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3. Neurofilament ELISA validation

Author

Petzold, Axel, Altintas, Ayse, Andreoni, Laura, Bartos, Ales, Berthele, Achim, Blankenstein, Marinus A., Buee, Luc, Castellazzi, Massimiliano, Cepok, Sabine, Comabella, Manuel, Constantinescu, Cris S., Deisenhammer, Florian, Deniz, Gunnur, Erten, Gaye, Espiño, Mercedes, Fainardi, Enrico, Franciotta, Diego, Freedman, Mark S., Giedraitis, Vilmantas, Gilhus, Nils Erik, Giovannoni, Gavin, Glabinski, Andrzej, Grieb, Pawel, Hartung, Hans-Peter, Hemmer, Bernhard, Herukka, Sanna-Kaisa, Hintzen, Rogier, Ingelsson, Martin, Jackson, Samuel, Jacobsen, Steve, Jafari, Naghmeh, Jalosinski, Marcin, Jarius, Sven, Kapaki, Elisabeth, Kieseier, Bernd C., Koel-Simmelink, Marleen J.A., Kornhuber, Johannes, Kuhle, Jens, Kurzepa, Jacek, Lalive, Patrice H., Lannfelt, Lars, Lehmensiek, Vera, Lewczuk, Piotr, Livrea, Paolo, Marnetto, Fabiana, Martino, Davide, Menge, Til, Norgren, Niklas, Papuć, Eva, Paraskevas, George P., Pirttilä, Tuula, Rajda, Cecília, Rejdak, Konrad, Ricny, Jan, Ripova, Daniela, Rosengren, Lars, Ruggieri, Maddalena, Schraen, Susanna, Shaw, Gerry, Sindic, Christian, Siva, Aksel, Stigbrand, Torgny, Stonebridge, Iva, Topcular, Baris, Trojano, Maria, Tumani, Hayrettin, Twaalfhoven, Harry A.M., Vécsei, László, Van Pesch, Vincent, Vanderstichele, Hugo, Vedeler, Christian, Verbeek, Marcel M., Villar, Luisa Maria, Weissert, Robert, Wildemann, Brigitte, Yang, Cui, Yao, Karen, and Teunissen, Charlotte E.

Published
2010
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17. CSF Biomarkers and Incipient Alzheimer Disease in Patients With Mild Cognitive Impairment

Author

Mattsson, Niklas, Zetterberg, Henrik, Hansson, Oskar, Andreasen, Niels, Parnetti, Lucilla, Jonsson, Michael, Herukka, Sanna-Kaisa, van der Flier, Wiesje M., Blankenstein, Marinus A., Ewers, Michael, Rich, Kenneth, Kaiser, Elmar, Verbeek, Marcel, Tsolaki, Magda, Mulugeta, Ezra, Rosén, Erik, Aarsland, Dag, Visser, Pieter Jelle, Schröder, Johannes, Marcusson, Jan, de Leon, Mony, Hampel, Harald, Scheltens, Philip, Pirttilä, Tuula, Wallin, Anders, Jönhagen, Maria Eriksdotter, Minthon, Lennart, Winblad, Bengt, and Blennow, Kaj

Published
2009
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18. Use of a genetic isolate to identify rare disease variants: C7 on 5p associated with MS

Author

Kallio, Suvi P., Jakkula, Eveliina, Purcell, Shaun, Suvela, Minna, Koivisto, Keijo, Tienari, Pentti J., Elovaara, Irina, Pirttilä, Tuula, Reunanen, Mauri, Bronnikov, Denis, Viander, Markku, Meri, Seppo, Hillert, Jan, Lundmark, Frida, Harbo, Hanne F., Lorentzen, Åslaug R., De Jager, Philip L., Daly, Mark J., Hafler, David A., Palotie, Aarno, Peltonen, Leena, and Saarela, Janna

Published
2009

30. Fine mapping of a multiple sclerosis locus to 2.5 Mb on chromosome 17q22–q24

Author

Saarela, Janna, Fejzo, Marlena Schoenberg, Chen, Daniel, Finnilä, Saara, Parkkonen, Maikki, Kuokkanen, Satu, Sobel, Eric, Tienari, Pentti J., Sumelahti, Marja-Liisa, Wikström, Juhani, Elovaara, Irina, Koivisto, Keijo, Pirttilä, Tuula, Reunanen, Mauri, Palotie, Aarno, and Peltonen, Leena

