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6. The natural history of multiple system atrophy: a prospective European cohort study

Author

Wenning, Gregor K, Geser, Felix, Krismer, Florian, Seppi, Klaus, Duerr, Susanne, Boesch, Sylvia, Köllensperger, Martin, Goebel, Georg, Pfeiffer, Karl P, Barone, Paolo, Pellecchia, Maria Teresa, Quinn, Niall P, Koukouni, Vasiliki, Fowler, Clare J, Schrag, Anette, Mathias, Christopher J, Giladi, Nir, Gurevich, Tanya, Dupont, Erik, Ostergaard, Karen, Nilsson, Christer F, Widner, Håkan, Oertel, Wolfgang, Eggert, Karla Maria, Albanese, Alberto, del Sorbo, Francesca, Tolosa, Eduardo, Cardozo, Adriana, Deuschl, Günther, Hellriegel, Helge, Klockgether, Thomas, Dodel, Richard, Sampaio, Cristina, Coelho, Miguel, Djaldetti, Ruth, Melamed, Eldad, Gasser, Thomas, Kamm, Christoph, Meco, Giuseppe, Colosimo, Carlo, Rascol, Olivier, Meissner, Wassilios G, Tison, François, and Poewe, Werner

Published
2013
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11. FUS pathology defines the majority of tau- and TDP-43-negative frontotemporal lobar degeneration

Author

Urwin, Hazel, Josephs, Keith A., Rohrer, Jonathan D., Mackenzie, Ian R., Neumann, Manuela, Authier, Astrid, Seelaar, Harro, Van Swieten, John C., Brown, Jeremy M., Johannsen, Peter, Nielsen, Jorgen E., Holm, Ida E., Dickson, Dennis W., Rademakers, Rosa, Graff-Radford, Neill R., Parisi, Joseph E., Petersen, Ronald C., Hatanpaa, Kimmo J., White III, Charles L., Weiner, Myron F., Geser, Felix, Van Deerlin, Vivianna M., Trojanowski, John Q., Miller, Bruce L., Seeley, William W., van der Zee, Julie, Kumar-Singh, Samir, Engelborghs, Sebastiaan, De Deyn, Peter P., Van Broeckhoven, Christine, Bigio, Eileen H., Deng, Han-Xiang, Halliday, Glenda M., Kril, Jillian J., Munoz, David G., Mann, David M., Pickering-Brown, Stuart M., Doodeman, Valerie, Adamson, Gary, Ghazi-Noori, Shabnam, Fisher, Elizabeth M. C., Holton, Janice L., Revesz, Tamas, Rossor, Martin N., Collinge, John, Mead, Simon, Isaacs, Adrian M., and The FReJA Consortium

Published
2010
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21. Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS

Author

Elden, Andrew C., Kim, Hyung-Jun, Hart, Michael P., Chen-Plotkin, Alice S., Johnson, Brian S., Fang, Xiaodong, Armakola, Maria, Geser, Felix, Greene, Robert, Lu, Min Min, Padmanabhan, Arun, Clay-Falcone, Dana, McCluskey, Leo, Elman, Lauren, Juhr, Denise, Gruber, Peter J., Rüb, Udo, Auburger, Georg, Trojanowski, John Q., Lee, Virginia M.-Y., Van Deerlin, Vivianna M., Bonini, Nancy M., and Gitler, Aaron D.

Published
2010
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23. Minocycline 1-year therapy in multiple-system-atrophy: Effect on clinical symptoms and [11C] (R)-PK11195 PET (MEMSA-trial)

Author

Dodel, Richard, Spottke, Annika, Gerhard, Alexander, Reuss, Alexander, Reinecker, Sylvia, Schimke, Nicole, Trenkwalder, Claudia, Sixel-Döring, Friederike, Herting, Birgit, Kamm, Christoph, Gasser, Thomas, Sawires, Martin, Geser, Felix, Köllensperger, Martin, Seppi, Klaus, Kloss, Manja, Krause, Martin, Daniels, Christine, Deuschl, Günther, Böttger, Silke, Naumann, Markus, Lipp, Axel, Gruber, Doreen, Kupsch, Andreas, Du, Yansheng, Turkheimer, Federico, Brooks, David J., Klockgether, Thomas, Poewe, Werner, Wenning, Gregor, Schade-Brittinger, Carmen, Oertel, Wolfgang H., and Eggert, Karla

