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Mutant huntingtin reduction in astrocytes slows disease progression in the bachd conditional huntington’s disease mouse model

https://doi.org/10.1093/hmg/ddy363
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What this work says

Outgoing claims: the papers this work cites, builds on, or argues with.

inferredcites →https://doi.org/10.1001/archneur.58.3.365openalex-snapshot
Glutamate Transporters in Neurologic Disease
inferredcites →https://doi.org/10.1002/ana.410270217openalex-snapshot
Degeneration of pyramidal projection neurons in Huntington's disease cortex
inferredcites →https://doi.org/10.1002/dvg.20287openalex-snapshot
Characterization of astrocyte‐specific conditional knockouts
inferredcites →https://doi.org/10.1006/nbdi.2001.0430openalex-snapshot
Impaired Glutamate Uptake in the R6 Huntington's Disease Transgenic Mice
inferredcites →https://doi.org/10.1007/978-1-4615-4685-6_6openalex-snapshot
Astrocytes as Active Participants of Glutamatergic Function and Regulators of its Homeostasis
inferredcites →https://doi.org/10.1007/bf00294227openalex-snapshot
Synaptophysin expression in the striatum in Huntington's disease
inferredcites →https://doi.org/10.1007/s11064-007-9463-1openalex-snapshot
Glutamate Uptake is Reduced in Prefrontal Cortex in Huntington’s Disease
inferredcites →https://doi.org/10.1007/s13311-019-00782-9openalex-snapshot
Cell-Autonomous and Non-cell-Autonomous Pathogenic Mechanisms in Huntington's Disease: Insights from In Vitro and In Vivo Models
inferredcites →https://doi.org/10.1016/0092-8674(93)90585-eopenalex-snapshot
A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes
inferredcites →https://doi.org/10.1016/0304-3940(86)90397-6openalex-snapshot
Reduced high-affinity glutamate uptake sites in the brains of patients with Huntington's disease
inferredcites →https://doi.org/10.1016/0896-6273(95)90345-3openalex-snapshot
Widespread expression of Huntington's disease gene (IT15) protein product
inferredcites →https://doi.org/10.1016/j.biopsych.2006.11.034openalex-snapshot
Psychiatric Symptoms in Huntington’s Disease before Diagnosis: The Predict-HD Study
inferredcites →https://doi.org/10.1016/j.mcn.2005.12.006openalex-snapshot
GFAP-positive progenitor cells produce neurons and oligodendrocytes throughout the CNS
inferredcites →https://doi.org/10.1016/j.molmed.2006.12.005openalex-snapshot
The tripartite synapse: roles for gliotransmission in health and disease
inferredcites →https://doi.org/10.1016/j.nbd.2009.05.007openalex-snapshot
Systematic behavioral evaluation of Huntington's disease transgenic and knock-in mouse models
inferredcites →https://doi.org/10.1016/j.nbd.2010.05.027openalex-snapshot
Palmitoylation and function of glial glutamate transporter-1 is reduced in the YAC128 mouse model of Huntington disease
inferredcites →https://doi.org/10.1016/j.nbd.2013.06.002openalex-snapshot
Enhanced Ca2+-dependent glutamate release from astrocytes of the BACHD Huntington's disease mouse model
inferredcites →https://doi.org/10.1016/j.nbd.2019.104635openalex-snapshot
Pathogenesis of SCA3 and implications for other polyglutamine diseases
inferredcites →https://doi.org/10.1016/j.neuron.2005.03.025openalex-snapshot
Pathological Cell-Cell Interactions Elicited by a Neuropathogenic Form of Mutant Huntingtin Contribute to Cortical Pathogenesis in HD Mice
inferredcites →https://doi.org/10.1016/j.neuron.2012.05.009openalex-snapshot
Sustained Therapeutic Reversal of Huntington's Disease by Transient Repression of Huntingtin Synthesis
inferredcites →https://doi.org/10.1016/j.neuron.2017.06.029openalex-snapshot
Neural Circuit-Specialized Astrocytes: Transcriptomic, Proteomic, Morphological, and Functional Evidence
inferredcites →https://doi.org/10.1016/j.neuroscience.2011.08.052openalex-snapshot
Pathophysiology of Huntington's disease: time-dependent alterations in synaptic and receptor function
inferredcites →https://doi.org/10.1016/s0014-4835(02)00278-6openalex-snapshot
Alpha-crystallin
inferredcites →https://doi.org/10.1016/s0166-2236(03)00141-3openalex-snapshot
Astrocyte-mediated control of cerebral microcirculation
inferredcites →https://doi.org/10.1016/s0959-4388(99)80043-9openalex-snapshot
Clearance of glutamate inside the synapse and beyond
inferredcites →https://doi.org/10.1037/a0020937openalex-snapshot
Neurocognitive signs in prodromal Huntington disease.