Published
2002

34. Pro-inflammatory interleukin-18 increases Alzheimer’s disease-associated amyloid-β production in human neuron-like cells

Author

Sutinen Elina M, Pirttilä Tuula, Anderson George, Salminen Antero, and Ojala Johanna O

Subjects
Interleukin-18, Inflammation, Amyloid-beta, Alzheimer’s disease, BACE, Presenilin, Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Background Alzheimer’s disease (AD) involves increased accumulation of amyloid-β (Aβ) plaques and neurofibrillary tangles as well as neuronal loss in various regions of the neocortex. Neuroinflammation is also present, but its role in AD is not fully understood. We previously showed increased levels of pro-inflammatory cytokine interleukin-18 (IL-18) in different regions of AD brains, where it co-localized with Aβ-plaques, as well as the ability of IL-18 to increase expression of glycogen synthase kinase-3β (GSK-3β) and cyclin dependent kinase 5, involved in hyperphosphorylation of tau-protein. Elevated IL-18 has been detected in several risk conditions for AD, including obesity, type-II diabetes, and cardiovascular diseases as well as in stress. Methods We differentiated SH-SY5Y neuroblastoma cells as neuron-like and exposed them to IL-18 for various times. We examined the protein levels of amyloid-β precursor protein (APP) and its processing products, its cleaving enzymes, involved in amyloidogenic processing of APP, and markers of apoptosis. Results IL-18 increased protein levels of the β-site APP-cleaving enzyme BACE-1, the N-terminal fragment of presenilin-1 and slightly presenilin enhancer 2, both of which are members of the γ-secretase complex, as well as Fe65, which is a binding protein of the C-terminus of APP and one regulator for GSK-3β. IL-18 also increased APP expression and phosphorylation, which preceded increased BACE-1 levels. Further, IL-18 altered APP processing, increasing Aβ40 production in particular, which was inhibited by IL-18 binding protein. Increased levels of soluble APPβ were detected in culture medium after the IL-18 exposure. IL-18 also increased anti-apoptotic bcl-xL levels, which likely counteracted the minor increase of the pro-apoptotic caspase-3. Lactate dehydrogenase activity in culture medium was unaffected. Conclusions The IL-18 induction of BACE-1, APP processing, and Aβ is likely to be linked to stress-associated adaptations in neurons during the course of normal functioning and development. However, in the course of wider changes in the aging brain, and particularly in AD, the effects of heightened or prolonged levels of IL-18 may contribute to the process of AD, including via increased Aβ.

Published
2012
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42. MS-taudin diagnoosi, lääkehoito ja kuntoutus

Author

Elovaara, Irina, Atula, Sari, Erälinna, Juha-Pekka, Färkkilä, Markus, Pirttilä, Tuula, Remes, Anne, Ruutiainen, Juhani, Varis, Tiina, and University of Tampere

