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3. Low prevalence of known pathogenic mutations in dominant PD genes: A Swedish multicenter study

Author

Puschmann, Andreas, Jiménez-Ferrer, Itzia, Lundblad-Andersson, Elin, Mårtensson, Emma, Hansson, Oskar, Odin, Per, Widner, Håkan, Brolin, Kajsa, Mzezewa, Ropafadzo, Kristensen, Jonas, Soller, Maria, Rödström, Emil Ygland, Ross, Owen A., Toft, Mathias, Breedveld, Guido J., Bonifati, Vincenzo, Brodin, Lovisa, Zettergren, Anna, Sydow, Olof, Linder, Jan, Wirdefeldt, Karin, Svenningsson, Per, Nissbrandt, Hans, Belin, Andrea Carmine, Forsgren, Lars, and Swanberg, Maria

Published
2019
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4. The Fat Mass and Obesity-Associated Protein (FTO) Regulates Locomotor Responses to Novelty via D2R Medium Spiny Neurons

Author

Ruud, Johan, Alber, Jens, Tokarska, Anna, Engström Ruud, Linda, Nolte, Hendrik, Biglari, Nasim, Lippert, Rachel, Lautenschlager, Änne, Cieślak, Przemysław E., Szumiec, Łukasz, Hess, Martin E., Brönneke, Hella S., Krüger, Marcus, Nissbrandt, Hans, Korotkova, Tatiana, Silberberg, Gilad, Rodriguez Parkitna, Jan, and Brüning, Jens C.

Published
2019
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7. The role of TREM2 R47H as a risk factor for Alzheimer's disease, frontotemporal lobar degeneration, amyotrophic lateral sclerosis, and Parkinson's disease

Author

Lill, Christina M., Rengmark, Aina, Pihlstrøm, Lasse, Fogh, Isabella, Shatunov, Aleksey, Sleiman, Patrick M., Wang, Li-San, Liu, Tian, Lassen, Christina F., Meissner, Esther, Alexopoulos, Panos, Calvo, Andrea, Chio, Adriano, Dizdar, Nil, Faltraco, Frank, Forsgren, Lars, Kirchheiner, Julia, Kurz, Alexander, Larsen, Jan P., Liebsch, Maria, Linder, Jan, Morrison, Karen E., Nissbrandt, Hans, Otto, Markus, Pahnke, Jens, Partch, Amanda, Restagno, Gabriella, Rujescu, Dan, Schnack, Cathrin, Shaw, Christopher E., Shaw, Pamela J., Tumani, Hayrettin, Tysnes, Ole-Bjørn, Valladares, Otto, Silani, Vincenzo, van den Berg, Leonard H., van Rheenen, Wouter, Veldink, Jan H., Lindenberger, Ulman, Steinhagen-Thiessen, Elisabeth, Teipel, Stefan, Perneczky, Robert, Hakonarson, Hakon, Hampel, Harald, von Arnim, Christine A.F., Olsen, Jørgen H., Van Deerlin, Vivianna M., Al-Chalabi, Ammar, Toft, Mathias, Ritz, Beate, and Bertram, Lars

Published
2015
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32. A Rare Truncating Mutation in ADH1C (G78Stop) Shows Significant Association With Parkinson Disease in a Large International Sample

Author

Buervenich, Silvia, Carmine, Andrea, Galter, Dagmar, Shahabi, Haydeh N., Johnels, Bo, Holmberg, Björn, Ahlberg, Jarl, Nissbrandt, Hans, Eerola, Johanna, Hellström, Olli, Tienari, Pentti J., Matsuura, Tohru, Ashizawa, Tetsuo, Wüllner, Ullrich, Klockgether, Thomas, Zimprich, Alexander, Gasser, Thomas, Hanson, Melissa, Waseem, Shamaila, Singleton, Andrew, McMahon, Francis J., Anvret, Maria, Sydow, Olof, and Olson, Lars

Published
2005

36. Association of Nrf2-encoding NFE2L2 haplotypes with Parkinson's disease

Author

Nilsson Michael, Blennow Kaj, Kurzawski Mateusz, Bialecka Monika, Drozdzik Marek, Nissbrandt Hans, Håkansson Anna, Bergström Petra, Celojevic Dragana, Nilsson Staffan, Landgren Sara, von Otter Malin, Hammarsten Ola, and Zetterberg Henrik