inferredcites →https://doi.org/10.1038/369744a0openalex-snapshot
Glutamate-mediated astrocyte–neuron signalling
inferredcites →https://doi.org/10.1038/ncomms11758openalex-snapshot
Human glia can both induce and rescue aspects of disease phenotype in Huntington disease
inferredcites →https://doi.org/10.1038/nm.3162openalex-snapshot
Astrocyte-derived ATP modulates depressive-like behaviors
inferredcites →https://doi.org/10.1038/nm.3514openalex-snapshot
Neuronal targets for reducing mutant huntingtin expression to ameliorate disease in a mouse model of Huntington's disease
inferredcites →https://doi.org/10.1038/nn.2467openalex-snapshot
A robust and high-throughput Cre reporting and characterization system for the whole mouse brain
inferredcites →https://doi.org/10.1038/nn.3691openalex-snapshot
Astrocyte Kir4.1 ion channel deficits contribute to neuronal dysfunction in Huntington's disease model mice
inferredcites →https://doi.org/10.1038/nn2047openalex-snapshot
Astrocytes as determinants of disease progression in inherited amyotrophic lateral sclerosis
inferredcites →https://doi.org/10.1038/npp.2010.74openalex-snapshot
Blockade of Astrocytic Glutamate Uptake in Rats Induces Signs of Anhedonia and Impaired Spatial Memory
inferredcites →https://doi.org/10.1038/npp.2012.105openalex-snapshot
Blockade of Astrocytic Glutamate Uptake in the Prefrontal Cortex Induces Anhedonia
inferredcites →https://doi.org/10.1073/pnas.0708285104openalex-snapshot
Therapeutic silencing of mutant huntingtin with siRNA attenuates striatal and cortical neuropathology and behavioral deficits
inferredcites →https://doi.org/10.1073/pnas.0911503106openalex-snapshot
Expression of mutant huntingtin in mouse brain astrocytes causes age-dependent neurological symptoms
inferredcites →https://doi.org/10.1073/pnas.1520639112openalex-snapshot
Translational profiling identifies a cascade of damage initiated in motor neurons and spreading to glia in mutant SOD1-mediated ALS
inferredcites →https://doi.org/10.1073/pnas.97.9.4926openalex-snapshot
d -Serine is an endogenous ligand for the glycine site of the N -methyl- d -aspartate receptor
inferredcites →https://doi.org/10.1083/jcb.200508072openalex-snapshot
Expression of mutant huntingtin in glial cells contributes to neuronal excitotoxicity
inferredcites →https://doi.org/10.1093/brain/awf180openalex-snapshot
Impaired glutamate transport and glutamate-glutamine cycling: downstream effects of the Huntington mutation
inferredcites →https://doi.org/10.1093/hmg/ddq212openalex-snapshot
In vivo expression of polyglutamine-expanded huntingtin by mouse striatal astrocytes impairs glutamate transport: a correlation with Huntington's disease subjects
inferredcites →https://doi.org/10.1093/hmg/ddw028openalex-snapshot
αB-Crystallin overexpression in astrocytes modulates the phenotype of the BACHD mouse model of Huntington's disease
inferredcites →https://doi.org/10.1097/00005072-198511000-00003openalex-snapshot
Neuropathological Classification of Huntingtonʼs Disease
inferredcites →https://doi.org/10.1097/00005072-199704000-00013openalex-snapshot
Changes of NMDA Receptor Subunit (NR1, NR2B) and Glutamate Transporter (GLT1) mRNA Expression in Huntingtonʼs Disease—An In Situ Hybridization Study
inferredcites →https://doi.org/10.1097/00005072-199805000-00001openalex-snapshot
Huntington Disease
inferredcites →https://doi.org/10.1111/j.1460-9568.2005.04396.xopenalex-snapshot
The fate of neural progenitor cells expressing astrocytic and radial glial markers in the postnatal rat dentate gyrus
inferredcites →https://doi.org/10.1139/cjpp-77-9-699openalex-snapshot
Astrocyte-induced modulation of synaptic transmission
inferredcites →https://doi.org/10.1152/physrev.00049.2005openalex-snapshot
Astrocyte Control of Synaptic Transmission and Neurovascular Coupling
inferredcites →https://doi.org/10.1177/38.1.2294148openalex-snapshot
Cellular distribution of alpha B-crystallin in non-lenticular tissues.
