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1.
  • Aarsland, Dag, et al. (författare)
  • Identification of Novel α-Synuclein Isoforms in Human Brain Tissue by using an Online NanoLC-ESI-FTICR-MS Method.
  • 2011
  • Ingår i: Neurochemical research. - 1573-6903. ; 36:11
  • Tidskriftsartikel (refereegranskat)abstract
    • Parkinson's disease (PD) and Dementia with Lewy bodies (DLB) are neurodegenerative diseases that are characterized by intra-neuronal inclusions of Lewy bodies in distinct brain regions. These inclusions consist mainly of aggregated α-synuclein (α-syn) protein. The present study used immunoprecipitation combined with nanoflow liquid chromatography (LC) coupled to high resolution electrospray ionization Fourier transform ion cyclotron resonance tandem mass spectrometry (ESI-FTICR-MS/MS) to determine known and novel isoforms of α-syn in brain tissue homogenates. N-terminally acetylated full-length α-syn (Ac-α-syn(1-140)) and two N-terminally acetylated C-terminally truncated forms of α-syn (Ac-α-syn(1-139) and Ac-α-syn(1-103)) were found. The different forms of α-syn were further studied by Western blotting in brain tissue homogenates from the temporal cortex Brodmann area 36 (BA36) and the dorsolateral prefrontal cortex BA9 derived from controls, patients with DLB and PD with dementia (PDD). Quantification of α-syn in each brain tissue fraction was performed using a novel enzyme-linked immunosorbent assay (ELISA).
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2.
  • Abramsson, Alexandra, 1973-, et al. (författare)
  • Proteomics Profiling of Single Organs from Individual Adult Zebrafish.
  • 2010
  • Ingår i: Zebrafish. - 1557-8542. ; 7:2, s. 161-168
  • Tidskriftsartikel (refereegranskat)abstract
    • Abstract The model organism zebrafish (Danio rerio) is extensively utilized in studies of developmental biology but is also being investigated in the context of a growing list of human age-related diseases. To facilitate such studies, we here present protein expression patterns of adult zebrafish organs, including blood, brain, fin, heart, intestine, liver, and skeletal muscle. Protein extracts were prepared from the different organs of two zebrafish and analyzed using liquid chromatography coupled to high-resolution tandem mass spectrometry. Zebrafish tissue was digested directly after minimal fractionation and cleaned up (the shotgun approach). Proteins were identified using Mascot software. In total, 1394 proteins were identified of which 644 were nonredundant. Of these, 373 demonstrated an organ-specific expression pattern and 57 had not been shown on protein level before. These data emphasize the need for increased research at the protein level to facilitate the selection of candidate proteins for targeted quantification and to refine systematic genetic network analysis in vertebrate development, biology, and disease.
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3.
  • Alves, Guido, et al. (författare)
  • CSF amyloid-β and tau proteins, and cognitive performance, in early and untreated Parkinson's Disease: the Norwegian ParkWest study
  • 2010
  • Ingår i: Journal of neurology, neurosurgery, and psychiatry. - 1468-330X. ; 81:10, s. 1080-1086
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Alzheimer's disease (AD) pathology is found in a considerable portion of patients with Parkinson's disease (PD), particularly those with early dementia (PDD). Altered cerebrospinal fluid (CSF) levels of amyloid-beta (Abeta) and tau proteins have been found in PDD, with intermediate changes for Abeta42 in non-demented PD. The authors investigated whether AD-related CSF protein levels are altered and relate to neuropsychological performance in early, untreated PD. Methods CSF concentrations of Abeta42, Abeta40 and Abeta38 were measured by electrochemiluminiscene and levels of total tau (T-tau) and phosphorylated tau (P-tau) by ELISA in 109 newly diagnosed, unmedicated, non-demented, community-based PD patients who had undergone comprehensive neuropsychological testing, and were compared with those of 36 age-matched normal controls and 20 subjects with mild AD. Results PD patients displayed significant reductions in Abeta42 (19%; p=0.009), Abeta40 (15.5%; p=0.008) and Abeta38 (23%; p=0.004) but not T-tau (p=0.816) or P-tau (p=0.531) compared with controls. CSF Abeta42 reductions in PD were less marked than in AD (53%; p=0.002). Sequential regression analyses demonstrated significant associations between CSF levels of Abeta42 (beta=0.205; p=0.019), Abeta40 (beta=0.378; p<0.001) and Abeta38 (beta=0.288; p=0.001) and memory impairment, but not executive-attentional or visuospatial dysfunction. Tau protein levels did not correlate with cognitive measures. Conclusion CSF Abeta levels are altered in a subset of patients with early PD and relate to memory impairment. Our study suggests that alterations in Abeta protein metabolism may contribute to the heterogeneity in pattern and course of cognitive decline associated with PD. Longitudinal studies are needed to clarify the clinical significance of CSF Abeta peptides as prognostic biomarkers in PD.