Subjects
Internal medicine, RC31-1245, Genetics, QH426-470
Abstract

Abstract Background Oxidative stress is heavily implicated in the pathogenic process of Parkinson's disease. Varying capacity to detoxify radical oxygen species through induction of phase II antioxidant enzymes in substantia nigra may influence disease risk. Here, we hypothesize that variation in NFE2L2 and KEAP1, the genes encoding the two major regulators of the phase II response, may affect the risk of Parkinson's disease. Methods The study included a Swedish discovery case-control material (165 cases and 190 controls) and a Polish replication case-control material (192 cases and 192 controls). Eight tag single nucleotide polymorphisms representing the variation in NFE2L2 and three representing the variation in KEAP1 were chosen using HapMap data and were genotyped using TaqMan Allelic Discrimination. Results We identified a protective NFE2L2 haplotype in both of our European case-control materials. Each haplotype allele was associated with five years later age at onset of the disease (p = 0.001) in the Swedish material, and decreased risk of PD (p = 2 × 10-6), with an odds ratio of 0.4 (95% CI 0.3-0.6) for heterozygous and 0.2 (95% CI 0.1-0.4) for homozygous carriers, in the Polish material. The identified haplotype includes a functional promoter haplotype previously associated with high transcriptional activity. Genetic variation in KEAP1 did not show any associations. Conclusion These data suggest that variation in NFE2L2 modifies the Parkinson's disease process and provide another link between oxidative stress and neurodegeneration.

Published
2010
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40. Glucagon-Like Peptide-1 and its Analogues Act in the Dorsal Raphe and Modulate Central Serotonin to Reduce Appetite and Body Weight

Author

Anderberg, Rozita H, Richard, Jennifer E, Eerola, Kim, Ferreras, Lorena Lopez, Nordbeck, Elin Banke, Hansson, Caroline, Nissbrandt, Hans, Berqquist, Filip, Gribble, Fiona M, Reimann, Frank, Wernstedt-Asterholm, Ingrid, Lamy, Christophe M., Skibicka, Karolina P, Gribble, Fiona [0000-0002-4232-2898], Reimann, Frank [0000-0001-9399-6377], and Apollo - University of Cambridge Repository

Subjects
endocrine system, obesity, food intake, Exendin-4, digestive, oral, and skin physiology, GLP-1, hormones, hormone substitutes, and hormone antagonists, serotonin
Abstract

Glucagon-like peptide-1 (GLP-1) and serotonin play critical roles in energy balance regulation. Both systems are exploited clinically as anti-obesity strategies. Surprisingly whether they interact in order to regulate energy balance is poorly understood. Here we investigated mechanisms by which GLP-1 and serotonin interact at the level of the CNS. Serotonin depletion impaired the ability of exendin-4, a clinically utilized GLP-1 analogue, to reduce body weight in rats, suggesting serotonin is a critical mediator of the energy balance impact of GLP-1R activation. Serotonin turnover and expression of 5HT2A and 5HT2C serotonin receptors in the hypothalamus were altered by GLP-1R activation. We demonstrate that 5HT2A, but surprisingly not 5HT2C, receptor is critical for weight-loss, anorexia and fat mass reduction induced by central GLP-1R activation. Importantly, central 5HT2A receptors are also required for peripherally injected liraglutide to reduce feeding and weight. Dorsal raphe (DR) harbors cell bodies of serotonin producing neurons that supply serotonin to the hypothalamic nuclei. We show that GLP-1R stimulation in DR is sufficient to induce hypophagia and increase electrical activity of the DR serotonin neurons. Finally our results disassociate brain metabolic and emotionality pathways impacted by GLP-1R activation. This study identifies serotonin as new critical neural substrate for GLP-1 impact on energy homeostasis, and expands the current map of brain areas impacted by GLP-1R activation.

Published
2017
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41. Testosterone is an endogenous regulator of BAFF and splenic B cell number

Author

Wilhelmson, Anna S., primary, Lantero Rodriguez, Marta, additional, Stubelius, Alexandra, additional, Fogelstrand, Per, additional, Johansson, Inger, additional, Buechler, Matthew B., additional, Lianoglou, Steve, additional, Kapoor, Varun N., additional, Johansson, Maria E., additional, Fagman, Johan B., additional, Duhlin, Amanda, additional, Tripathi, Prabhanshu, additional, Camponeschi, Alessandro, additional, Porse, Bo T., additional, Rolink, Antonius G., additional, Nissbrandt, Hans, additional, Turley, Shannon J., additional, Carlsten, Hans, additional, Mårtensson, Inga-Lill, additional, Karlsson, Mikael C. I., additional, and Tivesten, Åsa, additional

Published
2018
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42. Testosterone is an endogenous regulator of BAFF and splenic B cell number