Published
2010
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24. Clinical and Pathological Continuum of Multisystem TDP-43 Proteinopathies

Author

Geser, Felix, Martinez-Lage, Maria, Robinson, John, Uryu, Kunihiro, Neumann, Manuela, Brandmeir, Nicholas J., Xie, Sharon X., Kwong, Linda K., Elman, Lauren, McCluskey, Leo, Clark, Chris M., Malunda, Joe, Miller, Bruce L., Zimmerman, Earl A., Qian, Jiang, Van Deerlin, Vivianna, Grossman, Murray, Lee, Virginia M.-Y., and Trojanowski, John Q.

Published
2009

25. Red flags for multiple system atrophy

Author

Köllensperger, Martin, Geser, Felix, Seppi, Klaus, Stampfer-Kountchev, Michaela, Sawires, Martin, Scherfler, Christoph, Boesch, Sylvia, Mueller, Joerg, Koukouni, Vasiliki, Quinn, Niall, Pellecchia, Maria Teresa, Barone, Paolo, Schimke, Nicole, Dodel, Richard, Oertel, Wolfgang, Dupont, Erik, stergaard, Karen, Daniels, Christine, Deuschl, Günther, Gurevich, Tanya, Giladi, Nir, Coelho, Miguel, Sampaio, Cristina, Nilsson, Christer, Widner, Håkan, Sorbo, Francesca Del, Albanese, Alberto, Cardozo, Adriana, Tolosa, Eduardo, Abele, Michael, Klockgether, Thomas, Kamm, Christoph, Gasser, Thomas, Djaldetti, Ruth, Colosimo, Carlo, Meco, Giuseppe, Schrag, Anette, Poewe, Werner, and Wenning, Gregor K.

Published
2008
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29. Health-Related Quality of Life in Multiple System Atrophy

Author

Schrag, Anette, Geser, Felix, Stampfer-Kountchev, Michaela, Seppi, Klaus, Sawires, Martin, Köllensperger, Martin, Scherfler, Christoph, Quinn, Niall, Pellecchia, Maria T., Barone, Paolo, del Sorbo, Francesca, Albanese, Alberto, Ostergaard, Karen, Dupont, Erik, Cardozo, Adriana, Tolosa, Eduardo, Nilsson, Christer F., Widner, Håkan, Lindvall, Olle, Giladi, Nir, Gurevich, Tanya, Daniels, Christine, Deuschl, Günther, Coelho, Miguel, Sampaio, Cristina, Abele, Michael, Klockgether, Thomas, Schimke, Nicole, Eggert, Karla M., Oertel, Wolfgang, Djaldetti, Ruth, Colosimo, Carlo, Meco, Giuseppe, Poewe, Werner, and Wenning, Gregor K.

Published
2006
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31. Progression of multiple system atrophy (MSA): A prospective natural history study by the European MSA Study Group (EMSA SG)

Author

Geser, Felix, Wenning, Gregor K., Seppi, Klaus, Stampfer-Kountchev, Michaela, Scherfler, Christoph, Sawires, Martin, Frick, Carolin, Ndayisaba, Jean-Pierre, Ulmer, Hanno, Pellecchia, Maria T., Barone, Paolo, Kim, Hee T., Hooker, Juzar, Quinn, Niall P., Cardozo, Adriana, Tolosa, Eduardo, Abele, Michael, Klockgether, Thomas, stergaard, Karen, Dupont, Erik, Schimke, Nicole, Eggert, Karla M., Oertel, Wolfgang, Djaldetti, Ruth, and Poewe, Werner

Published
2006
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36. The Neuropathology of McLeod Syndrome.

Author

Walker, Ruth H., Saiki, Shinji, Danek, Adrian, Geser, Felix, Tolnay, Marcus, and Jung, H. H.