inferredcites →https://doi.org/10.1371/currents.hd.0ab4f3645aff523c56ecc8ccbe41a198openalex-snapshot
Increased Body Weight of the BAC HD Transgenic Mouse Model of Huntington’s Disease Accounts for Some but Not All of the Observed HD-like Motor Deficits
inferredcites →https://doi.org/10.1371/currents.hd.34957c4f8bd7cb1f5ec47381dfc811c3openalex-snapshot
Differential Synaptic and Extrasynaptic Glutamate-Receptor Alterations in Striatal Medium-Sized Spiny Neurons of Aged YAC128 Huntington’s Disease Mice
inferredcites →https://doi.org/10.1523/jneurosci.0116-08.2008openalex-snapshot
Expanded-Polyglutamine Huntingtin Protein Suppresses the Secretion and Production of a Chemokine (CCL5/RANTES) by Astrocytes
inferredcites →https://doi.org/10.1523/jneurosci.0168-16.2016openalex-snapshot
Mutant Huntingtin Impairs BDNF Release from Astrocytes by Disrupting Conversion of Rab3a-GTP into Rab3a-GDP
inferredcites →https://doi.org/10.1523/jneurosci.0857-08.2008openalex-snapshot
Full-Length Human Mutant Huntingtin with a Stable Polyglutamine Repeat Can Elicit Progressive and Selective Neuropathogenesis in BACHD Mice
inferredcites →https://doi.org/10.1523/jneurosci.14-03-01030.1994openalex-snapshot
GFAP promoter directs astrocyte-specific expression in transgenic mice
inferredcites →https://doi.org/10.1523/jneurosci.1418-17.2017openalex-snapshot
Mutant Huntingtin Inhibits αB-Crystallin Expression and Impairs Exosome Secretion from Astrocytes
inferredcites →https://doi.org/10.1523/jneurosci.19-16-06897.1999openalex-snapshot
Three-Dimensional Relationships between Hippocampal Synapses and Astrocytes
inferredcites →https://doi.org/10.1523/jneurosci.20-02-00666.2000openalex-snapshot
SNARE Protein-Dependent Glutamate Release from Astrocytes
inferredcites →https://doi.org/10.1523/jneurosci.2532-06.2006openalex-snapshot
Early Postnatal Astroglial Cells Produce Multilineage Precursors and Neural Stem Cells In Vivo
inferredcites →https://doi.org/10.1523/jneurosci.3539-10.2011openalex-snapshot
Differential Electrophysiological Changes in Striatal Output Neurons in Huntington's Disease
inferredcites →https://doi.org/10.1523/jneurosci.3693-15.2016openalex-snapshot
Dysfunctional Calcium and Glutamate Signaling in Striatal Astrocytes from Huntington's Disease Model Mice
inferredcites →https://doi.org/10.1523/jneurosci.4178-07.2008openalex-snapshot
A Transcriptome Database for Astrocytes, Neurons, and Oligodendrocytes: A New Resource for Understanding Brain Development and Function
inferredcites →https://doi.org/10.3233/jhd-140092openalex-snapshot
Widespread Heterogeneous Neuronal Loss Across the Cerebral Cortex in Huntington's Disease
inferredcites →https://doi.org/10.3389/fnmol.2019.00258openalex-snapshot
The Role of Microglia and Astrocytes in Huntington’s Disease
inferredcites →https://doi.org/10.3389/fnsys.2011.00046openalex-snapshot
Altered Balance of Activity in the Striatal Direct and Indirect Pathways in Mouse Models of Huntington's Disease

What points at this work

Incoming claims: where this work appears in other papers’ reference lists and arguments.

