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Book ; Online ; E-Book: Recent advances in Parkinson's disease

Björklund, Anders / Cenci, M. Angela

2020

Author's details	edited by Anders Björklund, M. Angela Cenci
Keywords	Parkinson's disease
Subject code	616.833
Language	English
Size	1 online resource (xx, 557 pages) :, illustrations
Publisher	Elsevier
Publishing place	Amsterdam, The Netherlands ; Oxford, England ; Cambridge, Massachusetts
Document type	Book ; Online ; E-Book
Remark	Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
ISBN	0-444-64261-7 ; 0-444-64260-9 ; 978-0-444-64261-5 ; 978-0-444-64260-8
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Cells, pathways, and models in dyskinesia research.

Cenci, M Angela / Kumar, Arvind

Current opinion in neurobiology

2024 Volume 84, Page(s) 102833

Abstract: L-DOPA-induced dyskinesia (LID) is the most common form of hyperkinetic movement disorder resulting from altered information processing in the cortico-basal ganglia network. We here review recent advances clarifying the altered interplay between striatal ...

Abstract	L-DOPA-induced dyskinesia (LID) is the most common form of hyperkinetic movement disorder resulting from altered information processing in the cortico-basal ganglia network. We here review recent advances clarifying the altered interplay between striatal output pathways in this movement disorder. We also review studies revealing structural and synaptic changes to the striatal microcircuitry and altered cortico-striatal activity dynamics in LID. We furthermore highlight the recent progress made in understanding the involvement of cerebellar and brain stem nuclei. These recent developments illustrate that dyskinesia research continues to provide key insights into cellular and circuit-level plasticity within the cortico-basal ganglia network and its interconnected brain regions.
MeSH term(s)	Humans ; Dyskinesia, Drug-Induced ; Levodopa/adverse effects ; Basal Ganglia ; Corpus Striatum ; Brain/metabolism
Chemical Substances	Levodopa (46627O600J)
Language	English
Publishing date	2024-01-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1078046-4
ISSN	1873-6882 ; 0959-4388
ISSN (online)	1873-6882
ISSN	0959-4388
DOI	10.1016/j.conb.2023.102833
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Zs.A 3260: Show issues

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Article ; Online: Structural-functional properties of direct-pathway striatal neurons at early and chronic stages of dopamine denervation.

Li, Chang / Elabi, Osama F / Fieblinger, Tim / Cenci, M Angela

The European journal of neuroscience

2023 Volume 59, Issue 6, Page(s) 1227–1241

Abstract: The dendritic arbour of striatal projection neurons (SPNs) is the primary anatomical site where dopamine and glutamate inputs to the basal ganglia functionally interact to control movement. These dendritic arbourisations undergo atrophic changes in ... ...

Abstract	The dendritic arbour of striatal projection neurons (SPNs) is the primary anatomical site where dopamine and glutamate inputs to the basal ganglia functionally interact to control movement. These dendritic arbourisations undergo atrophic changes in Parkinson's disease. A reduction in the dendritic complexity of SPNs is found also in animal models with severe striatal dopamine denervation. Using 6-hydroxydopamine (6-OHDA) lesions of the medial forebrain bundle as a model, we set out to compare morphological and electrophysiological properties of SPNs at an early versus a chronic stage of dopaminergic degeneration. Ex vivo recordings were performed in transgenic mice where SPNs forming the direct pathway (dSPNs) express a fluorescent reporter protein. At both the time points studied (5 and 28 days following 6-OHDA lesion), there was a complete loss of dopaminergic fibres through the dorsolateral striatum. A reduction in dSPN dendritic complexity and spine density was manifest at 28, but not 5 days post-lesion. At the late time point, dSPN also exhibited a marked increase in intrinsic excitability (reduced rheobase current, increased input resistance, more evoked action potentials in response to depolarising currents), which was not present at 5 days. The increase in neuronal excitability was accompanied by a marked reduction in inward-rectifying potassium (Kir) currents (which dampen the SPN response to depolarising stimuli). Our results show that dSPNs undergo delayed coordinate changes in dendritic morphology, intrinsic excitability and Kir conductance following dopamine denervation. These changes are predicted to interfere with the dSPN capacity to produce a normal movement-related output.
MeSH term(s)	Mice ; Animals ; Dopamine/metabolism ; Oxidopamine/toxicity ; Neurons/physiology ; Corpus Striatum/metabolism ; Mice, Transgenic ; Denervation
Chemical Substances	Dopamine (VTD58H1Z2X) ; Oxidopamine (8HW4YBZ748)
Language	English
Publishing date	2023-10-24
Publishing country	France
Document type	Journal Article
ZDB-ID	645180-9
ISSN	1460-9568 ; 0953-816X
ISSN (online)	1460-9568
ISSN	0953-816X
DOI	10.1111/ejn.16166
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Zs.A 2548: Show issues