Abstract

McLeod syndrome (MLS) belongs to the heterogeneous group of neuroacanthocytosis (NA) syndromes that are characterized by an involvement of the hematological and nervous systems. Central nervous system symptoms of MLS resemble Huntington's disease (HD) or choreoacanthocytosis (ChAc) and include a choreatic movement disorder, psychiatric abnormalities, cognitive decline, and generalized seizures. In MLS, rather non-specific pathological changes are present in the caudate nucleus, putamen and pallidum, which are characterized by neuronal loss and astrogliosis. ChAc may show an additional involvement of the substantia nigra and thalamus, and HD features more widespread pathology and the presence of distinctive intranuclear inclusions. Cortical pathology predominantly occurs in HD, is less pronounced in ChAc, and most likely present to an only minor extent in MLS. However, the nature of cortical, subcortical, and basal ganglia pathology in MLS remains to be investigated in more detail in larger autopsy series. [ABSTRACT FROM AUTHOR]

Published
2008
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37. Multiple System Atrophy.

Author

Tarsy, Daniel, Litvan, Irene, Geser, Felix, and Wenning, Gregor K.

Abstract

Multiple system atrophy (MSA) is a sporadic neurodegenerative disorder characterized clinically by various combinations of parkinsonian, autonomic, cerebellar, or pyramidal symptoms and signs and pathologically by cell loss, gliosis, and glial cytoplasmic inclusions in several brain and spinal cord structures. The term MSA was introduced in 1969, however cases of MSA were previously reported under the rubrics of striatonigral degeneration, olivopontocerebellar atrophy, Shy-Drager syndrome and idiopathic orthostatic hypotension. In the late 1990s, α-synuclein immunostaining was recognized as most sensitive marker of inclusion pathology in MSA: because of these advances in molecular pathogenesis, MSA has been firmly established as α-synucleinopathy along with Parkinson's disease (PD) and dementia with Lewy bodies. Recent epidemiological surveys have shown that MSA is not a rare disorder (∼5 cases per 100,000 population), and that misdiagnosis, especially with PD, is still common due to variable clinical presentations of MSA. However, the clinical picture of MSA in its full-blown form is distinctive. The patient is hypomimic with orofacial and anterior neck dystonia resulting in a grinning smile akin to "risus sardonicus" and sometimes disproportionate antecollis. The voice is often markedly impaired with a characteristic quivering high-pitched dysarthria. The motor disorder of MSA is often mixed with parkinsonism, cerebellar ataxia, limb dystonia, myoclonus, and pyramidal features occurring at the same time. However, akinesia and rigidity are the predominating features in 80% of patients, and cerebellar ataxia within the remaining 20%. According to the predominant motor presentation, MSA patients may be labeled as parkinsonian or cerebellar variant (MSA-P, MSA-C). The diagnosis of MSA is largely based on clinical expertise, and this is well illustrated by the consensus diagnostic criteria, which comprise clinical features only (divided into four domains including autonomic dysfunction, parkinsonism, cerebellar dysfunction, and corticospinal tract dysfunction). Nevertheless, several autonomic function, imaging, neurophysiological, and biochemical studies have been proposed in the last decade to help in the differential diagnosis of MSA. No drug treatment consistently benefits patients with this disease. Indeed, parkinsonism often shows a poor or unsustained response to chronic levodopa therapy, however, one-third of the patients may show a moderate-to-good dopaminergic response initially. There is no effective drug treatment for cerebellar ataxia. On the other hand, features of autonomic failure such as orthostatic hypotension, urinary retention or incontinence, constipation, and impotence, may often be relieved if recognized by the treating physician. Novel symptomatic and neuroprotective therapies are urgently required. [ABSTRACT FROM AUTHOR]

Published
2005
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38. Atypical Alzheimer's disease in an elderly United States resident with amyotrophic lateral sclerosis and pathological tau in spinal motor neurons.

Author

McCluskey, Leo F., Geser, Felix, Elman, Lauren B., Van Deerlin, Vivianna M., Robinson, John L., Lee, Virginia M.-Y., and Trojanowski, John Q.

Subjects
*PATHOPHYSIOLOGY of amyotrophic lateral sclerosis, *FRONTOTEMPORAL dementia, *DIAGNOSIS of neurological disorders
Abstract

The article presents a case study of a 650-year old female with sporadic amyotrophic lateral sclerosis (ALS), eye closure apraxia, and multisystem tau pathology for atypical Alzheimer's disease (AD) through brain and spinal cord morphology. A neuropathology diagnostic assessment was conducted through routined diagnostic techniques. The patient was diagnosed with clinically definitive ALS with frontotemporal degeneration (FTD) and died from respiratory failure three years after diagnosis.

Published
2014
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40. Presentation, diagnosis, and management of multiple system atrophy in Europe: Final analysis of the European multiple system atrophy registry.