Author

Wilhelmson, Anna S., Lantero Rodriguez, Marta, Stubelius, Alexandra, Fogelstrand, Per, Johansson, Inger, Buechler, Matthew B., Lianoglou, Steve, Kapoor, Varun N., Johansson, Maria E., Fagman, Johan B., Duhlin, Amanda, Tripathi, Prabhanshu, Camponeschi, Alessandro, Porse, Bo T., Rolink, Antonius G., Nissbrandt, Hans, Turley, Shannon J., Carlsten, Hans, Mårtensson, Inga-Lill, Karlsson, Mikael C. I., Tivesten, Åsa, Wilhelmson, Anna S., Lantero Rodriguez, Marta, Stubelius, Alexandra, Fogelstrand, Per, Johansson, Inger, Buechler, Matthew B., Lianoglou, Steve, Kapoor, Varun N., Johansson, Maria E., Fagman, Johan B., Duhlin, Amanda, Tripathi, Prabhanshu, Camponeschi, Alessandro, Porse, Bo T., Rolink, Antonius G., Nissbrandt, Hans, Turley, Shannon J., Carlsten, Hans, Mårtensson, Inga-Lill, Karlsson, Mikael C. I., and Tivesten, Åsa

Abstract

Testosterone deficiency in men is associated with increased risk for autoimmunity and increased B cell numbers through unknown mechanisms. Here we show that testosterone regulates the cytokine BAFF, an essential survival factor for B cells. Male mice lacking the androgen receptor have increased splenic B cell numbers, serum BAFF levels and splenic Baff mRNA. Testosterone deficiency by castration causes expansion of BAFF-producing fibroblastic reticular cells (FRCs) in spleen, which may be coupled to lower splenic noradrenaline levels in castrated males, as an α-adrenergic agonist decreases splenic FRC number in vitro. Antibody-mediated blockade of the BAFF receptor or treatment with the neurotoxin 6-hydroxydopamine revert the increased splenic B cell numbers induced by castration. Among healthy men, serum BAFF levels are higher in men with low testosterone. Our study uncovers a previously unrecognized regulation of BAFF by testosterone and raises important questions about BAFF in testosterone-mediated protection against autoimmunity.

Published
2018

44. Sustained effects of neonatal systemic lipopolysaccharide on IL-1β and Nrf2 in adult rat substantia nigra are partly normalized by a Spirulina enriched diet

Author

Patil, Jaspal, Matte, Ashok, Nissbrandt, Hans, Mallard, Carina, and Sandberg, Mats

Subjects
Lipopolysaccharides, NF-E2-Related Factor 2, Interleukin-1beta, Age Factors, Article, Rats, Rats, Sprague-Dawley, Substantia Nigra, Oxidative Stress, Treatment Outcome, Animals, Newborn, Spirulina, Animals, Dietary Proteins
Abstract

Neonatal infection can sensitize the adult substantia nigra (SN) to secondary insults, causing a decrease in antioxidant capacity which may lead to Parkinson's disease in adults. We studied the prolonged effect of systemic infection by (i.p.) administration of lipopolysaccharide (LPS) on interleukin (IL)-1β, the antioxidant regulator nuclear factor-erythroid 2-related factor 2 (Nrf2), and the peroxisome proliferator-activated receptor γ coactivator (PGC)-1α in rat SN.Five-day-old rat pups were treated with LPS (i.p. 2 mg/kg). After 65 days, the mRNA level of IL-1β was significantly increased, in parallel with a decrease in that of the rate-limiting enzyme in glutathione synthesis, the γ-glutamylcysteine ligase catalytic subunit (γGCLc), Nrf2, and brain-derived neurotrophic factor (BDNF). Protein levels of γGCLc and Nrf2 were decreased while IL-1β protein was significantly increased. These LPS-induced long-term changes correlated with a decrease in phosphorylated (active) AKT (pAKT) and phosphorylated (inactive) GSK-3β (pGSK-3β). In another set of experiments, a 0.1% Spirulina-containing diet was given to lactating mothers 24 h before the LPS treatment of the pups. The Spirulina-supplemented diet decreased IL-1β protein expression in SN and elevated the mRNA level of γGCLc, Nrf2 protein, PGC-1α protein, and pAKT.Early-life infection can negatively affect Nrf2, pAKT, and pGSK-3β for a long time in SN. A diet enriched with antioxidant and anti-inflammatory phytochemicals can partly restore some, but not all, of the effects on the antioxidant defense, possibly via normalizing effects on pAKT.

