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  1. AU="Beaumont, Vahri"
  2. AU="Sorrentino, Gregorio"
  3. AU="Matulionyte, Raimonda"
  4. AU="Afshar, Sabereh"
  5. AU=Armstrong James PK AU=Armstrong James PK
  6. AU="Leshem, Shahaf"
  7. AU="García-García, Ana"
  8. AU="Terrón, Alberto"
  9. AU=Hanel Martin
  10. AU="Saro-Buendía, Miguel"
  11. AU="John R. Kouvaris"
  12. AU="Tripathy, Ashutosh"
  13. AU="Sharpley, Ann L"
  14. AU="Kragt, Lea"
  15. AU="Cui, Yanyan"
  16. AU="Morton, Jennifer P"

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  1. Artikel ; Online: Cholinergic deficits selectively boost cortical intratelencephalic control of striatum in male Huntington's disease model mice.

    Pancani, Tristano / Day, Michelle / Tkatch, Tatiana / Wokosin, David L / González-Rodríguez, Patricia / Kondapalli, Jyothisri / Xie, Zhong / Chen, Yu / Beaumont, Vahri / Surmeier, D James

    Nature communications

    2023  Band 14, Heft 1, Seite(n) 1398

    Abstract: Huntington's disease (HD) is a progressive, neurodegenerative disease caused by a CAG triplet expansion in huntingtin. Although corticostriatal dysfunction has long been implicated in HD, the determinants and pathway specificity of this pathophysiology ... ...

    Abstract Huntington's disease (HD) is a progressive, neurodegenerative disease caused by a CAG triplet expansion in huntingtin. Although corticostriatal dysfunction has long been implicated in HD, the determinants and pathway specificity of this pathophysiology are not fully understood. Here, using a male zQ175
    Mesh-Begriff(e) Mice ; Male ; Animals ; Huntington Disease/metabolism ; Neurodegenerative Diseases/metabolism ; Corpus Striatum/metabolism ; Neostriatum/metabolism ; Cholinergic Agents/metabolism ; Disease Models, Animal ; Mice, Transgenic ; Huntingtin Protein/genetics ; Huntingtin Protein/metabolism
    Chemische Substanzen Cholinergic Agents ; Huntingtin Protein
    Sprache Englisch
    Erscheinungsdatum 2023-03-14
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-36556-3
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Enhanced striatopallidal gamma-aminobutyric acid (GABA)

    Perez-Rosello, Tamara / Gelman, Simon / Tombaugh, Geoffrey / Cachope, Roger / Beaumont, Vahri / Surmeier, D James

    Movement disorders : official journal of the Movement Disorder Society

    2019  Band 34, Heft 5, Seite(n) 684–696

    Abstract: Background: Huntington's disease (HD) is caused by a CAG repeat expansion in the huntingtin gene. This mutation leads to progressive dysfunction that is largely attributable to dysfunction of the striatum. The earliest signs of striatal pathology in HD ... ...

