Maass, Fabian

[["dc.bibliographiccitation.artnumber","625"],["dc.bibliographiccitation.journal","Frontiers in Neuroscience"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Roser, Anna-Elisa"],["dc.contributor.author","Caldi Gomes, Lucas"],["dc.contributor.author","Schünemann, Jonas"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2019-07-09T11:45:52Z"],["dc.date.available","2019-07-09T11:45:52Z"],["dc.date.issued","2018"],["dc.description.abstract","Parkinson’s disease (PD) is the second most common neurodegenerative disorder worldwide. Its main neuropathological hallmarks are the degeneration of dopaminergic neurons in the substantia nigra and alpha-synuclein containing protein inclusions, called Lewy Bodies. The diagnosis of idiopathic PD is still based on the assessment of clinical criteria, leading to an insufficient diagnostic accuracy. Additionally, there is no biomarker available allowing the prediction of the disease course or monitoring the response to therapeutic approaches. So far, protein biomarker candidates such as alpha-synuclein have failed to improve diagnosis of PD. Circulating microRNAs (miRNAs) in body fluids are promising biomarker candidates for PD, as they are easily accessible by nonor minimally-invasive procedures and changes in their expression are associated with pathophysiological processes relevant for PD. Advances in miRNA analysis methods resulted in numerous recent publications on miRNAs as putative biomarkers. Here, we discuss the applicability of different body fluids as sources for miRNA biomarkers, highlight technical aspects of miRNA analysis and give an overview on published studies investigating circulating miRNAs as biomarker candidates for diagnosis of PD and other Parkinsonian syndromes."],["dc.identifier.arxiv","30233304"],["dc.identifier.doi","10.3389/fnins.2018.00625"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15332"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59325"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/34"],["dc.language.iso","en"],["dc.notes.intern","DeepGreen Import"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | B09: Cytoskelettale Veränderungen tragen zu synapto-axonalen Fehlfunktionen in Morbus Parkinson bei"],["dc.relation.eissn","1662-453X"],["dc.relation.issn","1662-453X"],["dc.relation.workinggroup","RG Lingor (Translational Neurodegeneration)"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.subject.ddc","610"],["dc.title","Circulating miRNAs as Diagnostic Biomarkers for Parkinson’s Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","overview_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1259"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Diagnostics"],["dc.bibliographiccitation.volume","12"],["dc.contributor.affiliation","Emdina, Anna; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Hermann, Peter; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Varges, Daniela; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Nuhn, Sabine; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Goebel, Stefan; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Bunck, Timothy; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Maass, Fabian; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Schmitz, Matthias; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Llorens, Franc; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Kruse, Niels; 4Department of Neuropathology, University Medical Centre Göttingen, 37075 Göttingen, Germany; n.kruse@med.uni-goettingen.de"],["dc.contributor.affiliation","Lingor, Paul; 5Department of Neurology, Klinikum Rechts der Isar, Technical University of Munich, 80333 Munich, Germany; paul.lingor@tum.de"],["dc.contributor.affiliation","Mollenhauer, Brit; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Zerr, Inga; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.author","Emdina, Anna"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Varges, Daniela"],["dc.contributor.author","Nuhn, Sabine"],["dc.contributor.author","Goebel, Stefan"],["dc.contributor.author","Bunck, Timothy"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Mollenhauer, Brit"],["dc.date.accessioned","2022-06-01T09:39:57Z"],["dc.date.available","2022-06-01T09:39:57Z"],["dc.date.issued","2022"],["dc.date.updated","2022-06-05T20:43:26Z"],["dc.description.abstract","Biomarkers are increasingly recognized as tools in the diagnosis and prognosis of neurodegenerative diseases. No fluid biomarker for Parkinson’s disease (PD) has been established to date, but α-synuclein, a major component of Lewy bodies in PD and dementia with Lewy bodies (DLB), has become a promising candidate. Here, we investigated CSF α-synuclein in patients with PD (n = 28), PDD (n = 8), and DLB (n = 5), applying an electrochemiluminescence immunoassay. Median values were non-significantly (p = 0.430) higher in patients with PDD and DLB (287 pg/mL) than in PD (236 pg/mL). A group of n = 36 primarily non-demented patients with PD and PDD was clinically followed for up to two years. A higher baseline α-synuclein was associated with increases in Hoehn and Yahr classifications (p = 0.019) and Beck Depression Inventory scores (p < 0.001) as well as worse performance in Trail Making Test A (p = 0.017), Trail Making Test B (p = 0.043), and the Boston Naming Test (p = 0.002) at follow-up. Surprisingly, higher levels were associated with a better performance in semantic verbal fluency tests (p = 0.046). In summary, CSF α-synuclein