Subjects
Neurologia ja psykiatria - Neurology and psychiatry
Abstract

Mitä uutta päivityksessä? MS-taudin lääkehoito aloitetaan heti McDonaldin diagnostisten kriteereiden täytyttyä. Henkilöitä, joilla todetaan kliinisesti eriytynyt oireyhtymä (KEO) ja suurentunut riski saada MS-tauti (MS-tautiin sopivia muutoksia magneettikuvauksissa (MK) ja selkäydinnesteessä), seurataan MK:lla 3-6 kuukauden välein vuoden ajan ensimmäisestä kuvauksesta. Akuutti pahenemisvaihe hoidetaan suonensisäisellä tai suun kautta otettavalla jättiannoksisella kortikosteroidilla. Ensisijainen lääkehoito on beetainterferoni tai glatirameeriasetaatti. Beetainterferonihoidossa olevilta mitataan 12 ja 24 kuukauden kuluttua hoidon aloituksesta MxA-vaste. Jos vaste puuttuu toistetuissa määrityksissä, hoitoa on vaihdettava, ja mikäli vaste on vähäinen, mittaus toistetaan. Beetainterferoni- tai glatirameeriasetaattihoidosta huolimatta aktiivisen MS-taudin toissijainen lääkehoito on natalitsumabi. Immunomoduloiva hoito lopetetaan, mikäli tauti muuttuu toissijaisesti eteneväksi eikä ole enää immunologisesti aktiivinen. English summary: Update on Current Care guidelines: Diagnostics, treatment and rehabilitation of multiple sclerosis Treatment is initiated when the McDonald criteria for relapsing-remitting multiple sclerosis (RRMS) are fulfilled. High-risk patients with clinically isolated syndrome are followed using magnetic resonance imaging for one year after the first imaging. Interferon-β or glatiramer acetate are the first-line immunomodulating drugs (IMD) for RRMS. MxA protein is measured 12 and 24 months after initiation of Interferon-β to evaluate possible development of neutralizing antibodies. If MxA protein may not be detected repeatedly interferon-β treatment is discontinued. If the disease is active in spite of treatment with first-line IMD, natalizumab may be considered as a second-line therapy. IMD is stopped when the transition to secondary progressive phase has occurred (or upon transition to secondary progressive phase).

Published
2010

43. Genome-wide Association Study in a High-Risk Isolate for Multiple Sclerosis Reveals Associated Variants in STAT3 Gene

Author

Jakkula, Eveliina, Leppä, Virpi, Sulonen, Anna-Maija, Varilo, Teppo, Kallio, Suvi, Kemppinen, Anu, Purcell, Shaun, Koivisto, Keijo, Tienari, Pentti, Sumelahti, Marja-Liisa, Elovaara, Irina, Pirttilä, Tuula, Reunanen, Mauri, Aromaa, Arpo, Oturai, Annette Bang, Søndergaard, Helle Bach, Harbo, Hanne F., Mero, Inger-Lise, Gabriel, Stacey B., Mirel, Daniel B., Hauser, Stephen L., Kappos, Ludwig, Polman, Chris, De Jager, Philip L., Hafler, David A., Daly, Mark J., Palotie, Aarno, Saarela, Janna, and Peltonen, Leena

Published
2010
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46. CALHM1 P86L polymorphism does not alter amyloid-beta or tau in cerebrospinal fluid

Author

Giedraitis, Vilmantas, Glaser, Anna, Sarajärvi, Timo, Brundin, RoseMarie, Gunnarsson, Malin Degerman, Schjeide, Brit-Maren, Tanzi, Rudolph E, Helisalmi, Seppo, Pirttilä, Tuula, Kilander, Lena, Lannfelt, Lars, Soininen, Hilkka, Bertram, Lars, Ingelsson, Martin, Hiltunen, Mikko, Giedraitis, Vilmantas, Glaser, Anna, Sarajärvi, Timo, Brundin, RoseMarie, Gunnarsson, Malin Degerman, Schjeide, Brit-Maren, Tanzi, Rudolph E, Helisalmi, Seppo, Pirttilä, Tuula, Kilander, Lena, Lannfelt, Lars, Soininen, Hilkka, Bertram, Lars, Ingelsson, Martin, and Hiltunen, Mikko

Abstract

Recently, the P86L alteration in CALHM1 (calcium homeostasis modulator-1) was reported to be associated with Alzheimer's disease (AD). Moreover, the risk allele increased amyloid-beta (A beta) levels in conditioned media from cultured cells. Therefore, we hypothesized that CALHM1 P86L may modulate A beta or tau levels in cerebrospinal fluid (CSF). Nearly 200 individuals with AD or other cognitive disorders were included for CSF analysis and CALHM1 genotyping. No significant differences in CSF levels of A beta 42, tau or phospho-tau were found across the various CALHM1 genotypes. In conclusion, we found no evidence that CALHM1 P86L is associated with altered CSF levels of the investigated AD biomarkers.

Published
2010
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47. Neurofilament ELISA validation.