Author

Köllensperger, Martin, Geser, Felix, Ndayisaba, Jean-Pierre, Boesch, Sylvia, Seppi, Klaus, Ostergaard, Karen, Dupont, Erik, Cardozo, A., Tolosa, Eduardo, Abele, Michael, Klockgether, Thomas, Yekhlef, Farid, Tison, Francois, Daniels, Christine, Deuschl, Günther, Coelho, Miguel, Sampaio, Cristina, Bozi, Maria, Quinn, Niall, and Schrag, Anette

Abstract

Multiple system atrophy (MSA) is a Parkinson's Disease (PD)-like α-synucleinopathy clinically characterized by dysautonomia, parkinsonism, cerebellar ataxia, and pyramidal signs in any combination. We aimed to determine whether the clinical presentation of MSA as well as diagnostic and therapeutic strategies differ across Europe and Israel. In 19 European MSA Study Group centres all consecutive patients with a clinical diagnosis of MSA were recruited from 2001 to 2005. A standardized minimal data set was obtained from all patients. Four-hundred thirty-seven MSA patients from 19 centres in 10 countries were included. Mean age at onset was 57.8 years; mean disease duration at inclusion was 5.8 years. According to the consensus criteria 68% were classified as parkinsonian type (MSA-P) and 32% as cerebellar type (MSA-C) (probable MSA: 72%, possible MSA: 28%). Symptomatic dysautonomia was present in almost all patients, and urinary dysfunction (83%) more common than symptomatic orthostatic hypotension (75%). Cerebellar ataxia was present in 64%, and parkinsonism in 87%, of all cases. No significant differences in the clinical presentation were observed between the participating countries. In contrast, diagnostic work up and therapeutic strategies were heterogeneous. Less than a third of patients with documented orthostatic hypotension or neurogenic bladder disturbance were receiving treatment. This largest clinical series of MSA patients reported so far shows that the disease presents uniformly across Europe. The observed differences in diagnostic and therapeutic management including lack of therapy for dysautonomia emphasize the need for future guidelines in these areas. © 2010 Movement Disorder Society [ABSTRACT FROM AUTHOR]

Published
2010
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41. Minocycline 1-year therapy in multiple-system-atrophy: Effect on clinical symptoms and [11C] (R)-PK11195 PET (MEMSA-trial).

Author

Dodel, Richard, Spottke, Annika, Gerhard, Alexander, Reuss, Alexander, Reinecker, Sylvia, Schimke, Nicole, Trenkwalder, Claudia, Sixel-Döring, Friederike, Herting, Birgit, Kamm, Christoph, Gasser, Thomas, Sawires, Martin, Geser, Felix, Köllensperger, Martin, Seppi, Klaus, Kloss, Manja, Krause, Martin, Daniels, Christine, Deuschl, Günther, and Böttger, Silke

Abstract

The aim of the study was to investigate the efficacy of the antibiotic minocycline as a drug treatment in patients with Multiple-System-Atrophy Parkinson-type (MSA-P). Sixty-three patients were randomized to minocycline 200 mg/d (n = 32) or a matching placebo (n = 31). The primary outcome variable was the change in the value of the motor score of the Unified Multiple-System-Atrophy Rating-Scale (UMSARSII) from baseline to 48 weeks. Secondary outcome variables included subscores and individual Parkinsonian symptoms as determined by the UMSARS and the Unified-Parkinson's-Disease Rating-Scale (UPDRS). Health-related quality of life (HrQoL) was assessed using the EQ-5D and SF-12. 'Progression rate' was assumed to be reflected in the change in motor function over 48 weeks. At 24 weeks and 48 weeks of follow-up, there was a significant deterioration in motor scores in both groups, but neither the change in UMSARSII nor in UPDRSIII differed significantly between treatment groups, i.e. 'progression rate' was considered to be similar in both treatment arms. HrQoL did not differ among the two treatment arms. In a small subgroup of patients (n = 8; minocycline = 3, placebo = 5)[11C] (R)-PK11195-PET was performed. The three patients in the minocycline group had an attenuated mean increase in microglial activation as compared to the placebo group (P = 0.07) and in two of them individually showed decreased [11C] (R)-PK11195 binding actually decreased. These preliminary PET-data suggest that minocycline may interfere with microglial activation. The relevance of this observation requires further investigation. This prospective, 48 week, randomized, double-blind, multinational study failed to show a clinical effect of minocycline on symptom severity as assessed by clinical motor function. © 2009 Movement Disorder Society [ABSTRACT FROM AUTHOR]

Published
2010
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42. Multiple system atrophy: An update.