may be a potential prognostic marker for disease progression, affective symptoms, and executive cognitive function in PD. Larger-scaled studies have to validate these findings and the discordant results for single cognitive tests in this exploratory investigation."],["dc.identifier.doi","10.3390/diagnostics12051259"],["dc.identifier.pii","diagnostics12051259"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108601"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.eissn","2075-4418"],["dc.title","Baseline Cerebrospinal Fluid α-Synuclein in Parkinson’s Disease Is Associated with Disease Progression and Cognitive Decline"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Neurology"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","von Gottberg, Philipp"],["dc.contributor.author","Franz, Jonas"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2021-04-14T08:27:59Z"],["dc.date.available","2021-04-14T08:27:59Z"],["dc.date.issued","2021"],["dc.description.abstract","Fingolimod represents a highly effective disease-modifying drug in patients with active relapsing-remitting multiple sclerosis (RRMS). Its immunosuppressive effects can mediate adverse events like increased risk of cancer development or appearance of opportunistic infections. Progressive multifocal leukoencephalopathy (PML)–representing a severe opportunistic infection–has been only infrequently described during Fingolimod treatment. Here, we present a case of a 63-year-old women with pre-diagnosed RRMS who presented with new multiple cerebral lesions in a routine MRI scan, also including a tumefactive lesion in the left parietal lobe, eventually leading to the diagnosis of brain metastases derived by an adenocarcinoma of the lung. Additionally, a JCV-DNA-PCR in the cerebrospinal fluid revealed positive results, corresponding to a paraclinical progressive multifocal leukoencephalopathy. In conclusion, adverse events potentially associated with immunosuppression can occur during Fingolimod treatment. In this context, the occurrence of cancer and opportunistic infections should be carefully monitored. Here, we report a case in which JCV-DNA-PCR in the cerebrospinal fluid suggests asymptomatic PML and simultaneously lung cancer brain metastases developed. While it is rather unlikely that either event occurred as an adverse event of fingolimod treatment, a contributing effect cannot be formally excluded."],["dc.identifier.doi","10.3389/fneur.2021.561158"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17790"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82468"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-2295"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Case Report: Findings Suggestive of Paraclinical Progressive Multifocal Leukoencephalopathy and Lung Cancer-Derived Brain Metastases in an MS Patient Treated With Fingolimod"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Neurology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Koch, Jan C."],["dc.contributor.author","Kuttler, Josua"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Lengenfeld, Teresa"],["dc.contributor.author","Zielke, Eirini"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2020-12-10T18:44:33Z"],["dc.date.available","2020-12-10T18:44:33Z"],["dc.date.issued","2020"],["dc.description.abstract","The Rho kinase (ROCK) inhibitor Fasudil is a promising drug for a disease-modifying therapy of amyotrophic lateral sclerosis (ALS). In preclinical models, Fasudil was shown to increase motor neuron survival, inhibit axonal degeneration, enhance axonal regeneration and modulate microglial function in vitro and in vivo. It prolonged survival and improved motor function of SOD1-G93A-mice. Recently, a phase IIa clinical trial has been commenced to investigate the safety, tolerability, and efficacy of Fasudil in ALS patients at an early stage of disease (ROCK-ALS trial, NCT03792490, Eudra-CT-Nr.: 2017-003676-31). Although Fasudil has been approved in Japan for many years for the treatment of vasospasms following subarachnoid hemorrhage and is known to have a favorable side effect profile in these patients, there is no data on its use in human patients with ALS or any other neurodegenerative conditions. Here, we report the first three cases of compassionate use of Fasudil in patients with ALS. Between May 2017 and February 2019, one male (66 years old) and two female (62 and 68 years old) subjects with probable or definite ALS according to the El Escorial criteria (one of the females having a pathogenic SOD1 mutation) were administered Fasudil 30 mg intravenously twice daily over 45 min on 20 consecutive working days. Blood pressure, heart rate and routine laboratory tests were constantly controlled. All three subjects tolerated the Fasudil infusions well without any obvious side effects. Interestingly, the slow vital capacity showed a significant increase in one of the patients. Taken together, we report here the first compassionate use of the ROCK inhibitor Fasudil in three ALS patients, which was well-tolerated."],["dc.identifier.doi","10.3389/fneur.2020.00173"],["dc.identifier.eissn","1664-2295"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17427"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78500"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-2295"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Compassionate Use of the ROCK Inhibitor Fasudil in Three Patients With Amyotrophic Lateral Sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","105"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Zella, Maria"],["dc.contributor.author","Metzdorf, Judith"],["dc.contributor.author","Ostendorf, Friederike"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Muhlack, Siegfried"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Haghikia, Aiden"],["dc.contributor.author","Tönges, Lars"],["dc.date.accessioned","2021-06-01T10:48:47Z"],["dc.date.available","2021-06-01T10:48:47Z"],["dc.date.issued","2019"],["dc.description.abstract","The etiology of Parkinson’s disease (PD) is significantly influenced by disease-causing changes in the protein alpha-Synuclein (aSyn). It can trigger and promote intracellular stress and thereby impair the function of dopaminergic neurons. However, these damage mechanisms do not only extend to neuronal cells, but also affect most glial cell populations, such as astroglia and microglia, but also T lymphocytes, which can no longer maintain the homeostatic CNS milieu because they produce neuroinflammatory responses to aSyn pathology. Through precise neuropathological examination, molecular characterization of biomaterials, and the use of PET technology, it has been clearly demonstrated that neuroinflammation is involved in human PD. In this review, we provide an in-depth overview of the pathomechanisms that aSyn elicits in models of disease and focus on the affected glial cell and lymphocyte populations and their interaction with pathogenic aSyn species. The interplay between aSyn and glial cells is analyzed both in the basic research setting and in the context of human neuropathology. Ultimately, a strong rationale builds up to therapeutically reduce the burden of pathological aSyn in the CNS. The current antibody-based approaches to lower the amount of aSyn and thereby alleviate neuroinflammatory responses is finally discussed as novel therapeutic strategies for PD."],["dc.identifier.doi","10.3390/cells8020105"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86052"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.publisher","MDPI"],["dc.relation.eissn","2073-4409"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Novel Immunotherapeutic Approaches to Target Alpha-Synuclein and Related Neuroinflammation in Parkinson’s Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","673"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Brain Sciences"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Lange, Claudia"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Hassoun, Lina"],["dc.contributor.author","Bouter, Caroline"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Schott, Björn Hendrik"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Fitzner, Dirk"],["dc.date.accessioned","2021-08-12T07:45:51Z"],["dc.date.available","2021-08-12T07:45:51Z"],["dc.date.issued","2021"],["dc.description.abstract","(1) Background: autoimmune encephalitis associated with neurexin-3α antibodies is a seldom reported disease entity often accompanied by a severe clinical neuropsychiatric syndrome. (2) Method: we report on the case of a 58-year-old man diagnosed with neurexin-3α-associated autoimmune encephalitis revealing cognitive decline and depression before the proof of neurexin-3α antibodies. He underwent neuropsychological testing, peripheral blood and cerebrospinal fluid analysis, neuroimaging and electroencephalography. (3) Results: our patient’s main clinical feature was amnestic cognitive decline in combination with depressive symptoms. CSF analysis showed elevated phosphorylated tau protein 181 and positive proof of serum neurexin-3α antibodies in a cell-based assay. An 18F-FDG-PET/CT of the brain initially showed bilateral cerebral hypometabolism prefrontal and parietal, which was absent in follow up. The brain MRI was unremarkable. EEG recordings showed frontotemporal slowing in the theta and delta range. (4) Conclusions: taken together, we assumed autoimmune encephalitis associated with serum neurexin-3α antibodies. To the best of our knowledge, we are the first to report on a predominantly mild clinical manifestation entailing amnestic mild cognitive impairment in addition to depression, thus broadening the clinical spectrum associated with neurexin-3α antibodies."],["dc.description.abstract","(1) Background: autoimmune encephalitis associated with neurexin-3α antibodies is a seldom reported disease entity often accompanied by a severe clinical neuropsychiatric syndrome. (2) Method: we report on the case of a 58-year-old man diagnosed with neurexin-3α-associated autoimmune encephalitis revealing cognitive decline and depression before the proof of neurexin-3α antibodies. He underwent neuropsychological testing, peripheral blood and cerebrospinal fluid analysis, neuroimaging and electroencephalography. (3) Results: our patient’s main clinical feature was amnestic cognitive decline in combination with depressive symptoms. CSF analysis showed elevated phosphorylated tau protein 181 and positive proof of serum neurexin-3α antibodies in a cell-based assay. An 18F-FDG-PET/CT of the brain initially showed bilateral cerebral hypometabolism prefrontal and parietal, which was absent in follow up. The brain MRI was unremarkable. EEG recordings showed frontotemporal slowing in the theta and delta range. (4) Conclusions: taken together, we assumed autoimmune encephalitis associated with serum neurexin-3α antibodies. To the best of our knowledge, we are the first to report on a predominantly mild clinical manifestation entailing amnestic mild cognitive impairment in addition to depression, thus broadening the clinical spectrum associated with neurexin-3α antibodies."