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4.
  • Andersson, M, et al. (författare)
  • The cognitive profile and CSF biomarkers in dementia with Lewy bodies and Parkinson's disease dementia.
  • 2011
  • Ingår i: International journal of geriatric psychiatry. - 1099-1166. ; 26:1, s. 100-5
  • Tidskriftsartikel (refereegranskat)abstract
    • Dementia with Lewy bodies (DLB) and Parkinson&#39;s disease dementia (PDD) may be viewed as different points on a continuum reflecting the regional burden and distribution of pathology. An important clinical consideration is overlapping Alzheimer&#39;s disease (AD) pathology, since it has been reported that associated AD pathology in DLB shortens survival and leads to a more rapid cognitive decline. We aimed to investigate cerebrospinal fluid (CSF) biomarkers and the associated cognitive profile in DLB and PDD.
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5.
  • Andreasen, Niels, et al. (författare)
  • Changes in CSF acetyl- and butyrylcholinesterase activity after long-term treatment with AChE inhibitors in Alzheimer's disease.
  • 2011
  • Ingår i: Acta neurologica Scandinavica. - 1600-0404. ; 124:2, s. 122-129
  • Tidskriftsartikel (refereegranskat)abstract
    • Parnetti L, Chiasserini D, Andreasson U, Ohlson M, Hüls C, Zetterberg H, Minthon L, Wallin ÅK, Andreasen N, Talesa VN, Blennow K. Changes in CSF acetyl- and butyrylcholinesterase activity after long-term treatment with AChE inhibitors in Alzheimer&#39;s disease.Acta Neurol Scand: DOI: 10.1111/j.1600-0404.2010.01435.x. © 2010 John Wiley &amp; Sons A/S. Objectives - To measure cerebrospinal fluid (CSF) activity of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) in patients with Alzheimer&#39;s disease (AD) participating in randomized clinical trials from three European centers, before and after long-term treatment with different AChE inhibitors (AChEIs). Materials and methods - Of the 144 patients included in the study, 104 were treated with donepezil, 15 with galantamine, 16 with rivastigmine, and nine with placebo. CSF AChE and BChE activities were measured at baseline and after 1- year treatment. Results - Donepezil and galantamine groups showed a significant increase in CSF AChE activity at follow-up, while no changes for BChE activity were observed; in donepezil group, a positive correlation between plasma concentration and AChE activity was documented. Conversely, in rivastigmine group, a decrease in CSF activity of both enzymes was observed. CSF AChE and BChE activities were not correlated with the clinical outcome in any group considered. CSF biomarkers did not show any change after treatment. Conclusions - AChEIs differently influence the activity of target enzymes in CSF independent of their pharmacodynamic effects.
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6.
  • 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&#39;s disease (PD), Alzheimer&#39;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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7.
  • Andreasen, Niels, et al. (författare)
  • Neuroinflammation Screening in Immunotherapy Trials against Alzheimer's Disease.
  • 2010
  • Ingår i: International journal of Alzheimer's disease. - 2090-0252. ; :638379
  • Tidskriftsartikel (refereegranskat)abstract
    • Due to side effects in the form of meningoencephalitis in the interrupted phase II AN1792 trial of active antiamyloid β(Aβ) immunization against Alzheimer's disease (AD), there has been concern that anti-Aβ immunization may cause destructive neuroinflammation. Here, we report on two patients fulfilling clinical AD criteria who were diagnosed with Lyme neuroborreliosis during screening before inclusion in anti-Aβ immunotherapy trials. The two cases illustrate the necessity of careful biochemical screening for neuroinflammatory/neuroinfectious conditions before an AD diagnosis is made and before clinical AD patients are included in trials of therapy that could impact the immune system. Should the two cases have been included and deteriorated, additional investigations might have led to the erroneous conclusion that therapy-induced meningoencephalitis had occurred.
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8.
  • Andreasen, Niels, et al. (författare)
  • No neurochemical evidence of brain injury after blast overpressure by repeated explosions or firing heavy weapons.
