 42). In man, one study suggests that a polymorphism (rs8702, 56,836G > C) in the kinesin light chain 1 gene (KNS2) may affect the risk of Alzheimer's disease (AD). To further assess KNS2 as a susceptibility gene for AD we analyzed 802 patients with sporadic AD and 286 controls, 134 longitudinally followed patients with mild cognitive impairment (MCI) and 39 cognitively stable controls for the rs8702 polymorphism. The rs8702 polymorphism did not influence risk of AD (p=0.46). However, rs8702 interacted with APOE epsilon 4 carrier status in AD (p=0.006) and influenced cerebrospinal fluid levels of hyper-phosphorylated tau in MCI patients who converted to AD during follow-up (p=0.018). These findings support earlier indications that genetic variability in the KNS2 gene may play a role during early stages of AD pathogenesis.
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2.
  • Andreasen, Niels, et al. (författare)
  • Kinesin Light Chain 1 Gene Haplotypes in Three Conformational Diseases.
  • 2010
  • Ingår i: Neuromolecular medicine. - 1559-1174. ; 12:3, s. 229-236
  • Tidskriftsartikel (refereegranskat)abstract
    • A functional intracellular transport system is essential to maintain cell shape and function especially in elongated cells, e.g. neurons and lens fibre cells. Impaired intracellular transport has been suggested as a common pathological mechanism for age-related diseases characterised by protein aggregation. Here, we hypothesise that common genetic variation in the transport protein kinesin may influence the risk of Parkinson's disease (PD), Alzheimer's disease (AD) and age-related cataract. This case-control study involves a PD material (165 cases and 190 controls), an AD material (653 cases and 845 controls) and a cataract material (495 cases and 183 controls). Genetic variation in the kinesin light chain 1-encoding gene (KLC1) was tagged by six tag single nucleotide polymorphisms (SNPs). Single SNPs and haplotypes were analysed for associations with disease risk, age parameters, mini-mental state examination scores and cerebrospinal fluid biomarkers for AD using logistic or linear regression. Genetic variation in KLC1 did not influence risk of PD. Weak associations with risk of AD were seen for rs8007903 and rs3212079 (P (c) = 0.04 and P (c) = 0.02, respectively). Two SNPs (rs8007903 and rs8702) influenced risk of cataract (P (c) = 0.0007 and P (c) = 0.04, respectively). However, the allele of rs8007903 that caused increased risk of AD caused reduced risk of cataract, speaking against a common functional effect of this particular SNP in the two diseases. Haplotype analyses did not add significantly to the associations found in the single SNP analyses. Altogether, these results do not convincingly support KLC1 as a major susceptibility gene in any of the studied diseases, although there is a small effect of KLC1 in relation to cataract.
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3.
  • Boström, Fredrik, et al. (författare)
  • Cerebrospinal Fluid Total Tau Is Associated with Shorter Survival in Dementia with Lewy Bodies.
  • 2009
  • Ingår i: Dementia and geriatric cognitive disorders. - 1421-9824. ; 28:4, s. 314-319
  • Tidskriftsartikel (refereegranskat)abstract
    • A pathology typical of dementia with Lewy bodies (DLB) has been demonstrated to increase mortality to a greater extent than the pathology of Alzheimer's disease (AD). However, mortality in DLB has also been shown to increase with concomitant AD pathology. Furthermore, in a recent publication, we showed that there is a robust and specific increase in CSF calcium and magnesium in DLB patients compared to both AD patients and controls. Thus, in order to explore the influence of CSF AD markers and trace element concentrations on mortality in DLB, we undertook a longitudinal prospective study of 47 clinically diagnosed DLB patients and 157 AD patients as well as 49 healthy volunteers. Both AD and DLB patients showed an increased mortality compared to the healthy controls (relative risk: 10 and 8, respectively; p < 0.001). Increased levels of CSF total tau were associated with increased mortality among the DLB patients (p < 0.05), but not among the AD patients or controls. Gender, age, MMSE score, Abeta42 concentration and phosphorylated tau, and CSF trace element concentrations did not influence survival in the obtained models.
4.
  • Buchhave, Peder, et al. (författare)
  • Elevated plasma levels of soluble CD40 in incipient Alzheimer's disease.