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3390/brainsci11060673"],["dc.identifier.pii","brainsci11060673"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88559"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.relation.eissn","2076-3425"],["dc.rights","CC BY 4.0"],["dc.title","Mild Amnestic Cognitive Impairment and Depressive Symptoms in Autoimmune Encephalitis Associated with Serum Anti-Neurexin-3α Autoantibodies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Neurology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.affiliation","Maass, Fabian; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Hermann, Peter; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Varges, Daniela; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Nuhn, Sabine; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","van Riesen, Christoph; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Jamous, Ala; 3Department of Neuroradiology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Focke, Niels K.; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Hewitt, Manuel; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Leha, Andreas; 4Department of Medical Statistics, University Medical Center, Göttingen, Germany"],["dc.contributor.affiliation","Bähr, Mathias; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Zerr, Inga; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Varges, Daniela"],["dc.contributor.author","Nuhn, Sabine"],["dc.contributor.author","van Riesen, Christoph"],["dc.contributor.author","Jamous, Ala"],["dc.contributor.author","Focke, Niels K."],["dc.contributor.author","Hewitt, Manuel"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2022-08-04T08:31:14Z"],["dc.date.available","2022-08-04T08:31:14Z"],["dc.date.issued","2022-07-19"],["dc.date.updated","2022-08-02T14:39:19Z"],["dc.description.abstract","The objective of the study was to characterize the pattern of cognitive dysfunction in patients with multiple system atrophy (MSA) applying a standardized neuropsychological assessment. A total of 20 patients with the diagnosis of probable or possible MSA were enrolled for neuropsychological assessment applying the CERAD plus battery. All patients were tested at baseline and 14/20 patients received additional follow-up assessments (median follow-up of 24 months). Additionally, relationship between cortical thickness values/subcortical gray matter volumes and CERAD subitems was evaluated at baseline in a subgroup of 13/20 patients. Trail Making Test (TMT) was the most sensitive CERAD item at baseline with abnormal performance (z-score < −1.28) in one or both pathological TMT items (TMT-A, TMT-B) in 60% of patients with MSA. Additionally, there was a significant inverse correlation between the volume of the left and the right accumbens area and the TMT A item after adjusting for age (left side: p = 0.0009; right side p = 0.003). Comparing both subtypes, patients with MSA-C had significant lower values in phonemic verbal fluency (p = 0.04) and a trend for lower values in semantic verbal fluency (p = 0.06) compared to MSA-P. Additionally, patients with MSA-C showed significantly worse performance in the TMT-B task (p = 0.04) and a trend for worse performance in the TMT-A task (p = 0.06). Concerning longitudinal follow-up, a significant worsening in the TMT-B (p = 0.03) can be reported in MSA. In conclusion, frontal-executive dysfunction presents the hallmark of cognitive impairment in MSA."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3389/fneur.2022.881369"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112628"],["dc.language.iso","en"],["dc.relation.eissn","1664-2295"],["dc.rights","CC BY 4.0"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Prospective CERAD Neuropsychological Assessment in Patients With Multiple System Atrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Aging Neuroscience"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Canaslan, Sezgi"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Villar-Piqué, Anna"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Gmitterová, Karin"],["dc.contributor.author","Varges, Daniela"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2021-12-01T09:24:03Z"],["dc.date.available","2021-12-01T09:24:03Z"],["dc.date.issued","2021"],["dc.description.abstract","Alpha-synucleinopathies, such as Parkinson\\’s disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA), are a class of neurodegenerative diseases. A diagnosis may be challenging because clinical symptoms partially overlap, and there is currently no reliable diagnostic test available. Therefore, we aimed to identify a suitable marker protein in cerebrospinal fluid (CSF) to distinguish either between different types of alpha-synucleinopathies or between alpha-synucleinopathies and controls. In this study, the regulation of different marker protein candidates, such as alpha-synuclein (a-Syn), neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), and total tau (tau) in different types of alpha-synucleinopathies, had been analyzed by using an ultrasensitive test system called single-molecule array (SIMOA). Interestingly, we observed that CSF-NfL was significantly elevated in patients with DLB and MSA compared to patients with PD or control donors. To differentiate between groups, receiver