Author

UCL - SSS/IONS/CEMO - Pôle Cellulaire et moléculaire, UCL - (SLuc) Service de neurologie, Petzold, Axel, Altintas, Ayse, Andreoni, Laura, Bartos, Ales, Berthele, Achim, Blankenstein, Marinus A, Buee, Luc, Castellazzi, Massimiliano, Cepok, Sabine, Comabella, Manuel, Constantinescu, Cris S, Deisenhammer, Florian, Deniz, Gunnur, Erten, Gaye, Espiño, Mercedes, Fainardi, Enrico, Franciotta, Diego, Freedman, Mark S, Giedraitis, Vilmantas, Gilhus, Nils Erik, Giovannoni, Gavin, Glabinski, Andrzej, Grieb, Pawel, Hartung, Hans-Peter, Hemmer, Bernhard, Herukka, Sanna-Kaisa, Hintzen, Rogier, Ingelsson, Martin, Jackson, Samuel, Jacobsen, Steve, Jafari, Naghmeh, Jalosinski, Marcin, Jarius, Sven, Kapaki, Elisabeth, Kieseier, Bernd C, Koel-Simmelink, Marleen J A, Kornhuber, Johannes, Kuhle, Jens, Kurzepa, Jacek, Lalive, Patrice H, Lannfelt, Lars, Lehmensiek, Vera, Lewczuk, Piotr, Livrea, Paolo, Marnetto, Fabiana, Martino, Davide, Menge, Til, Norgren, Niklas, Papuć, Eva, Paraskevas, George P, Pirttilä, Tuula, Rajda, Cecília, Rejdak, Konrad, Ricny, Jan, Ripova, Daniela, Rosengren, Lars, Ruggieri, Maddalena, Schraen, Susanna, Shaw, Gerry, Sindic, Christian, Siva, Aksel, Stigbrand, Torgny, Stonebridge, Iva, Topcular, Baris, Trojano, Maria, Tumani, Hayrettin, Twaalfhoven, Harry A M, Vécsei, László, Van Pesch, Vincent, Vanderstichele, Hugo, Vedeler, Christian, Verbeek, Marcel M, Villar, Luisa Maria, Weissert, Robert, Wildemann, Brigitte, Yang, Cui, Yao, Karen, Teunissen, Charlotte E, UCL - SSS/IONS/CEMO - Pôle Cellulaire et moléculaire, UCL - (SLuc) Service de neurologie, Petzold, Axel, Altintas, Ayse, Andreoni, Laura, Bartos, Ales, Berthele, Achim, Blankenstein, Marinus A, Buee, Luc, Castellazzi, Massimiliano, Cepok, Sabine, Comabella, Manuel, Constantinescu, Cris S, Deisenhammer, Florian, Deniz, Gunnur, Erten, Gaye, Espiño, Mercedes, Fainardi, Enrico, Franciotta, Diego, Freedman, Mark S, Giedraitis, Vilmantas, Gilhus, Nils Erik, Giovannoni, Gavin, Glabinski, Andrzej, Grieb, Pawel, Hartung, Hans-Peter, Hemmer, Bernhard, Herukka, Sanna-Kaisa, Hintzen, Rogier, Ingelsson, Martin, Jackson, Samuel, Jacobsen, Steve, Jafari, Naghmeh, Jalosinski, Marcin, Jarius, Sven, Kapaki, Elisabeth, Kieseier, Bernd C, Koel-Simmelink, Marleen J A, Kornhuber, Johannes, Kuhle, Jens, Kurzepa, Jacek, Lalive, Patrice H, Lannfelt, Lars, Lehmensiek, Vera, Lewczuk, Piotr, Livrea, Paolo, Marnetto, Fabiana, Martino, Davide, Menge, Til, Norgren, Niklas, Papuć, Eva, Paraskevas, George P, Pirttilä, Tuula, Rajda, Cecília, Rejdak, Konrad, Ricny, Jan, Ripova, Daniela, Rosengren, Lars, Ruggieri, Maddalena, Schraen, Susanna, Shaw, Gerry, Sindic, Christian, Siva, Aksel, Stigbrand, Torgny, Stonebridge, Iva, Topcular, Baris, Trojano, Maria, Tumani, Hayrettin, Twaalfhoven, Harry A M, Vécsei, László, Van Pesch, Vincent, Vanderstichele, Hugo, Vedeler, Christian, Verbeek, Marcel M, Villar, Luisa Maria, Weissert, Robert, Wildemann, Brigitte, Yang, Cui, Yao, Karen, and Teunissen, Charlotte E

Abstract

This multi-center validation study identified the lack of preparation of accurate and consistent protein standards as the main reason for a poor inter-laboratory CV. This issue is also relevant to other protein biomarkers based on this type of assay and will need to be solved in order to achieve an acceptable level of analytical accuracy. The raw data of this study is available online.