    Abstract Background: Huntington's disease (HD) is caused by a CAG repeat expansion in the huntingtin gene. This mutation leads to progressive dysfunction that is largely attributable to dysfunction of the striatum. The earliest signs of striatal pathology in HD are found in indirect pathway gamma-Aminobutyric acid (GABA)-ergic spiny projection neurons that innervate the external segment of the globus pallidus (GPe). What is less clear is whether the synaptic coupling of spiny projection neurons with GPe neurons changes in HD.
    Objectives: The principal goal of this study was to determine whether striatopallidal synaptic transmission was altered in 2 mouse models of HD.
    Methods: Striatopallidal synaptic transmission was studied using electrophysiological and optogenetic approaches in ex vivo brain slices from 2 HD models: Q175 heterozygous (het) and R6/2 mice.
    Results: Striatopallidal synaptic transmission increased in strength with the progression of behavioral deficits in Q175 and R6/2 mice. The alteration in synaptic transmission was evident in both prototypical and arkypallidal GPe neurons. This change did not appear attributable to an increase in the probability of GABA release but, rather, to an enhancement in the postsynaptic response to GABA released at synaptic sites. This alteration significantly increased the ability of striatopallidal axon terminals to pause ongoing GPe activity.
    Conclusions: In 2 mouse models of HD, striatopallidal synaptic transmission increased in parallel with the progression of behavioral deficits. This adaptation could compensate in part for the concomitant deficit in the ability of corticostriatal signals to activate spiny projection neurons and pause GPe activity. © 2019 International Parkinson and Movement Disorder Society.
    Mesh-Begriff(e) Animals ; Corpus Striatum/metabolism ; Disease Models, Animal ; Electric Stimulation ; Electrophysiological Phenomena ; GABAergic Neurons/metabolism ; Gene Knock-In Techniques ; Globus Pallidus/metabolism ; Huntingtin Protein/genetics ; Huntington Disease/genetics ; Huntington Disease/metabolism ; Inhibitory Postsynaptic Potentials/physiology ; Mice ; Neostriatum/metabolism ; Neural Pathways/metabolism ; Neurons/metabolism ; Optogenetics ; Patch-Clamp Techniques ; Synaptic Transmission/physiology ; gamma-Aminobutyric Acid/metabolism
    Chemische Substanzen Htt protein, mouse ; Huntingtin Protein ; gamma-Aminobutyric Acid (56-12-2)
    Sprache Englisch
    Erscheinungsdatum 2019-02-06
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 607633-6
    ISSN 1531-8257 ; 0885-3185
    ISSN (online) 1531-8257
    ISSN 0885-3185
    DOI 10.1002/mds.27622
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: Phosphodiesterase 9A Inhibition Facilitates Corticostriatal Transmission in Wild-Type and Transgenic Rats That Model Huntington's Disease.

    Chakroborty, Shreaya / Manfredsson, Fredric P / Dec, Alexander M / Campbell, Peter W / Stutzmann, Grace E / Beaumont, Vahri / West, Anthony R

    Frontiers in neuroscience

    2020  Band 14, Seite(n) 466

    Abstract: Huntington's disease (HD) results from abnormal expansion in CAG trinucleotide repeats within the HD gene, a mutation which leads to degeneration of striatal medium-sized spiny neurons (MSNs), deficits in corticostriatal transmission, and loss of motor ... ...

    Abstract Huntington's disease (HD) results from abnormal expansion in CAG trinucleotide repeats within the HD gene, a mutation which leads to degeneration of striatal medium-sized spiny neurons (MSNs), deficits in corticostriatal transmission, and loss of motor control. Recent studies also indicate that metabolism of cyclic nucleotides by phosphodiesterases (PDEs) is dysregulated in striatal networks in a manner linked to deficits in corticostriatal transmission. The current study assessed cortically-evoked firing in electrophysiologically-identified MSNs and fast-spiking interneurons (FSIs) in aged (9-11 months old) wild-type (WT) and BACHD transgenic rats (TG5) treated with vehicle or the selective PDE9A inhibitor PF-04447943. WT and TG5 rats were anesthetized with urethane and single-unit activity was isolated during low frequency electrical stimulation of the ipsilateral motor cortex. Compared to WT controls, MSNs recorded in TG5 animals exhibited decreased spike probability during cortical stimulation delivered at low to moderate stimulation intensities. Moreover, large increases in onset latency of cortically-evoked spikes and decreases in spike probability were observed in FSIs recorded in TG5 animals. Acute systemic administration of the PDE9A inhibitor PF-04447943 significantly decreased the onset latency of cortically-evoked spikes in MSNs recorded in WT and TG5 rats. PDE9A inhibition also increased the proportion of MSNs responding to cortical stimulation and reversed deficits in spike probability observed in TG5 rats. As PDE9A is a cGMP specific enzyme, drugs such as PF-04447943 which act to facilitate striatal cGMP signaling and glutamatergic corticostriatal transmission could be useful therapeutic agents for restoring striatal function and alleviating motor and cognitive symptoms associated with HD.
    Sprache Englisch
    Erscheinungsdatum 2020-06-03
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2411902-7
    ISSN 1662-453X ; 1662-4548
    ISSN (online) 1662-453X
    ISSN 1662-4548
    DOI 10.3389/fnins.2020.00466
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  4. Artikel ; Online: HDinHD: A Rich Data Portal for Huntington's Disease Research.

