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  1. Article ; Online: Neuronal Presentation of Antigen and Its Possible Role in Parkinson's Disease.

    Hobson, Benjamin D / Sulzer, David

    Journal of Parkinson's disease

    2022  Volume 12, Issue s1, Page(s) S137–S147

    Abstract: Patients with Parkinson's disease (PD) and other synucleinopathies often exhibit autoimmune features, including CD4+ and some CD8+ T lymphocytes that recognize epitopes derived from alpha-synuclein. While neurons have long been considered to not present ... ...

    Abstract Patients with Parkinson's disease (PD) and other synucleinopathies often exhibit autoimmune features, including CD4+ and some CD8+ T lymphocytes that recognize epitopes derived from alpha-synuclein. While neurons have long been considered to not present antigens, recent data indicate that they can be induced to do so, particularly in response to interferons and other forms of stress. Here, we review literature on neuronal antigen presentation and its potential role in PD. Although direct evidence for CD8+ T cell-mediated neuronal death is lacking in PD, neuronal antigen presentation appears central to the pathology of Rasmussen's encephalitis, a pediatric neurological disorder driven by cytotoxic T cell infiltration and neuroinflammation. Emerging data suggest that T cells enter the brain in PD and other synucleinopathies, where the majority of neuromelanin-containing substantia nigra and locus coeruleus neurons express MHC Class I molecules. In cell culture, CD8+ T cell recognition of antigen:MHC Class I complexes on neuronal membranes leads to cytotoxic responses and neuronal cell death. Recent animal models suggest the possibility of T cell autoreactivity to mitochondrial antigens in PD. It remains unclear if neuronal antigen presentation plays a role in PD or other neurodegenerative disorders, and efforts are underway to better elucidate the potential impact of autoimmune responses on neurodegeneration.
    MeSH term(s) Animals ; Epitopes ; Histocompatibility Antigens Class I ; Interferons ; Neurons/metabolism ; Parkinson Disease/metabolism ; Synucleinopathies ; alpha-Synuclein/metabolism
    Chemical Substances Epitopes ; Histocompatibility Antigens Class I ; alpha-Synuclein ; Interferons (9008-11-1)
    Language English
    Publishing date 2022-03-07
    Publishing country Netherlands
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2620609-2
    ISSN 1877-718X ; 1877-7171
    ISSN (online) 1877-718X
    ISSN 1877-7171
    DOI 10.3233/JPD-223153
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6964: Show issues Location:
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  2. Article ; Online: Tailoring the Gibbs Free Energy of the Nitroxide Exchange Reaction: Substituent and Solvent Effects.

    Sulzer, David / Bihlmeier, Angela

    The journal of physical chemistry. A

    2021  Volume 125, Issue 35, Page(s) 7616–7624

    Abstract: A quantum chemical study of the nitroxide exchange reaction is presented. Inspired by the recent use of this reaction in the synthesis of dynamic covalent polymer networks, we studied the influence of substituents and solvents on the Gibbs free energy, ... ...

    Abstract A quantum chemical study of the nitroxide exchange reaction is presented. Inspired by the recent use of this reaction in the synthesis of dynamic covalent polymer networks, we studied the influence of substituents and solvents on the Gibbs free energy, which plays a crucial role for both the reversibility of the reaction and the extent of product formation. We provide accurate benchmark values based on CCSD(T) and COSMO-RS theory for a series of structural modifications and make suggestions for improving the molecular building blocks used so far.
    Language English
    Publishing date 2021-08-30
    Publishing country United States
    Document type Journal Article
    ISSN 1520-5215
    ISSN (online) 1520-5215
    DOI 10.1021/acs.jpca.1c04864
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  3. Article ; Online: The chemical tools for imaging dopamine release.

    Post, Michael R / Sulzer, David

    Cell chemical biology

    2021  Volume 28, Issue 6, Page(s) 748–764

    Abstract: Dopamine is a modulatory neurotransmitter involved in learning, motor functions, and reward. Many neuropsychiatric disorders, including Parkinson's disease, autism, and schizophrenia, are associated with imbalances or dysfunction in the dopaminergic ... ...