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inferred← citeshttps://doi.org/10.1002/stem.3103openalex-snapshot
Mesenchymal stem cells alleviate AQP-4-dependent glymphatic dysfunction and improve brain distribution of antisense oligonucleotides in BACHD mice
inferred← citeshttps://doi.org/10.1007/978-3-031-40858-8_564-1openalex-snapshot
Cognitive Disability and Inflammation in Huntington’s Disease
inferred← citeshttps://doi.org/10.1007/978-3-032-18296-8_26openalex-snapshot
Experimental Therapeutic Approaches: Molecular, Genetic, and Behavioral
inferred← citeshttps://doi.org/10.1007/978-981-13-9913-8_14openalex-snapshot
Astrocytes in Huntington’s Disease
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Caenorhabditis elegans as a Model Organism in Neurological Research
inferred← citeshttps://doi.org/10.1007/s00415-023-12109-yopenalex-snapshot
Plasma GFAP and its association with disease severity in Huntington’s disease
inferred← citeshttps://doi.org/10.1007/s12035-021-02451-5openalex-snapshot
Accumulation of Endogenous Mutant Huntingtin in Astrocytes Exacerbates Neuropathology of Huntington Disease in Mice
inferred← citeshttps://doi.org/10.1007/s12192-020-01101-4openalex-snapshot
Small heat shock proteins in neurodegenerative diseases
inferred← citeshttps://doi.org/10.1007/s13311-019-00782-9openalex-snapshot
Cell-Autonomous and Non-cell-Autonomous Pathogenic Mechanisms in Huntington's Disease: Insights from In Vitro and In Vivo Models
inferred← citeshttps://doi.org/10.1007/s13311-023-01357-5openalex-snapshot
Contribution of Glial Cells to Polyglutamine Diseases: Observations from Patients and Mouse Models
inferred← citeshttps://doi.org/10.1016/b978-0-12-821565-4.00012-2openalex-snapshot
Neurodegenerative diseases
inferred← citeshttps://doi.org/10.1016/b978-0-323-95672-7.00013-3openalex-snapshot
Genetic mouse models to explore Huntington's disease mechanisms and therapeutic strategies
inferred← citeshttps://doi.org/10.1016/b978-0-323-98818-6.00001-7openalex-snapshot
Immunology and microbiome: Implications for motor systems
inferred← citeshttps://doi.org/10.1016/j.bbr.2021.113230openalex-snapshot
The absence of the aryl hydrocarbon receptor in the R6/1 transgenic mouse model of Huntington’s disease improves the neurological phenotype
inferred← citeshttps://doi.org/10.1016/j.celrep.2021.109308openalex-snapshot
Cell-intrinsic glial pathology is conserved across human and murine models of Huntington’s disease
inferred← citeshttps://doi.org/10.1016/j.celrep.2023.112198openalex-snapshot
Tumor Suppressor p53 Regulates Heat Shock Factor 1 Protein Degradation in Huntington's Disease
inferred← citeshttps://doi.org/10.1016/j.expneurol.2020.113358openalex-snapshot
Differential effects of SNARE-dependent gliotransmission on behavioral phenotypes in a mouse model of Huntington's disease
inferred← citeshttps://doi.org/10.1016/j.jns.2024.122979openalex-snapshot
Cerebrospinal fluid glial fibrillary acidic protein, in contrast to amyloid beta protein, is associated with disease symptoms in Huntington's disease
inferred← citeshttps://doi.org/10.1016/j.nbd.2019.04.015openalex-snapshot
Astrocyte transduction is required for rescue of behavioral phenotypes in the YAC128 mouse model with AAV-RNAi mediated HTT lowering therapeutics
inferred← citeshttps://doi.org/10.1016/j.nbd.2019.104635openalex-snapshot
Pathogenesis of SCA3 and implications for other polyglutamine diseases
inferred← citeshttps://doi.org/10.1016/j.nbd.2020.104951openalex-snapshot
Use of adeno-associated virus-mediated delivery of mutant huntingtin to study the spreading capacity of the protein in mice and non-human primates
inferred← citeshttps://doi.org/10.1016/j.nbd.2020.104957openalex-snapshot
Glia in neurodegeneration: Drivers of disease or along for the ride?