  • 2011
  • Ingår i: Acta neurologica Scandinavica. - 1600-0404. ; 123, s. 245-51
  • Tidskriftsartikel (refereegranskat)abstract
    • Blennow K, Jonsson M, Andreasen N, Rosengren L, Wallin A, Hellström PA, Zetterberg H. No neurochemical evidence of brain injury after blast overpressure by repeated explosions or firing heavy weapons.Acta Neurol Scand: DOI: 10.1111/j.1600-0404.2010.01408.x .(c) 2010 John Wiley & Sons A/S. Background - Psychiatric and neurological symptoms are common among soldiers exposed to blast without suffering a direct head injury. It is not known whether such symptoms are direct consequences of blast overpressure. Objective - To examine if repeated detonating explosions or firing if of heavy weapons is associated with neurochemical evidence of brain damage. Materials and methods - Three controlled experimental studies. In the first, army officers were exposed to repeated firing of a FH77B howitzer or a bazooka. Cerebrospinal fluid (CSF) was taken post-exposure to measure biomarkers for brain damage. In the second, officers were exposed for up to 150 blasts by firing a bazooka, and in the third to 100 charges of detonating explosives of 180 dB. Serial serum samples were taken after exposure. Results were compared with a control group consisting of 19 unexposed age-matched healthy volunteers. Results - The CSF biomarkers for neuronal/axonal damage (tau and neurofilament protein), glial cell injury (GFAP and S-100b), blood-brain barrier damage (CSF/serum albumin ratio) and hemorrhages (hemoglobin and bilirubin) and the serum GFAP and S-100b showed normal and stable levels in all exposed officers. Discussion - Repeated exposure to high-impact blast does not result in any neurochemical evidence of brain damage. These findings are of importance for soldiers regularly exposed to high-impact blast when firing artillery shells or other types of heavy weapons.
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9.
  • Balldin, Jan, 1935-, et al. (författare)
  • Gamma-glutamyltransferase in alcohol use disorders: Modification of decision limits in relation to treatment goals?
  • 2010
  • Ingår i: Scandinavian journal of clinical and laboratory investigation. - 1502-7686. ; 70:2, s. 71-74
  • Tidskriftsartikel (refereegranskat)abstract
    • Abstract Serum gamma-glutamyltransferase (GGT) is recommended as a marker for alcohol use disorders by the Swedish National Guidelines for Addiction, although it has a low sensitivity and specificity. GGT is inexpensive and easily accessible but additional knowledge is required on how to use the marker in patients with various levels of alcohol intake. Levels of GGT were obtained from 37 male social drinkers (< 100 grams pure alcohol weekly) and 18 former alcohol-dependent males with long-term (6 +/- 5 years) abstinence. Reproducibility was calculated through repeated blood samplings. Mean serum activity of GGT, in former alcohol-dependent males, was 0.26 microkat/L with an intra-class correlation coefficient of 0.85. In social drinkers, these figures were 0.34 microkat/L and 0.92, respectively. In treatment of males, with the goal of abstinence, upper reference limit is suggested to be 0.40 microkat/L. Goals of non-harmful drinking (< 100 grams weekly) suggest higher limits (0.62 microkat/L). Thirty percent increase of GGT should be suggestive of relapse.
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10.
  • Berggren, Ulf, 1948-, et al. (författare)
  • Dopamine D2 Receptor Genotype Is Associated with Increased Mortality at a 10-Year Follow-up of Alcohol-Dependent Individuals.
  • 2010
  • Ingår i: Alcohol and alcoholism. - 1464-3502. ; 45:1, s. 1-5
  • Tidskriftsartikel (refereegranskat)abstract
    • AIMS: Because the TAQ1 A1 allele may be associated with alcohol-related medical illnesses, and medical illnesses in alcohol-dependent individuals are associated with increased mortality, we test the hypothesis that the TAQ1 A1 allele of the DRD2 gene is associated with increased mortality in alcohol-dependent individuals. METHODS: Following an index treatment episode, a 10-year follow-up study in 366 alcohol-dependent individuals was performed. The TAQ1 A1/A2 DRD2 genotype and allele frequencies were compared between those deceased and those still living at the 10-year point. In addition, the genotype and allele frequencies of these alcohol-dependent individuals were compared to that in 578 control subjects. RESULTS: The prevalence of the A1 allele differed between the deceased and living patients and the controls: 47% of the deceased were A1+, compared to 37% of the living patients and 32% of the controls. The frequency of the TAQ1 A1/A2 genotype also differed between the groups. Thus, 43% had the A1/A2 genotype in comparison with 32% in the living patients and 29% in the controls. The TAQ 1 A1 allele frequency differed between the groups. The frequency of A1 allele was 25% in the deceased patients compared to 21% in the living patients and 17% in the controls. CONCLUSION: The TAQ I A1 allele of the DRD2 gene (or DRD2 gene region) was associated with increased mortality over a 10-year period in alcohol-dependent individuals.
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