Published
2016

46. Glucagon-Like Peptide 1 and Its Analogs Act in the Dorsal Raphe and Modulate Central Serotonin to Reduce Appetite and Body Weight

Author

Anderberg, Rozita H., primary, Richard, Jennifer E., additional, Eerola, Kim, additional, López-Ferreras, Lorena, additional, Banke, Elin, additional, Hansson, Caroline, additional, Nissbrandt, Hans, additional, Berqquist, Filip, additional, Gribble, Fiona M., additional, Reimann, Frank, additional, Wernstedt Asterholm, Ingrid, additional, Lamy, Christophe M., additional, and Skibicka, Karolina P., additional

Published
2017
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48. Genetic associations of Nrf2-encoding variants with Parkinson's disease - a multicenter study

Author

Otter, Malin von, Bergstrm, Petra, Quattrone, Aldo, De Marco, Elvira Valeria, Annesi, Grazia, Sderkvist, Peter, Bezzina Wettinger, Stephanie, Drozdzik, Marek, Bialecka, Monika, Nissbrandt, Hans, Klein, Christine, Nilsson, Michael, Hammarsten, Ola, Nilsson, Staffan, and Zetterberg, Henrik

Subjects
Parkinson's disease, Transcription factors -- Research, Single nucleotide polymorphisms
Abstract

Background: The transcription factor Nrf2, encoded by the gene, is an important regulator of the cellular protection against oxidative stress. Parkinson's disease is a neurodegenerative disease highly associated with oxidative stress. In a previously published study, we reported associations of haplotypes with risk and age at onset of idiopathic Parkinson's disease in a Swedish discovery material and a Polish replication material. Here, we have extended the replication study and performed meta-analyses including the Polish material and four new independent European patient-control materials. Furthermore, all SNPs included in the haplotype windows were investigated individually for associations with Parkinson's disease in meta-analyses including all six materials. Methods: Totally 1038 patients and 1600 control subjects were studied. Based on previous haplotype associations with Parkinson's disease, five tag SNPs were genotyped by allelic discrimination and three functional promoter SNPs were genotyped by sequencing. The impact of individual SNPs and haplotypes on risk and age at onset of Parkinson's disease were investigated in each material individually and in meta-analyses of the obtained results. Results: Meta-analyses of haplotypes showed association of haplotype GAAAA, including the fully functional promoter haplotype AGC, with decreased risk (OR=0.8 per allele, p=0.012) and delayed onset (+1.1 years per allele, p=0.048) of Parkinson's disease. These results support the previously observed protective effect of this haplotype in the first study. Further, meta-analyses of the SNPs included in the haplotypes revealed four SNPs associated with age at onset of Parkinson's disease (rs7557529 G>A, -1.0 years per allele, p=0.042; rs35652124 A>G, -1.1 years per allele, p=0.045; rs2886161 A>G, -1.2 years per allele, p=0.021; rs1806649 G>A, +1.2 years per allele, p=0.029). One of these (rs35652124) is a functional SNP located in the promoter. No individual SNP was associated with risk of Parkinson's disease. Conclusion: Our results support the hypothesis that variation in the gene, encoding a central protein in the cellular protection against oxidative stress, may contribute to the pathogenesis of Parkinson's disease. Functional studies are now needed to explore these results further., peer-reviewed

Published
2014

49. Testosterone is an endogenous regulator of BAFF and splenic B cell number.

Author

Buechler, Matthew B., Lantero Rodriguez, Marta, Fogelstrand, Per, Johansson, Inger, Tivesten, Åsa, Wilhelmson, Anna S., Duhlin, Amanda, Karlsson, Mikael C. I., Tripathi, Prabhanshu, Camponeschi, Alessandro, Mårtensson, Inga-Lill, Rolink, Antonius G., Nissbrandt, Hans, Porse, Bo T., Carlsten, Hans, Stubelius, Alexandra, Lianoglou, Steve, Kapoor, Varun N., Turley, Shannon J., and Johansson, Maria E.

Subjects
TESTOSTERONE, HORMONE deficiencies, HORMONE regulation, SPLEEN, TALL-1 (Protein), AUTOIMMUNITY
Abstract

Testosterone deficiency in men is associated with increased risk for autoimmunity and increased B cell numbers through unknown mechanisms. Here we show that testosterone regulates the cytokine BAFF, an essential survival factor for B cells. Male mice lacking the androgen receptor have increased splenic B cell numbers, serum BAFF levels and splenic Baff mRNA. Testosterone deficiency by castration causes expansion of BAFF-producing fibroblastic reticular cells (FRCs) in spleen, which may be coupled to lower splenic noradrenaline levels in castrated males, as an α-adrenergic agonist decreases splenic FRC number in vitro. Antibody-mediated blockade of the BAFF receptor or treatment with the neurotoxin 6- hydroxydopamine revert the increased splenic B cell numbers induced by castration. Among healthy men, serum BAFF levels are higher in men with low testosterone. Our study uncovers a previously unrecognized regulation of BAFF by testosterone and raises important questions about BAFF in testosterone-mediated protection against autoimmunity. [ABSTRACT FROM AUTHOR]

Published
2018
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