inferred← citeshttps://doi.org/10.1016/j.nbd.2020.104963openalex-snapshot
The contribution of glial cells to Huntington's disease pathogenesis
inferred← citeshttps://doi.org/10.1016/j.neuron.2022.01.006openalex-snapshot
Uninterrupted CAG repeat drives striatum-selective transcriptionopathy and nuclear pathogenesis in human Huntingtin BAC mice
inferred← citeshttps://doi.org/10.1016/j.neuron.2025.08.009openalex-snapshot
On astrocyte-neuron interactions: Broad insights from the striatum
inferred← citeshttps://doi.org/10.1016/j.neuropharm.2019.03.027openalex-snapshot
Astroglial monoacylglycerol lipase controls mutant huntingtin-induced damage of striatal neurons
inferred← citeshttps://doi.org/10.1016/j.neurot.2026.e00859openalex-snapshot
Silmitasertib, an FDA-designated orphan CK2 inhibitor, ameliorates neuropathology and motor dysfunction in a Huntington's disease mouse model
inferred← citeshttps://doi.org/10.1016/j.pneurobio.2021.102089openalex-snapshot
Glucose metabolic crosstalk and regulation in brain function and diseases
inferred← citeshttps://doi.org/10.1016/j.tins.2019.06.003openalex-snapshot
Astrocyte–Neuron Interactions in the Striatum: Insights on Identity, Form, and Function
inferred← citeshttps://doi.org/10.1038/s41392-023-01628-9openalex-snapshot
Astrocytes in human central nervous system diseases: a frontier for new therapies
inferred← citeshttps://doi.org/10.1038/s41467-024-50626-0openalex-snapshot
Multi-omic analysis of Huntington’s disease reveals a compensatory astrocyte state
inferred← citeshttps://doi.org/10.1038/s41573-022-00390-xopenalex-snapshot
Function and therapeutic value of astrocytes in neurological diseases
inferred← citeshttps://doi.org/10.1038/s41583-022-00641-1openalex-snapshot
Astrocyte contribution to dysfunction, risk and progression in neurodegenerative disorders
inferred← citeshttps://doi.org/10.1038/s41591-023-02566-3openalex-snapshot
Microglia and complement mediate early corticostriatal synapse loss and cognitive dysfunction in Huntington’s disease
inferred← citeshttps://doi.org/10.1038/s41598-022-21900-2openalex-snapshot
Fragment-based virtual screening identifies a first-in-class preclinical drug candidate for Huntington’s disease
inferred← citeshttps://doi.org/10.1080/13543784.2020.1804552openalex-snapshot
Huntingtin-lowering strategies for Huntington’s disease
inferred← citeshttps://doi.org/10.1080/13543784.2024.2348738openalex-snapshot
Inflammation and Huntington’s disease – a neglected therapeutic target?
inferred← citeshttps://doi.org/10.1093/brain/awz363openalex-snapshot
Microglial depletion prevents extracellular matrix changes and striatal volume reduction in a model of Huntington's disease
inferred← citeshttps://doi.org/10.1093/hmg/ddac303openalex-snapshot
An altered extracellular matrix–integrin interface contributes to Huntington’s disease-associated CNS dysfunction in glial and vascular cells
inferred← citeshttps://doi.org/10.1093/hmg/ddz009openalex-snapshot
Mutant huntingtin expression in microglia is neither required nor sufficient to cause the Huntington’s disease-like phenotype in BACHD mice
inferred← citeshttps://doi.org/10.1101/2020.08.06.20169524openalex-snapshot
Kynurenine pathway metabolites in cerebrospinal fluid and blood as potential biomarkers in Huntington’s disease
inferred← citeshttps://doi.org/10.1101/2020.11.03.367326openalex-snapshot
Modulating glial genes involved in synaptic function mitigates pathogenesis and behavioral deficits in a Drosophila model of Huntington’s Disease
inferred← citeshttps://doi.org/10.1101/2021.11.29.470488openalex-snapshot
Striatal compartmentalization and clustering of different subtypes of astrocytes is altered in the zQ175 Huntington’s disease mouse model
inferred← citeshttps://doi.org/10.1101/2021.12.03.471180openalex-snapshot
Microglia Mediate Early Corticostriatal Synapse Loss and Cognitive Dysfunction in Huntington’s Disease Through Complement-Dependent Mechanisms