Author

Wenning, Gregor K., Geser, Felix, Stampfer-Kountchev, Michaela, and Tison, François

Abstract

Multiple system atrophy (MSA) is a sporadic neurodegenerative disorder that usually manifests in the early sixth decade of life and progresses relentlessly with a mean survival of 9 years. Clinically, MSA is dominated by autonomic/urogenital failure, which may be associated with either levodopa ( L-dopa) -unresponsive parkinsonism in 80% of cases (MSA-P subtype) or with cerebellar ataxia in 20% of cases (MSA-C subtype). Pathologically, MSA is characterized by a neuronal multisystem degeneration and abnormal glial cytoplasmic inclusions containing α-synuclein aggregates. Pharmacological treatment of motor features is disappointing except for a transient L-dopa response in a minority of MSA-P patients. In contrast, autonomic and urogenital features of MSA should be identified early on, because they can be treated effectively in many instances. Neuroprotective strategies are presently unavailable, however, two multicentre European trials have been launched to evaluate the effects of riluzole and human recombinant growth hormone on disease progression in MSA. Clearly, further randomised, controlled trials are required to identify effective symptomatic or neuroprotective agents in MSA. Several in vivo models have become available to allow a careful preselection of candidate agents. Several research groups have been formed in Europe (EMSA-SG, NNIPPS) and United States (NAMSA-SG), providing a framework for coordinated trial activity in MSA. © 2003 Movement Disorder Society [ABSTRACT FROM AUTHOR]

Published
2003
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45. Development and Validation of a Prognostic Model to Predict Overall Survival in Multiple System Atrophy.

Author

Eschlboeck S, Goebel G, Eckhardt C, Fanciulli A, Raccagni C, Boesch S, Djamshidian A, Heim B, Mahlknecht P, Mair K, Nachbauer W, Scherfler C, Stockner H, Poewe W, Seppi K, Kiechl S, Wenning G, Krismer F, Barone P, Pellecchia MT, Quinn NP, Fowler CJ, Schrag A, Giladi N, Gurevich T, Ostergaard K, Widner H, Oertel W, Albanese A, Tolosa E, Deuschl G, Klockgether T, Dodel R, Sampaio C, Melamed E, Gasser T, Colosimo C, Rascol O, Meissner W, Tison F, Geser F, Duerr S, Boesch S, Köllensperger M, Koukouni V, Mathias CJ, Dupont E, Nilsson CF, Eggert KM, Del Sorbo F, Cardozo A, Hellriegel H, Coelho M, Djaldetti R, Kamm C, and Meco G

Abstract

Background: Multiple system atrophy (MSA) is a devastating disease characterized by a variable combination of motor and autonomic symptoms. Previous studies identified numerous clinical factors to be associated with shorter survival., Objective: To enable personalized patient counseling, we aimed at developing a risk model of survival based on baseline clinical symptoms., Methods: MSA patients referred to the Movement Disorders Unit in Innsbruck, Austria, between 1999 and 2016 were retrospectively analyzed. Kaplan-Meier curves and multivariate Cox regression analysis with least absolute shrinkage and selection operator penalty for variable selection were performed to identify prognostic factors. A nomogram was developed to estimate the 7 years overall survival probability. The performance of the predictive model was validated and calibrated internally using bootstrap resampling and externally using data from the prospective European MSA Study Group Natural History Study., Results: A total of 210 MSA patients were included in this analysis, of which 124 patients died. The median survival was 7 years. The following clinical variables were found to significantly affect overall survival and were included in the nomogram: age at symptom onset, falls within 3 years of onset, early autonomic failure including orthostatic hypotension and urogenital failure, and lacking levodopa response. The time-dependent area under curve for internal and external validation was >0.7 within the first 7 years of the disease course. The model was well calibrated showing good overlap between predicted and actual survival probability at 7 years., Conclusion: The nomogram is a simple tool to predict survival on an individual basis and may help to improve counseling and treatment of MSA patients., (© 2023 The Authors. Movement Disorders Clinical Practice published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.)