    Aaronson, Jeff / Beaumont, Vahri / Blevins, Richard A / Andreeva, Viktoria / Murasheva, Irina / Shneyderman, Anastasia / Armah, Kabenla / Gill, Rob / Chen, Jian / Rosinski, Jim / Park, Larry C / Coppola, Giovanni / Munoz-Sanjuan, Ignacio / Vogt, Thomas F

    Journal of Huntington's disease

    2021  Band 10, Heft 3, Seite(n) 405–412

    Abstract: HDinHD (Huntington's Disease in High Definition; HDinHD.org) is an open online portal for the HD research community that presents a synthesized view of HD-related scientific data. Here, we present a broad overview of HDinHD and highlight the newly ... ...

    Abstract HDinHD (Huntington's Disease in High Definition; HDinHD.org) is an open online portal for the HD research community that presents a synthesized view of HD-related scientific data. Here, we present a broad overview of HDinHD and highlight the newly launched HDinHD Explorer tool that enables researchers to discover and explore a wide range of diverse yet interconnected HD-related data. We demonstrate the utility of HDinHD Explorer through data mining of a single collection of newly released in vivo therapeutic intervention study reports alongside previously published reports.
    Mesh-Begriff(e) Humans ; Huntington Disease/genetics
    Sprache Englisch
    Erscheinungsdatum 2021-08-15
    Erscheinungsland Netherlands
    Dokumenttyp Letter ; Research Support, Non-U.S. Gov't
    ZDB-ID 2673033-9
    ISSN 1879-6400 ; 1879-6397
    ISSN (online) 1879-6400
    ISSN 1879-6397
    DOI 10.3233/JHD-210491
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  5. Artikel ; Online: Unravelling and Exploiting Astrocyte Dysfunction in Huntington's Disease.

    Khakh, Baljit S / Beaumont, Vahri / Cachope, Roger / Munoz-Sanjuan, Ignacio / Goldman, Steven A / Grantyn, Rosemarie

    Trends in neurosciences

    2017  Band 40, Heft 7, Seite(n) 422–437

    Abstract: Astrocytes are abundant within mature neural circuits and are involved in brain disorders. Here, we summarize our current understanding of astrocytes and Huntington's disease (HD), with a focus on correlative and causative dysfunctions of ion homeostasis, ...

    Abstract Astrocytes are abundant within mature neural circuits and are involved in brain disorders. Here, we summarize our current understanding of astrocytes and Huntington's disease (HD), with a focus on correlative and causative dysfunctions of ion homeostasis, calcium signaling, and neurotransmitter clearance, as well as on the use of transplanted astrocytes to produce therapeutic benefit in mouse models of HD. Overall, the data suggest that astrocyte dysfunction is an important contributor to the onset and progression of some HD symptoms in mice. Additional exploration of astrocytes in HD mouse models and humans is needed and may provide new therapeutic opportunities to explore in conjunction with neuronal rescue and repair strategies.
    Mesh-Begriff(e) Animals ; Astrocytes/pathology ; Astrocytes/physiology ; Astrocytes/transplantation ; Humans ; Huntington Disease/pathology ; Huntington Disease/physiopathology ; Huntington Disease/therapy
    Sprache Englisch
    Erscheinungsdatum 2017-05-31
    Erscheinungsland England
    Dokumenttyp Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 282488-7
    ISSN 1878-108X ; 0378-5912 ; 0166-2236
    ISSN (online) 1878-108X
    ISSN 0378-5912 ; 0166-2236
    DOI 10.1016/j.tins.2017.05.002
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  6. Artikel ; Online: Identification of a Potent, Selective, and Brain-Penetrant Rho Kinase Inhibitor and its Activity in a Mouse Model of Huntington's Disease.