  • 2009
  • Ingår i: Neuroscience letters. - 0304-3940. ; 450:1, s. 56-9
  • Tidskriftsartikel (refereegranskat)abstract
    • CD40 is a member of the tumor necrosis factor receptor super-family and has been suggested to play a role in the metabolism of beta-amyloid (Abeta) in Alzheimer's disease (AD). However, the role of CD40-signalling in incipient AD has not yet been studied. We investigated the plasma levels of soluble CD40 (sCD40) and the soluble CD40 ligand (sCD40L) at baseline in 136 subjects with mild cognitive impairment (MCI) and 30 age-matched controls. Sixty of the 136 MCI cases converted to AD (MCI-AD) during a clinical follow-up period of 4-7 years. The baseline levels of sCD40, but not sCD40L, were elevated in MCI-AD cases when compared to age-matched controls (Mann-Whitney U-test, p=0.02). However, MCI patients who were cognitively stable or developed vascular dementia during follow-up did not have significantly increased levels of sCD40 or sCD40L when compared to controls. The levels of sCD40 correlated to decreased baseline performance on mini-mental state examination (MMSE) in both controls (r(s)=-0.37, p<0.05) and MCI-AD cases (r(s)=-0.29, p<0.05). Finally, the plasma levels of sCD40 correlated with the levels of soluble amyloid precursor protein-alpha (sAPP-alpha) (r(s)=0.28, p<0.01) and sAPP-beta (r(s)=0.23, p<0.05) in cerebrospinal fluid. In conclusion, CD40-signalling might play a role in the pathogenesis of early AD.
5.
  • Gerhardsson, Lars, 1952-, et al. (författare)
  • Concentrations of metals, beta-amyloid and tau-markers in cerebrospinal fluid in patients with Alzheimer's disease.
  • 2009
  • Ingår i: Dementia and geriatric cognitive disorders. - 1421-9824. ; 28:1, s. 88-94
  • Tidskriftsartikel (refereegranskat)abstract
    • Background/Aims: In this study, metal concentrations were related to the levels of well-known Alzheimer markers in cerebrospinal fluid (CSF), such as amyloid-beta (A beta), total tau (T-tau) and phosphorylated-tau (P-tau). Methods: Concentrations of 19 metals (Mg, Ca, V, Mn, Fe, Co, Ni, Cu, Zn, Se, Rb, Sr, Mo, Cd, Sn, Sb, Cs, Hg and Pb by inductively coupled plasma-mass spectrometry) and the levels of A beta, T-tau and P-tau in CSF were determined (xMAP technology) in 264 patients with Alzheimer's disease ( AD), and in 54 healthy referents. Results: The AD subjects showed positive correlations between CSF-T-tau and CSF-P-tau versus CSF-Mn (r(s) = 0.22, p = 0.004; r(s) = 0.18, p = 0.021). CSF-T-tau, however, showed a negative correlation with CSF-Cs (r(s) = -0.17; p = 0.027). In subjects with severe AD, CSF-A beta showed a strong positive correlation with CSF-Cs (r(s) = 0.49; p = 0.026), while CSF-T-tau showed a strong negative correlation with CSF-Cs (r(s) = -0.49; p = 0.026). Also, CSF P-tau was negatively associated with CSF-Cs (r(s) = -0.41; p = 0.06). Conclusion: The different relationships between the CSF-levels of A beta and tau-markers versus the levels of CSF-Mn and CSF-Cs may be due to different binding affinity between these metals and metal binding proteins in the CSF and the surrounding brain. Copyright (c) 2009 S. Karger AG, Basel
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6.
7.
  • Hansson, Oskar, et al. (författare)
  • Combined rCBF and CSF biomarkers predict progression from mild cognitive impairment to Alzheimer's disease.
  • 2009
  • Ingår i: Neurobiology of aging. - 1558-1497. ; 30:2, s. 165-73
  • Tidskriftsartikel (refereegranskat)abstract
    • This study aimed to identify preclinical Alzheimer's disease (AD) in patients with mild cognitive impairment (MCI) using measurements of both regional cerebral blood flow (rCBF) and cerebrospinal fluid (CSF) biomarkers. Baseline rCBF assessments (133Xe method) were performed in 70 patients with MCI who were cognitively stable for 4–6 years, 69 patients with MCI who subsequently developed AD, and 33 healthy individuals. CSF was collected at baseline and analyzed for β-amyloid1–42, total tau and phophorylated tau. In contrast to patients with stable MCI, those who subsequently developed AD had decreased rCBF in the temporo-parietal cortex already at baseline. The relative risk of future progression to AD was particularly increased in MCI patients with decreased rCBF in parietal cortex (hazard ratio 3.1, P < 0.0001). Subjects with pathological levels of both CSF tau and β-amyloid1–42 were also at high risk of developing AD (hazard ratio 13.4, P < 0.0001). The MCI patients with a combination of decreased parietal rCBF and pathological CSF biomarkers at baseline had a substantially increased risk of future development of AD, with a hazard ratio of 24.3 (P < 0.0001), when compared to those with normal CSF biomarkers. Moreover, decreased parietal rCBF (but not CSF biomarkers) was associated with a more rapid progression to AD. In conclusion, the combination of rCBF and CSF biomarkers improves the risk assessment of progression to AD in patients with MCI.