Published
2010

48. Cerebrospinal fluid {beta}-amyloid 42 and tau proteins as biomarkers of Alzheimer-type pathologic changes in the brain

Author

Tapiola, Tero, Alafuzoff, Irina, Herukka, Sanna-Kaisa, Parkkinen, Laura, Hartikainen, Päivi, Soininen, Hilkka, Pirttilä, Tuula, Tapiola, Tero, Alafuzoff, Irina, Herukka, Sanna-Kaisa, Parkkinen, Laura, Hartikainen, Päivi, Soininen, Hilkka, and Pirttilä, Tuula

Abstract

BACKGROUND: There is a clear need to develop an objective diagnostic test for Alzheimer disease (AD). Changes in the levels of cerebrospinal fluid (CSF) tau protein and beta-amyloid 42 (Abeta42) peptide in patients with AD have been well documented, but the relationship between these biomarkers and neuropathologic changes in the brain is not established. OBJECTIVE: To study the relationship between antemortem CSF biomarker levels and Alzheimer-type neuropathologic changes in the brain. DESIGN: Cross-sectional study to correlate levels of CSF Abeta42, total tau, and phosphorylated tau protein with neuropathologic changes in the brain. SETTING: Academic research. Patients The study included 123 patients (79 with clinically diagnosed AD, 29 with other dementia, and 15 with other neurologic disease). All underwent clinical evaluation and provided antemortem lumbar CSF samples, and neuropathologic data were collected from September 11, 1990, to March 13, 2003, in the Department of Neuroscience and Neurology, University of Kuopio, Kuopio, Finland. MAIN OUTCOME MEASURES: Levels of CSF Abeta42, total tau, and phosphorylated tau protein were measured using standard commercial immunoassays. Neuropathologic evaluations included the classic silver impregnation method and immunohistochemistry for Abeta, hyperphosphorylated tau, and alpha-synuclein. RESULTS: Cerebrospinal fluid Abeta42 and tau protein levels were related to amyloid load and the presence of neurofibrillary pathologic abnormalities in the brain. Cerebrospinal fluid Abeta42 level correlated inversely with total Abeta load in the brain, and CSF tau level correlated with results of immunohistochemistry for hyperphosphorylated tau and with the presence of neocortical neurofibrillary tangles. In multivariate logistic regression analysis, the number of neuritic plaques in the brain remained a significant predictor of decreased CSF Abeta42 level and of increased CSF tau level. Based on the ratio of phosphorylated tau leve

Published
2009
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49. Interferon Regulatory Factor 5 (IRF5) Gene Variants are Associated with Multiple Sclerosis in Three Distinct Populations

Author

Kristjansdottir, Gudlaug, Sandling, Johanna K, Bonetti, Alessandro, Roos, Izaura M, Milani, Lili, Wang, Chuan, Gustafsdottir, Sigrun M, Sigurdsson, Snaevar, Lundmark, Anders, Tienari, Pentti J, Koivisto, Keijo, Elovaara, Irina, Pirttilä, Tuula, Reunanen, Mauri, Peltonen, Leena, Saarela, Janna, Hillert, Jan, Olsson, Tomas, Landegren, Ulf, Alcina, Antonio, Fernández, Oscar, Leyva, Laura, Guerrero, Miguel, Lucas, Miguel, Izquierdo, Guillermo, Matesanz, Fuencisla, Syvänen, Ann-Christine, Kristjansdottir, Gudlaug, Sandling, Johanna K, Bonetti, Alessandro, Roos, Izaura M, Milani, Lili, Wang, Chuan, Gustafsdottir, Sigrun M, Sigurdsson, Snaevar, Lundmark, Anders, Tienari, Pentti J, Koivisto, Keijo, Elovaara, Irina, Pirttilä, Tuula, Reunanen, Mauri, Peltonen, Leena, Saarela, Janna, Hillert, Jan, Olsson, Tomas, Landegren, Ulf, Alcina, Antonio, Fernández, Oscar, Leyva, Laura, Guerrero, Miguel, Lucas, Miguel, Izquierdo, Guillermo, Matesanz, Fuencisla, and Syvänen, Ann-Christine