    Ladduwahetty, Tammy / Lee, Matthew R / Maillard, Michel C / Cachope, Roger / Todd, Daniel / Barnes, Michael / Beaumont, Vahri / Chauhan, Alka / Gallati, Caroline / Haughan, Alan F / Kempf, Georg / Luckhurst, Christopher A / Matthews, Kim / McAllister, George / Mitchell, Philip / Patel, Hiral / Rose, Mark / Saville-Stones, Elizabeth / Steinbacher, Stefan /
    Stott, Andrew J / Thatcher, Emma / Tierney, Jason / Urbonas, Liudvikas / Munoz-Sanjuan, Ignacio / Dominguez, Celia

    Journal of medicinal chemistry

    2022  Band 65, Heft 14, Seite(n) 9819–9845

    Abstract: The Rho kinase (ROCK) pathway is implicated in the pathogenesis of several conditions, including neurological diseases. In Huntington's disease (HD), ROCK is implicated in mutant huntingtin (HTT) aggregation and neurotoxicity, and members of the ROCK ... ...

    Abstract The Rho kinase (ROCK) pathway is implicated in the pathogenesis of several conditions, including neurological diseases. In Huntington's disease (HD), ROCK is implicated in mutant huntingtin (HTT) aggregation and neurotoxicity, and members of the ROCK pathway are increased in HD mouse models and patients. To validate this mode of action as a potential treatment for HD, we sought a potent, selective, central nervous system (CNS)-penetrant ROCK inhibitor. Identifying a compound that could be dosed orally in mice with selectivity against other AGC kinases, including protein kinase G (PKG), whose inhibition could potentially activate the ROCK pathway, was paramount for the program. We describe the optimization of published ligands to identify a novel series of ROCK inhibitors based on a piperazine core. Morphing of the early series developed in-house by scaffold hopping enabled the identification of a compound exhibiting high potency and desired selectivity and demonstrating a robust pharmacodynamic (PD) effect by the inhibition of ROCK-mediated substrate (MYPT1) phosphorylation after oral dosing.
    Mesh-Begriff(e) Animals ; Brain/metabolism ; Disease Models, Animal ; Huntingtin Protein/metabolism ; Huntington Disease/drug therapy ; Mice ; Protein Kinase Inhibitors/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; rho-Associated Kinases
    Chemische Substanzen Huntingtin Protein ; Protein Kinase Inhibitors ; rho-Associated Kinases (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2022-07-11
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 218133-2
    ISSN 1520-4804 ; 0022-2623
    ISSN (online) 1520-4804
    ISSN 0022-2623
    DOI 10.1021/acs.jmedchem.2c00474
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  7. Artikel ; Online: Developing HDAC4-Selective Protein Degraders To Investigate the Role of HDAC4 in Huntington's Disease Pathology.

    Macabuag, Natsuko / Esmieu, William / Breccia, Perla / Jarvis, Rebecca / Blackaby, Wesley / Lazari, Ovadia / Urbonas, Liudvikas / Eznarriaga, Maria / Williams, Rachel / Strijbosch, Annelieke / Van de Bospoort, Rhea / Matthews, Kim / Clissold, Cole / Ladduwahetty, Tammy / Vater, Huw / Heaphy, Patrick / Stafford, Douglas G / Wang, Hong-Jun / Mangette, John E /
    McAllister, George / Beaumont, Vahri / Vogt, Thomas F / Wilkinson, Hilary A / Doherty, Elizabeth M / Dominguez, Celia

    Journal of medicinal chemistry

    2022  Band 65, Heft 18, Seite(n) 12445–12459

    Abstract: Huntington's disease (HD) is a lethal autosomal dominant neurodegenerative disorder resulting from a CAG repeat expansion in the huntingtin ( ...