8.
  • Landgren, Sara, 1980-, et al. (författare)
  • No Association of VEGF Polymorphims with Alzheimer's Disease.
  • 2010
  • Ingår i: Neuromolecular medicine. - 1559-1174. ; 12:3, s. 224-8
  • Tidskriftsartikel (refereegranskat)abstract
    • The vascular hypothesis of Alzheimer's disease (AD) has brought the vascular endothelial growth factor (VEGF) into focus. The genomic region including the VEGF gene has been linked to AD and single nucleotide polymorphisms (SNPs) of the VEGF have in previous studies been associated with AD risk. To further evaluate these findings, we genotyped two SNPs in the VEGF gene (rs699947 -2578) and rs1570360 -1154) by TaqMan Allelic Discrimination in a study sample including AD patients (n = 801) and controls (n = 286). In a subgroup of the population these SNPs were analyzed in relation to APOE epsilon 4 genotype, to cerebrospinal fluid biomarkers (T-tau, P-tau, and beta(42)-Amyloid) as well as to neuropathological markers for AD (neurofibrillary tangles and senile plaques). No significant associations with risk for AD or any of the studied biomarkers could be found in this study, thus not supporting VEGF as being a major risk gene for AD.
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9.
  • Ray, Sandip, et al. (författare)
  • Classification and prediction of clinical Alzheimer's diagnosis based on plasma signaling proteins
  • 2007
  • Ingår i: NATURE MEDICINE. - 1078-8956. ; 13:11, s. 1359-1362
  • Tidskriftsartikel (refereegranskat)abstract
    • A molecular test for Alzheimer's disease could lead to better treatment and therapies. We found 18 signaling proteins in blood plasma that can be used to classify blinded samples from Alzheimer's and control subjects with close to 90% accuracy and to identify patients who had mild cognitive impairment that progressed to Alzheimer's disease 2-6 years later. Biological analysis of the 18 proteins points to systemic dysregulation of hematopoiesis, immune responses, apoptosis and neuronal support in presymptomatic Alzheimer's disease.
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10.
  • Rüetschi, Ulla, 1962-, et al. (författare)
  • Identification of CSF biomarkers for frontotemporal dementia using SELDI-TOF.
  • 2005
  • Ingår i: Experimental neurology. - 0014-4886. ; 196:2, s. 273-81
  • Tidskriftsartikel (refereegranskat)abstract
    • This investigation describes the discovery of novel possible cerebrospinal fluid (CSF) biomarkers for frontotemporal dementia (FTD) using surface-enhanced laser desorption/ionization time-of-flight (SELDI-TOF) mass spectrometry (MS). Sixteen clinically diagnosed FTD patients and 12 non-demented controls were included in the study. CSF was collected and analyzed for protein expression by SELDI-TOF MS. The samples were analyzed on four different array surfaces using two different energy-absorbing molecules as matrices. In total each sample was subjected to eight different surface/matrix conditions. About 2000 protein peaks (mass/charge ratios) were detected. Forty-two peaks were differentially expressed in FTD (P < 0.01). After exclusion of peaks with low signal-to-noise ratio and/or poor resolution and peaks representing differentially charged proteins, 10 peaks remained, five of which were increased and five decreased in FTD cases compared to controls. Using partial least square discriminant analysis (PLS-DA), the combination of these biomarkers discriminated FTD from non-demented controls with a sensitivity of 94%, a specificity of 83% and an accuracy of 89%. Five of the peaks were purified further and identified by tandem MS as a fragment of neurosecretory protein VGF, transthyretin, S-cysteinylated transthyretin, truncated cystatin C and a fragment of chromogranin B. With use of these potential biomarkers, FTD can be distinguished from control subjects with high accuracy in this pilot study.
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