operating characteristic (ROC) curve analysis resulted in a very good diagnostic accuracy as indicated by the area under the curve (AUC) values of 0.87–0.92 for CSF-NfL. Furthermore, we observed that GFAP and tau were slightly increased either in DLB or MSA, while a-Syn levels remained unregulated. Our study suggests NfL as a promising marker to discriminate between different types of alpha-synucleinopathies or between DLB/MSA and controls."],["dc.description.abstract","Alpha-synucleinopathies, such as Parkinson’s disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA), are a class of neurodegenerative diseases. A diagnosis may be challenging because clinical symptoms partially overlap, and there is currently no reliable diagnostic test available. Therefore, we aimed to identify a suitable marker protein in cerebrospinal fluid (CSF) to distinguish either between different types of alpha-synucleinopathies or between alpha-synucleinopathies and controls. In this study, the regulation of different marker protein candidates, such as alpha-synuclein (a-Syn), neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), and total tau (tau) in different types of alpha-synucleinopathies, had been analyzed by using an ultrasensitive test system called single-molecule array (SIMOA). Interestingly, we observed that CSF-NfL was significantly elevated in patients with DLB and MSA compared to patients with PD or control donors. To differentiate between groups, receiver operating characteristic (ROC) curve analysis resulted in a very good diagnostic accuracy as indicated by the area under the curve (AUC) values of 0.87–0.92 for CSF-NfL. Furthermore, we observed that GFAP and tau were slightly increased either in DLB or MSA, while a-Syn levels remained unregulated. Our study suggests NfL as a promising marker to discriminate between different types of alpha-synucleinopathies or between DLB/MSA and controls."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3389/fnagi.2021.717930"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94835"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1663-4365"],["dc.relation.orgunit","Klinik für Neurologie"],["dc.rights","CC BY 4.0"],["dc.title","Detection of Cerebrospinal Fluid Neurofilament Light Chain as a Marker for Alpha-Synucleinopathies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","15"],["dc.bibliographiccitation.journal","Frontiers in Neuroscience"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Joppe, Karina"],["dc.contributor.author","Roser, Anna-Elisa"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2019-07-09T11:49:58Z"],["dc.date.available","2019-07-09T11:49:58Z"],["dc.date.issued","2019"],["dc.description.abstract","The homeostasis of iron is of fundamental importance in the central nervous system (CNS) to ensure biological processes such as oxygen transport, mitochondrial respiration or myelin synthesis. Dyshomeostasis and accumulation of iron can be observed during aging and both are shared characteristics of several neurodegenerative diseases. Iron-mediated generation of reactive oxygen species (ROS) may lead to protein aggregation and cellular toxicity. The process of misfolding and aggregation of neuronal proteins such as α-synuclein, Tau, amyloid beta (Aβ), TDP-43 or SOD1 is a common hallmark of many neurodegenerative disorders and iron has been shown to facilitate protein aggregation. Thus, both, iron and aggregating proteins are proposed to amplify their detrimental effects in the disease state. In this review, we give an overview on effects of iron on aggregation of different proteins involved in neurodegeneration. Furthermore, we discuss the proposed mechanisms of iron-mediated toxicity and protein aggregation emphasizing the red-ox chemistry and protein-binding properties of iron. Finally, we address current therapeutic approaches harnessing iron chelation as a disease-modifying intervention in neurodegenerative disorders, such as Parkinson's disease, Alzheimer's disease, and amyotrophic lateral sclerosis."],["dc.identifier.doi","10.3389/fnins.2019.00015"],["dc.identifier.pmid","30723395"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15821"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59666"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/15"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | B09: Cytoskelettale Veränderungen tragen zu synapto-axonalen Fehlfunktionen in Morbus Parkinson bei"],["dc.relation.issn","1662-4548"],["dc.relation.workinggroup","RG Lingor (Translational Neurodegeneration)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","The Contribution of Iron to Protein Aggregation Disorders in the Central Nervous System"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Rikker, Sebastian"],["dc.contributor.author","Dambeck, Vivian"],["dc.contributor.author","Warth, Carmina"],["dc.contributor.author","Tatenhorst, Lars"],["dc.contributor.author","Csoti, Ilona"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2021-04-14T08:25:46Z"],["dc.date.available","2021-04-14T08:25:46Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1038/s41598-020-65503-1"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17459"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81725"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2045-2322"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Increased alpha-synuclein tear fluid levels in patients with Parkinson’s disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]