    Abstract Huntington's disease (HD) is a lethal autosomal dominant neurodegenerative disorder resulting from a CAG repeat expansion in the huntingtin (
    Mesh-Begriff(e) Animals ; Disease Models, Animal ; Drug Development ; Histone Deacetylases/metabolism ; Huntingtin Protein/genetics ; Huntingtin Protein/metabolism ; Huntington Disease/genetics ; Mice ; Neurons/metabolism ; Proteolysis ; Ubiquitins
    Chemische Substanzen Huntingtin Protein ; Ubiquitins ; Hdac5 protein, mouse (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98)
    Sprache Englisch
    Erscheinungsdatum 2022-09-13
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 218133-2
    ISSN 1520-4804 ; 0022-2623
    ISSN (online) 1520-4804
    ISSN 0022-2623
    DOI 10.1021/acs.jmedchem.2c01149
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  8. Artikel ; Online: In vitro phosphodiesterase 10A (PDE10A) binding in whole hemisphere human brain using the PET radioligand [

    Svedberg, Marie M / Varnäs, Katarina / Varrone, Andrea / Mitsios, Nicholas / Mulder, Jan / Gulyás, Balázs / Beaumont, Vahri / Munoz-Sanjuan, Ignacio / Zaleska, Margaret M / Schmidt, Christopher J / Halldin, Christer / Mrzljak, Ladislav

    Brain research

    2019  Band 1711, Seite(n) 140–145

    Abstract: Highly specific and sensitive biomarkers for pathologies related to dysfunctions in the basal ganglia circuit are of great value to assess therapeutic efficacy not only clinically to establish an early diagnosis, but also in terms of monitoring the ... ...

    Abstract Highly specific and sensitive biomarkers for pathologies related to dysfunctions in the basal ganglia circuit are of great value to assess therapeutic efficacy not only clinically to establish an early diagnosis, but also in terms of monitoring the efficacy of therapeutic interventions and decelerated neurodegeneration. The phosphodiesterase 10A (PDE10A) enzyme plays a central role in striatal signaling and is implicated in several neuropsychiatric disorders involving striatal pathology, such as Huntingtońs disease (HD) and schizophrenia. Inhibition of PDE10A activates the neurons in the striatum and consequently leads to alteration of behavioral aspects modulated by the striatal circuit. [
    Mesh-Begriff(e) Adult ; Aged ; Basal Ganglia/enzymology ; Basal Ganglia/metabolism ; Brain/diagnostic imaging ; Brain/enzymology ; Cadaver ; Corpus Striatum/enzymology ; Corpus Striatum/metabolism ; Female ; Fluorine Radioisotopes ; Humans ; Male ; Middle Aged ; Neostriatum/enzymology ; Neostriatum/metabolism ; Phosphoric Diester Hydrolases/metabolism ; Phthalimides ; Positron-Emission Tomography/methods ; Quinazolinones ; Radiopharmaceuticals
    Chemische Substanzen 2-(2-(3-(4-(2-fluoroethoxy)phenyl)-7-methyl-4-oxo-3,4-dihydroquinazolin-2-yl)ethyl)-4-isopropoxyisoindoline-1,3-dione ; Fluorine Radioisotopes ; Phthalimides ; Quinazolinones ; Radiopharmaceuticals ; PDE10A protein, human (EC 3.1.4.-) ; Phosphoric Diester Hydrolases (EC 3.1.4.-)
    Sprache Englisch
    Erscheinungsdatum 2019-01-18
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1200-2
    ISSN 1872-6240 ; 0006-8993
    ISSN (online) 1872-6240
    ISSN 0006-8993
    DOI 10.1016/j.brainres.2019.01.021
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  9. Artikel: Evaluation of 5-(Trifluoromethyl)-1,2,4-oxadiazole-Based Class IIa HDAC Inhibitors for Huntington's Disease.