Published
2023
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46. Pathological TDP-43 distinguishes sporadic amyotrophic lateral sclerosis from amyotrophic lateral sclerosis with SOD1 mutations.

Author

Mackenzie IR, Bigio EH, Ince PG, Geser F, Neumann M, Cairns NJ, Kwong LK, Forman MS, Ravits J, Stewart H, Eisen A, McClusky L, Kretzschmar HA, Monoranu CM, Highley JR, Kirby J, Siddique T, Shaw PJ, Lee VM, and Trojanowski JQ

Subjects
Humans, Immunohistochemistry, Medulla Oblongata pathology, Motor Cortex pathology, Mutation genetics, Spinal Cord pathology, Superoxide Dismutase-1, Ubiquitin genetics, Amyotrophic Lateral Sclerosis genetics, Amyotrophic Lateral Sclerosis pathology, DNA-Binding Proteins genetics, Superoxide Dismutase genetics
Abstract

Objective: Amyotrophic lateral sclerosis (ALS) is a common, fatal motor neuron disorder with no effective treatment. Approximately 10% of cases are familial ALS (FALS), and the most common genetic abnormality is superoxide dismutase-1 (SOD1) mutations. Most ALS research in the past decade has focused on the neurotoxicity of mutant SOD1, and this knowledge has directed therapeutic strategies. We recently identified TDP-43 as the major pathological protein in sporadic ALS. In this study, we investigated TDP-43 in a larger series of ALS cases (n = 111), including familial cases with and without SOD1 mutations., Methods: Ubiquitin and TDP-43 immunohistochemistry was performed on postmortem tissue from sporadic ALS (n = 59), ALS with SOD1 mutations (n = 15), SOD-1-negative FALS (n = 11), and ALS with dementia (n = 26). Biochemical analysis was performed on representative cases from each group., Results: All cases of sporadic ALS, ALS with dementia, and SOD1-negative FALS had neuronal and glial inclusions that were immunoreactive for both ubiquitin and TDP-43. Cases with SOD1 mutations had ubiquitin-positive neuronal inclusions; however, no cases were immunoreactive for TDP-43. Biochemical analysis of postmortem tissue from sporadic ALS and SOD1-negative FALS demonstrated pathological forms of TDP-43 that were absent in cases with SOD1 mutations., Interpretation: These findings implicate pathological TDP-43 in the pathogenesis of sporadic ALS. In contrast, the absence of pathological TDP-43 in cases with SOD1 mutations implies that motor neuron degeneration in these cases may result from a different mechanism, and that cases with SOD1 mutations may not be the familial counterpart of sporadic ALS.

Published
2007
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47. Failure of neuronal protection by inhibition of glial activation in a rat model of striatonigral degeneration.

Author

Stefanova N, Mitschnigg M, Ghorayeb I, Diguet E, Geser F, Tison F, Poewe W, and Wenning GK

Subjects
Animals, Male, Minocycline pharmacology, Minocycline therapeutic use, Neuroglia drug effects, Neurons drug effects, Neuroprotective Agents pharmacology, Rats, Rats, Wistar, Striatonigral Degeneration prevention & control, Disease Models, Animal, Neuroglia metabolism, Neurons metabolism, Neuroprotective Agents therapeutic use, Striatonigral Degeneration metabolism
Abstract

Previous studies in rodent models of neurodegenerative disorders have demonstrated that minocycline exerts neuroprotective effects unrelated to its antimicrobial action. The purpose of the present study was to analyze whether minocycline exhibits neuroprotective activity in a rat model of striatonigral degeneration (SND), the core pathology underlying levodopa-unresponsive parkinsonism associated with multiple system atrophy (MSA). We observed no significant effect of minocycline on locomotor impairment in double-lesioned SND rats. Minocycline significantly suppressed astroglial and microglial activation (P < 0.01); however, 3'5'-monophosphate-regulated phosphoprotein (DARPP 32) immunohistochemistry revealed no significant differences in striatal lesion volume of minocycline-treated versus untreated control SND rats. Furthermore, there was no protection of nigral dopaminergic neurons in the double-lesion model. We conclude that despite its astrocytic and microglial suppression, minocycline failed to attenuate lesion-induced neuronal damage in the SND rat model., (2004 Wiley-Liss, Inc.)

Published
2004
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