    Abstract Dopamine is a modulatory neurotransmitter involved in learning, motor functions, and reward. Many neuropsychiatric disorders, including Parkinson's disease, autism, and schizophrenia, are associated with imbalances or dysfunction in the dopaminergic system. Yet, our understanding of these pervasive public health issues is limited by our ability to effectively image dopamine in humans, which has long been a goal for chemists and neuroscientists. The last two decades have witnessed the development of many molecules used to trace dopamine. We review the small molecules, nanoparticles, and protein sensors used with fluorescent microscopy/photometry, MRI, and PET that shape dopamine research today. None of these tools observe dopamine itself, but instead harness the biology of the dopamine system-its synthetic and metabolic pathways, synaptic vesicle cycle, and receptors-in elegant ways. Their advantages and weaknesses are covered here, along with recent examples and the chemistry and biology that allow them to function.
    MeSH term(s) Dopamine/analysis ; Dopamine/metabolism ; Humans ; Parkinson Disease/diagnosis ; Parkinson Disease/metabolism
    Chemical Substances Dopamine (VTD58H1Z2X)
    Language English
    Publishing date 2021-04-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ISSN 2451-9448
    ISSN (online) 2451-9448
    DOI 10.1016/j.chembiol.2021.04.005
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  4. Article: 5-HT1B receptors mediate dopaminergic inhibition of vesicular fusion and GABA release from striatonigral synapses.

    Molinari, Maya / Lieberman, Ori J / Sulzer, David / Santini, Emanuela / Borgkvist, Anders

    bioRxiv : the preprint server for biology

    2024  

    Abstract: The substantia nigra pars reticulata (SNr), a crucial basal ganglia output nucleus, contains a dense expression of dopamine D1 receptors (D1Rs), along with dendrites belonging to dopaminergic neurons of substantia nigra pars compacta. These D1Rs are ... ...

    Abstract The substantia nigra pars reticulata (SNr), a crucial basal ganglia output nucleus, contains a dense expression of dopamine D1 receptors (D1Rs), along with dendrites belonging to dopaminergic neurons of substantia nigra pars compacta. These D1Rs are primarily located on the terminals of striatonigral medium spiny neurons, suggesting their involvement in the regulation of neurotransmitter release from the direct pathway in response to somatodendritic dopamine release. To explore the hypothesis that D1Rs modulate GABA release from striatonigral synapses, we conducted optical recordings of striatonigral activity and postsynaptic patch-clamp recordings from SNr neurons in the presence of dopamine and D1R agonists. We found that dopamine inhibits optogenetically triggered striatonigral GABA release by modulating vesicle fusion and Ca
    Language English
    Publishing date 2024-03-14
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.03.14.584991
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  5. Article ; Online: Developmental regulation of thalamus-driven pauses in striatal cholinergic interneurons.

    McGuirt, Avery / Pigulevskiy, Irena / Sulzer, David

    iScience

    2022  Volume 25, Issue 11, Page(s) 105332

    Abstract: In response to salient sensory cues, the tonically active striatal cholinergic interneuron (ChI) exhibits a characteristic synchronized "pause" thought to facilitate learning and the execution of motivated behavior. We report that thalamostriatal-driven ... ...

    Abstract In response to salient sensory cues, the tonically active striatal cholinergic interneuron (ChI) exhibits a characteristic synchronized "pause" thought to facilitate learning and the execution of motivated behavior. We report that thalamostriatal-driven ChI pauses are enhanced in
    Language English
    Publishing date 2022-10-13
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2022.105332
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  6. Article: Similarities and differences between nigral and enteric dopaminergic neurons unravel distinctive involvement in Parkinson's disease.

    Chalazonitis, Alcmène / Rao, Meenakshi / Sulzer, David

    NPJ Parkinson's disease

    2022  Volume 8, Issue 1, Page(s) 50

    Abstract: In addition to the well-known degeneration of midbrain dopaminergic neurons, enteric neurons can also be affected in neurodegenerative disorders such as Parkinson's disease (PD). Dopaminergic neurons have recently been identified in the enteric nervous ... ...