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Article ; Online: Non-dopaminergic approaches to the treatment of motor complications in Parkinson's disease.

Cenci, M Angela / Skovgård, Katrine / Odin, Per

Neuropharmacology

2022 Volume 210, Page(s) 109027

Abstract: Dopamine replacement therapy with l-DOPA is the most efficacious symptomatic treatment for Parkinson's disease, but its utility is limited by a development of motor fluctuations and abnormal involuntary movements (dyskinesia) in the majority of patients. ...

Abstract	Dopamine replacement therapy with l-DOPA is the most efficacious symptomatic treatment for Parkinson's disease, but its utility is limited by a development of motor fluctuations and abnormal involuntary movements (dyskinesia) in the majority of patients. These complications are attributed to the combined effects of dopaminergic degeneration and non-physiological reinstatement of dopamine transmission by the standard oral medications. There is substantial evidence that this altered state of dopamine transmission causes pathophysiological changes to a variety of non-dopaminergic neurotransmitter systems in the brain. This evidence has prompted an interest in developing drugs that target non-dopaminergic receptors for the purpose of improving l-DOPA-induced dyskinesia and/or motor fluctuations. We here review all the most important categories of non-dopaminergic targets that have been investigated so far, but with a particular focus on modulators of glutamatergic and serotonergic transmission, which continue to inspire significant efforts towards clinical translation. In particular, we discuss both the experimental rationale and the clinical experience thus far gained from studying 5-HT1A and 5-HT1B receptor agonists, NMDA and AMPA receptor antagonists, mGluR5 negative allosteric modulators, mGluR4 positive allosteric modulators, and adenosine A2a receptor antagonists. We also review compounds with complex pharmacological properties that are already used clinically or about to enter an advanced phase of clinical development (amantadine, safinamide, zonisamide, pridopidine, mesdopetam). We conclude with an outlook on possible directions to address unmet needs and improve the chance of successful translation in this therapeutic area.
MeSH term(s)	Antiparkinson Agents/adverse effects ; Dopamine ; Dyskinesia, Drug-Induced/drug therapy ; Humans ; Levodopa/adverse effects ; Parkinson Disease/drug therapy
Chemical Substances	Antiparkinson Agents ; Levodopa (46627O600J) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2022-03-12
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2022.109027
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Article ; Online: Preface: The evolving scenario of Parkinson's research.

Björklund, Anders / Cenci, M Angela

Progress in brain research

2019 Volume 252, Page(s) xix–xx

MeSH term(s)	Biomedical Research ; Humans ; Parkinson Disease
Language	English
Publishing date	2019-11-23
Publishing country	Netherlands
Document type	Editorial ; Introductory Journal Article
ISSN	1875-7855 ; 0079-6123
ISSN (online)	1875-7855
ISSN	0079-6123
DOI	10.1016/S0079-6123(20)30032-7
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Article ; Online: Animal models for preclinical Parkinson's research: An update and critical appraisal.

Cenci, M Angela / Björklund, Anders

Progress in brain research

2020 Volume 252, Page(s) 27–59

Abstract: Animal models of Parkinson's disease (PD) are essential to investigate pathogenic pathways at the whole-organism level. Moreover, they are necessary for a preclinical investigation of potential new therapies. Different pathological features of PD can be ... ...