    Stott, Andrew J / Maillard, Michel C / Beaumont, Vahri / Allcock, David / Aziz, Omar / Borchers, Alexander H / Blackaby, Wesley / Breccia, Perla / Creighton-Gutteridge, Gillian / Haughan, Alan F / Jarvis, Rebecca E / Luckhurst, Christopher A / Matthews, Kim L / McAllister, George / Pollack, Scott / Saville-Stones, Elizabeth / Van de Poël, Amanda J / Vater, Huw D / Vann, Julie /
    Williams, Rachel / Yates, Dawn / Muñoz-Sanjuán, Ignacio / Dominguez, Celia

    ACS medicinal chemistry letters

    2021  Band 12, Heft 3, Seite(n) 380–388

    Abstract: Using an iterative structure-activity relationship driven approach, we identified a CNS-penetrant 5-(trifluoromethyl)-1,2,4-oxadiazole (TFMO, ...

    Abstract Using an iterative structure-activity relationship driven approach, we identified a CNS-penetrant 5-(trifluoromethyl)-1,2,4-oxadiazole (TFMO,
    Sprache Englisch
    Erscheinungsdatum 2021-02-11
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 1948-5875
    ISSN 1948-5875
    DOI 10.1021/acsmedchemlett.0c00532
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  10. Artikel ; Online: Age- and sex-related changes in cortical and striatal nitric oxide synthase in the Q175 mouse model of Huntington's disease.

    Padovan-Neto, Fernando E / Jurkowski, Lauren / Murray, Conor / Stutzmann, Grace E / Kwan, Mei / Ghavami, Afshin / Beaumont, Vahri / Park, Larry C / West, Anthony R

    Nitric oxide : biology and chemistry

    2018  Band 83, Seite(n) 40–50

    Abstract: In Huntington's disease (HD), corticostriatal and striatopallidal projection neurons preferentially degenerate as a result of mutant huntingtin expression. Pathological deficits in nitric oxide (NO) signaling have also been reported in corticostriatal ... ...

    Abstract In Huntington's disease (HD), corticostriatal and striatopallidal projection neurons preferentially degenerate as a result of mutant huntingtin expression. Pathological deficits in nitric oxide (NO) signaling have also been reported in corticostriatal circuits in HD, however, the impact of age and sex on nitrergic transmission is not well characterized. Thus, we utilized NADPH-diaphorase (NADPH-d) histochemistry and qPCR assays to assess neuronal NO synthase (nNOS) activity/expression in aged male and female Q175 heterozygous mice. Compared to age-matched controls, male Q175 mice exhibited reductions in NADPH-d staining in the motor cortex at 21, but not, 16 months of age. Comparisons across genotypes showed that striatal NADPH-d staining was significantly decreased at both 16 and 21 months of age. Comparisons within sexes in 21 month old mice revealed a decrease in striatal NADPH-d staining in males, but no changes were detected in females. Significant correlations between cortical and striatal NADPH-d staining deficits were also observed in males and females at both ages. To directly assess the role of constitutively active NOS isoforms in these changes, nNOS and endothelial NOS (eNOS) mRNA expression levels were examined in R6/2 (3 month old) and Q175 (11.5 month old) mice using qPCR assays. nNOS transcript expression was decreased in the cortex (40%) and striatum (54%) in R6/2 mice. nNOS mRNA down-regulation in striatum of Q175 animals was more modest (19%), and no changes were detected in cortex. eNOS expression was not changed in the cortex or striatum of Q175 mice. The current findings point to age-dependent deficits in nNOS activity in the HD cortex and striatum which appear first in the striatum and are more pronounced in males. Together, these observations and previous studies indicate that decreases in nitrergic transmission progress with age and are likely to contribute to corticostriatal circuit pathophysiology particularly in male patients with HD.
    Mesh-Begriff(e) Aging/metabolism ; Animals ; Disease Models, Animal ; Female ; Humans ; Huntington Disease/metabolism ; Male ; Mice ; Mice, Transgenic ; Nitric Oxide Synthase/genetics ; Nitric Oxide Synthase/metabolism ; Sex Characteristics
    Chemische Substanzen Nitric Oxide Synthase (EC 1.14.13.39)
    Sprache Englisch
    Erscheinungsdatum 2018-12-05
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1362794-6
    ISSN 1089-8611 ; 1089-8603
    ISSN (online) 1089-8611
    ISSN 1089-8603
    DOI 10.1016/j.niox.2018.12.002
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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