    Abstract In addition to the well-known degeneration of midbrain dopaminergic neurons, enteric neurons can also be affected in neurodegenerative disorders such as Parkinson's disease (PD). Dopaminergic neurons have recently been identified in the enteric nervous system (ENS). While ENS dopaminergic neurons have been shown to degenerate in genetic mouse models of PD, analyses of their survival in enteric biopsies of PD patients have provided inconsistent results to date. In this context, this review seeks to highlight the distinctive and shared factors and properties that control the evolution of these two sets of dopaminergic neurons from neuronal precursors to aging neurons. Although their cellular sources and developmental times of origin differ, midbrain and ENS dopaminergic neurons express many transcription factors in common and their respective environments express similar neurotrophic molecules. For example, Foxa2 and Sox6 are expressed by both populations to promote the specification, differentiation, and long-term maintenance of the dopaminergic phenotype. Both populations exhibit sustained patterns of excitability that drive intrinsic vulnerability over time. In disorders such as PD, colon biopsies have revealed aggregation of alpha-synuclein in the submucosal plexus where dopaminergic neurons reside and lack blood barrier protection. Thus, these enteric neurons may be more susceptible to neurotoxic insults and aggregation of α-synuclein that spreads from gut to midbrain. Under sustained stress, inefficient autophagy leads to neurodegeneration, GI motility dysfunction, and PD symptoms. Recent findings suggest that novel neurotrophic factors such as CDNF have the potential to be used as neuroprotective agents to prevent and treat ENS symptoms of PD.
    Language English
    Publishing date 2022-04-22
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2819218-7
    ISSN 2373-8057
    ISSN 2373-8057
    DOI 10.1038/s41531-022-00308-9
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  7. Article ; Online: Norepinephrine release in the cerebellum contributes to aversive learning.

    Stanley, Adrien T / Post, Michael R / Lacefield, Clay / Sulzer, David / Miniaci, Maria Concetta

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 4852

    Abstract: The modulation of dopamine release from midbrain projections to the striatum has long been demonstrated in reward-based learning, but the synaptic basis of aversive learning is far less characterized. The cerebellum receives axonal projections from the ... ...

    Abstract The modulation of dopamine release from midbrain projections to the striatum has long been demonstrated in reward-based learning, but the synaptic basis of aversive learning is far less characterized. The cerebellum receives axonal projections from the locus coeruleus, and norepinephrine release is implicated in states of arousal and stress, but whether aversive learning relies on plastic changes in norepinephrine release in the cerebellum is unknown. Here we report that in mice, norepinephrine is released in the cerebellum following an unpredicted noxious event (a foot-shock) and that this norepinephrine release is potentiated powerfully with fear acquisition as animals learn that a previously neutral stimulus (tone) predicts the aversive event. Importantly, both chemogenetic and optogenetic inhibition of the locus coeruleus-cerebellum pathway block fear memory without impairing motor function. Thus, norepinephrine release in the cerebellum is modulated by experience and underlies aversive learning.
    MeSH term(s) Mice ; Animals ; Avoidance Learning/physiology ; Norepinephrine/metabolism ; Locus Coeruleus/physiology ; Cerebellum/metabolism ; Mesencephalon/metabolism
    Chemical Substances Norepinephrine (X4W3ENH1CV)
    Language English
    Publishing date 2023-08-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-40548-8
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  8. Article: T cells, α-synuclein and Parkinson disease.

    Garretti, Francesca / Monahan, Connor / Sette, Alessandro / Agalliu, Dritan / Sulzer, David

    Handbook of clinical neurology

    2022  Volume 184, Page(s) 439–455

    Abstract: The notion that autoimmune responses to α-synuclein may be involved in the pathogenesis of this disorder stems from reports that mutations in α-synuclein or certain alleles of the major histocompatibility complex (MHC) are associated with the disease and ...