Abstract

BACKGROUND: IRF5 is a transcription factor involved both in the type I interferon and the toll-like receptor signalling pathways. Previously, IRF5 has been found to be associated with systemic lupus erythematosus, rheumatoid arthritis and inflammatory bowel diseases. Here we investigated whether polymorphisms in the IRF5 gene would be associated with yet another disease with features of autoimmunity, multiple sclerosis (MS). METHODS: We genotyped nine single nucleotide polymorphisms and one insertion-deletion polymorphism in the IRF5 gene in a collection of 2337 patients with MS and 2813 controls from three populations: two case-control cohorts from Spain and Sweden, and a set of MS trio families from Finland. RESULTS: Two single nucleotide polymorphism (SNPs) (rs4728142, rs3807306), and a 5 bp insertion-deletion polymorphism located in the promoter and first intron of the IRF5 gene, showed association signals with values of p<0.001 when the data from all cohorts were combined. The predisposing alleles were present on the same common haplotype in all populations. Using electrophoretic mobility shift assays we observed allele specific differences in protein binding for the SNP rs4728142 and the 5 bp indel, and by a proximity ligation assay we demonstrated increased binding of the transcription factor SP1 to the risk allele of the 5 bp indel. CONCLUSION: These findings add IRF5 to the short list of genes shown to be associated with MS in more than one population. Our study adds to the evidence that there might be genes or pathways that are common in multiple autoimmune diseases, and that the type I interferon system is likely to be involved in the development of these diseases.

Published
2008
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50. Applicability of current staging/categorization of alpha-synuclein pathology and their clinical relevance.

Author

Parkkinen, Laura, Pirttilä, Tuula, Alafuzoff, Irina, Parkkinen, Laura, Pirttilä, Tuula, and Alafuzoff, Irina

Abstract

In Parkinson's disease (PD) and dementia with Lewy bodies (DLB) alpha-synuclein (alphaS) pathology is seen that displays a predictable topographic distribution. There are two staging/categorization systems, i.e. Braak's and McKeith's, currently in use for the assessment of alphaS pathology. The aim of these diagnostic strategies in pathology is, in addition to assess the stage/severity of pathology, to assess the probabilities of the related clinical symptomatology i.e. dementia and extrapyramidal symptoms (EPS). Herein, we assessed the applicability of these two staging/categorization systems and the frequency of dementia and EPS in a cohort of 226 alphaS-positive-subjects. These subject were selected from a large autopsy sample (n = 1,720), irrespective of the clinical presentation, based on the detection of alphaS-immunoreactivity (IR) in one of the most vulnerable nuclei; in the dorsal motor nucleus of vagus, substantia nigra and basal forebrain. The frequency of alphaS-IR lesions in this large cohort was 14% (248 out of 1,720). If applicable, each of the 226 subjects with all required material available was assigned a neuropathological stage/category of PD/DLB and finally the neuropathological data was analyzed in relation to dementia and EPS. 83% of subjects showed a distribution pattern of alphaS-IR that was compatible with the current staging/categorization systems. Around 55% of subjects with widespread alphaS pathology (Braak's PD stages 5-6) lacked clinical signs of dementia or EPS. Similarly, in respect to those subjects that fulfilled the McKeith criteria for diffuse neocortical category and displaying only mild concomitant Alzheimer's disease-related pathology, only 48% were demented and 54% displayed EPS. It is noteworthy that some subjects (17%) deviated from the suggested caudo-rostral propagation suggesting alternative routes of progression, perhaps due to concomitant diseases and genetic predisposition. In conclusion, our results do indeed confirm

Published
2008
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