Abstract	Animal models of Parkinson's disease (PD) are essential to investigate pathogenic pathways at the whole-organism level. Moreover, they are necessary for a preclinical investigation of potential new therapies. Different pathological features of PD can be induced in a variety of invertebrate and vertebrate species using toxins, drugs, or genetic perturbations. Each model has a particular utility and range of applicability. Invertebrate PD models are particularly useful for high throughput-screening applications, whereas mammalian models are needed to explore complex motor and non-motor features of the human disease. Here, we provide a comprehensive review and critical appraisal of the most commonly used mammalian models of PD, which are produced in rats and mice. A substantial loss of nigrostriatal dopamine neurons is necessary for the animal to exhibit a hypokinetic motor phenotype responsive to dopaminergic agents, thus resembling clinical PD. This level of dopaminergic neurodegeneration can be induced using specific neurotoxins, environmental toxicants, or proteasome inhibitors. Alternatively, nigrostriatal dopamine degeneration can be induced via overexpression of α-synuclein using viral vectors or transgenic techniques. In addition, protein aggregation pathology can be triggered by inoculating preformed fibrils of α-synuclein in the substantia nigra or the striatum. Thanks to the conceptual and technical progress made in the past few years a vast repertoire of well-characterized animal models are currently available to address different aspects of PD in the laboratory.
MeSH term(s)	Animals ; Biomedical Research ; Disease Models, Animal ; Parkinson Disease/metabolism ; Parkinson Disease/pathology ; Parkinson Disease/physiopathology
Language	English
Publishing date	2020-03-21
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1875-7855 ; 0079-6123
ISSN (online)	1875-7855
ISSN	0079-6123
DOI	10.1016/bs.pbr.2020.02.003
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Article ; Online: Non-Apoptotic Caspase-3 Activation Mediates Early Synaptic Dysfunction of Indirect Pathway Neurons in the Parkinsonian Striatum.

Fieblinger, Tim / Li, Chang / Espa, Elena / Cenci, M Angela

International journal of molecular sciences

2022 Volume 23, Issue 10

Abstract: Non-apoptotic caspase-3 activation is critically involved in dendritic spine loss and synaptic dysfunction in Alzheimer's disease. It is, however, not known whether caspase-3 plays similar roles in other pathologies. Using a mouse model of clinically ... ...

Abstract	Non-apoptotic caspase-3 activation is critically involved in dendritic spine loss and synaptic dysfunction in Alzheimer's disease. It is, however, not known whether caspase-3 plays similar roles in other pathologies. Using a mouse model of clinically manifest Parkinson's disease, we provide the first evidence that caspase-3 is transiently activated in the striatum shortly after the degeneration of nigrostriatal dopaminergic projections. This caspase-3 activation concurs with a rapid loss of dendritic spines and deficits in synaptic long-term depression (LTD) in striatal projection neurons forming the indirect pathway. Interestingly, systemic treatment with a caspase inhibitor prevents both the spine pruning and the deficit of indirect pathway LTD without interfering with the ongoing dopaminergic degeneration. Taken together, our data identify transient and non-apoptotic caspase activation as a critical event in the early plastic changes of indirect pathway neurons following dopamine denervation.
MeSH term(s)	Caspase 3/metabolism ; Corpus Striatum/metabolism ; Dopamine/metabolism ; Neostriatum/metabolism ; Neurons/metabolism
Chemical Substances	Caspase 3 (EC 3.4.22.-) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2022-05-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23105470
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Article ; Online: Dopamine Agonist Cotreatment Alters Neuroplasticity and Pharmacology of Levodopa-Induced Dyskinesia.

Espa, Elena / Song, Lu / Skovgård, Katrine / Fanni, Silvia / Cenci, M Angela

Movement disorders : official journal of the Movement Disorder Society

2023 Volume 38, Issue 3, Page(s) 410–422

Abstract: Background: Current models of levodopa (L-dopa)-induced dyskinesia (LID) are obtained by treating dopamine-depleted animals with L-dopa. However, patients with LID receive combination therapies that often include dopamine agonists.: Objective: Using ... ...