    Abstract The notion that autoimmune responses to α-synuclein may be involved in the pathogenesis of this disorder stems from reports that mutations in α-synuclein or certain alleles of the major histocompatibility complex (MHC) are associated with the disease and that dopaminergic and norepinephrinergic neurons in the midbrain can present antigenic epitopes. Here, we discuss recent evidence that a defined set of peptides derived from α-synuclein act as antigenic epitopes displayed by specific MHC alleles and drive helper and cytotoxic T cell responses in patients with PD. Moreover, phosphorylated α-synuclein may activate T cell responses in a less restricted manner in PD. While the roles for the acquired immune system in disease pathogenesis remain unknown, preclinical animal models and in vitro studies indicate that T cells may interact with neurons and exert effects related to neuronal death and neuroprotection. These findings suggest that therapeutics that target T cells and ameliorate the incidence or disease severity of inflammatory bowel disorders or CNS autoimmune diseases such as multiple sclerosis may be useful in PD.
    MeSH term(s) Animals ; Dopamine ; Humans ; Neurons ; Parkinson Disease/genetics ; T-Lymphocytes ; alpha-Synuclein
    Chemical Substances alpha-Synuclein ; Dopamine (VTD58H1Z2X)
    Language English
    Publishing date 2022-01-14
    Publishing country Netherlands
    Document type Journal Article ; Review
    ISSN 0072-9752
    ISSN 0072-9752
    DOI 10.1016/B978-0-12-819410-2.00023-0
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  9. Article ; Online: The Synaptic Autophagy Cycle.

    Lieberman, Ori J / Sulzer, David

    Journal of molecular biology

    2019  Volume 432, Issue 8, Page(s) 2589–2604

    Abstract: Macroautophagy (hereafter referred to as autophagy) is an evolutionarily conserved pathway in which proteins and organelles are delivered to the lysosome for degradation. In neurons, autophagy was originally described as associated with disease states ... ...

    Abstract Macroautophagy (hereafter referred to as autophagy) is an evolutionarily conserved pathway in which proteins and organelles are delivered to the lysosome for degradation. In neurons, autophagy was originally described as associated with disease states and neuronal survival. Over the last decade, however, evidence has accumulated that autophagy controls synaptic function in both the axon and dendrite. Here, we review this literature, highlighting the role of autophagy in the pre- and postsynapse, synaptic plasticity, and behavior. We end by discussing open questions in the field of synaptic autophagy.
    MeSH term(s) Animals ; Autophagy ; Cell Survival ; Humans ; Neurodegenerative Diseases/pathology ; Neuronal Plasticity ; Neurons/pathology
    Language English
    Publishing date 2019-12-20
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80229-3
    ISSN 1089-8638 ; 0022-2836
    ISSN (online) 1089-8638
    ISSN 0022-2836
    DOI 10.1016/j.jmb.2019.12.028
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 867: Show issues Location:
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  10. Article ; Online: Misfolded GBA/β-glucocerebrosidase impairs ER-quality control by chaperone-mediated autophagy in Parkinson disease.

    Kuo, Sheng-Han / Tasset, Inmaculada / Cuervo, Ana Maria / Sulzer, David

    Autophagy

    2022  Volume 18, Issue 12, Page(s) 3050–3052

    Abstract: Inhibition of chaperone-mediated autophagy (CMA), a selective type of lysosomal degradation for intracellular proteins, may contribute to pathogenesis in neurodegenerative diseases including Parkinson disease (PD). Pathogenic variants of PD-related ... ...

    Abstract Inhibition of chaperone-mediated autophagy (CMA), a selective type of lysosomal degradation for intracellular proteins, may contribute to pathogenesis in neurodegenerative diseases including Parkinson disease (PD). Pathogenic variants of PD-related proteins that reside in the cytosol, including SNCA/alpha-synuclein, LRRK2 (leucine rich repeat kinase 2), UCHL1 (ubiquitin Cterminal hydrolase 1) and VPS35 (VPS35 retromer complex component), exert inhibitory effects on CMA. Decreased CMA activity has also been reported in sporadic PD patients, consistent with an association between CMA inhibition and PD. We have now reported the first example of CMA dysfunction caused by a non-cytosolic PD-related protein, GBA/β-glucocerebrosidase, the most common genetic risk factor for PD, which uncovers a new role for CMA in endoplasmic reticulum (ER) quality control.
    MeSH term(s) Humans ; alpha-Synuclein/metabolism ; Chaperone-Mediated Autophagy ; Endoplasmic Reticulum/metabolism ; Glucosylceramidase/genetics ; Glucosylceramidase/metabolism ; Lysosomes/metabolism ; Mutation ; Parkinson Disease/metabolism ; Quality Control ; Protein Folding
    Chemical Substances alpha-Synuclein ; Glucosylceramidase (EC 3.2.1.45) ; GBA protein, human (EC 3.2.1.45)
    Language English
    Publishing date 2022-05-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2022.2071383
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    Zs.A 6741: Show issues Location:
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