Abstract	Background: Current models of levodopa (L-dopa)-induced dyskinesia (LID) are obtained by treating dopamine-depleted animals with L-dopa. However, patients with LID receive combination therapies that often include dopamine agonists. Objective: Using 6-hydroxydopamine-lesioned rats as a model, we aimed to establish whether an adjunct treatment with the D2/3 agonist ropinirole impacts on patterns of LID-related neuroplasticity and drug responses. Methods: Different regimens of L-dopa monotreatment and L-dopa-ropinirole cotreatment were compared using measures of hypokinesia and dyskinesia. Striatal expression of ∆FosB and angiogenesis markers were studied immunohistochemically. Antidyskinetic effects of different drug categories were investigated in parallel groups of rats receiving either L-dopa monotreatment or L-dopa combined with ropinirole. Results: We defined chronic regimens of L-dopa monotreatment and L-dopa-ropinirole cotreatment inducing overall similar abnormal involuntary movement scores. Compared with the monotreatment group, animals receiving the L-dopa-ropinirole combination exhibited an overall lower striatal expression of ∆FosB with a distinctive compartmental distribution. The expression of angiogenesis markers and blood-brain barrier hyperpermeability was markedly reduced after L-dopa-ropinirole cotreatment compared with L-dopa monotreatment. Moreover, significant group differences were detected upon examining the response to candidate antidyskinetic drugs. In particular, compounds modulating D1 receptor signaling had a stronger effect in the L-dopa-only group, whereas both amantadine and the selective NMDA antagonist MK801 produced a markedly larger antidyskinetic effect in L-dopa-ropinirole cotreated animals. Conclusions: Cotreatment with ropinirole altered LID-related neuroplasticity and pharmacological response profiles. The impact of adjuvant dopamine agonist treatment should be taken into consideration when investigating LID mechanisms and candidate interventions in both clinical and experimental settings. © 2023 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
MeSH term(s)	Rats ; Animals ; Levodopa/therapeutic use ; Dopamine Agonists/pharmacology ; Dopamine Agonists/therapeutic use ; Antiparkinson Agents/therapeutic use ; Rats, Sprague-Dawley ; Dyskinesia, Drug-Induced/drug therapy ; Oxidopamine ; Disease Models, Animal
Chemical Substances	Levodopa (46627O600J) ; Dopamine Agonists ; Antiparkinson Agents ; Oxidopamine (8HW4YBZ748)
Language	English
Publishing date	2023-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	607633-6
ISSN	1531-8257 ; 0885-3185
ISSN (online)	1531-8257
ISSN	0885-3185
DOI	10.1002/mds.29301
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Article ; Online: Translating scientific advances into disease-modifying therapies for Parkinson's Disease.

Cenci, M Angela / Olanow, C Warren

Experimental neurology

2017 Volume 298, Issue Pt B, Page(s) 135–136

Language	English
Publishing date	2017-12
Publishing country	United States
Document type	Editorial
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2017.10.011
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Article ; Online: Glutamatergic pathways as a target for the treatment of dyskinesias in Parkinson's disease.

Cenci, M Angela

Biochemical Society transactions

2014 Volume 42, Issue 2, Page(s) 600–604

Abstract: PD (Parkinson's disease) is characterized by some typical motor features that are caused by striatal dopamine depletion and respond well to dopamine-replacement therapy with L-dopa. Unfortunately, the majority of PD patients treated with L-dopa develop ... ...

Abstract	PD (Parkinson's disease) is characterized by some typical motor features that are caused by striatal dopamine depletion and respond well to dopamine-replacement therapy with L-dopa. Unfortunately, the majority of PD patients treated with L-dopa develop abnormal involuntary movements (dyskinesias) within a few years. The mechanisms underlying the development of LIDs (L-dopa-induced dyskinesias) involve, on one hand, a presynaptic dysregulation of dopamine release and clearance and, on the other hand, an abnormal postsynaptic response to dopamine in the brain. There is a large amount of evidence that these dopamine-dependent mechanisms are modulated by glutamatergic pathways and glutamate receptors. The present article summarizes the pathophysiological role of glutamatergic pathways in LID and reviews pre-clinical and clinical results obtained using pharmacological modulators of different classes and subtypes of glutamate receptors to treat parkinsonian dyskinesias.
MeSH term(s)	Animals ; Dyskinesias/metabolism ; Dystonia/metabolism ; Humans ; Levodopa/therapeutic use ; Neurodegenerative Diseases/metabolism ; Parkinson Disease/metabolism
Chemical Substances	Levodopa (46627O600J)
Language	English
Publishing date	2014-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	184237-7
ISSN	1470-8752 ; 0300-5127
ISSN (online)	1470-8752
ISSN	0300-5127
DOI	10.1042/BST20140006
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