inferred← citeshttps://doi.org/10.1101/2022.09.10.507291openalex-snapshot
Mapping the glial transcriptome in Huntington’s disease using snRNAseq: Selective disruption of glial signatures across brain regions
inferred← citeshttps://doi.org/10.1101/2023.09.08.556867openalex-snapshot
Multi-OMIC analysis of Huntington disease reveals a neuroprotective astrocyte state
inferred← citeshttps://doi.org/10.1101/2024.06.16.599193openalex-snapshot
Single-cell variations of circadian clock and immune gene expression in microglia and neurodegeneration
inferred← citeshttps://doi.org/10.1101/cshperspect.a041375openalex-snapshot
Glia in Neurodegenerative Disease
inferred← citeshttps://doi.org/10.1111/jnc.15360openalex-snapshot
Kynurenine pathway metabolites in cerebrospinal fluid and blood as potential biomarkers in Huntington's disease
inferred← citeshttps://doi.org/10.1111/nan.12682openalex-snapshot
Effects of mutant huntingtin inactivation on Huntington disease‐related behaviours in the BACHD mouse model
inferred← citeshttps://doi.org/10.1111/nyas.14977openalex-snapshot
Astrocytic contributions to Huntington's disease pathophysiology
inferred← citeshttps://doi.org/10.1126/scitranslmed.aaw8546openalex-snapshot
Astrocyte molecular signatures in Huntington’s disease
inferred← citeshttps://doi.org/10.1177/09636897221105499openalex-snapshot
Therapeutic Potential of Astrocyte Transplantation
inferred← citeshttps://doi.org/10.1177/1073858420972662openalex-snapshot
Synaptic Dysfunction in Huntington’s Disease: Lessons from Genetic Animal Models
inferred← citeshttps://doi.org/10.1177/18796397251338207openalex-snapshot
Neuroinflammation in Huntington's disease: Causes, consequences, and treatment strategies
inferred← citeshttps://doi.org/10.1186/s13073-022-01134-7openalex-snapshot
Towards elucidating disease-relevant states of neurons and glia by CRISPR-based functional genomics
inferred← citeshttps://doi.org/10.1186/s40478-019-0726-2openalex-snapshot
Endogenous mouse huntingtin is highly abundant in cranial nerve nuclei, co-aggregates to Abeta plaques and is induced in reactive astrocytes in a transgenic mouse model of Alzheimer’s disease
inferred← citeshttps://doi.org/10.1186/s40478-022-01379-8openalex-snapshot
CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.1186/s40478-024-01871-3openalex-snapshot
Mapping the glial transcriptome in Huntington’s disease using snRNAseq: selective disruption of glial signatures across brain regions
inferred← citeshttps://doi.org/10.1186/s40478-025-02054-4openalex-snapshot
Astrocyte-neuron combined targeting for CYP46A1 gene therapy in Huntington’s disease
inferred← citeshttps://doi.org/10.1242/dmm.052002openalex-snapshot
Modulation of SNARE-dependent exocytosis in astrocytes improves neuropathology in Huntington's disease
inferred← citeshttps://doi.org/10.1242/dmm.052513openalex-snapshot
Mutant huntingtin expression in somatostatin-positive interneurons contributes to neurophysiological and behavioral phenotypes in BACHD mice
inferred← citeshttps://doi.org/10.12703/r/10-77openalex-snapshot
Huntington’s disease mouse models: unraveling the pathology caused by CAG repeat expansion
inferred← citeshttps://doi.org/10.1515/revneuro-2024-0043openalex-snapshot
Research progress on astrocyte-derived extracellular vesicles in the pathogenesis and treatment of neurodegenerative diseases
inferred← citeshttps://doi.org/10.1523/jneurosci.0998-21.2022openalex-snapshot
Neuroimmunometabolism: A New Pathological Nexus Underlying Neurodegenerative Disorders
inferred← citeshttps://doi.org/10.21203/rs.3.rs-1562535/v1openalex-snapshot
Fragment-based virtual screening identifies a first-in-class preclinical drug candidate for Huntington’s disease
inferred← citeshttps://doi.org/10.21203/rs.3.rs-3827959/v1openalex-snapshot
Investigating the Gliogenic Genes and Signaling Pathways in the Pathogenesis of Huntington’s Disease: A Systematic Review
inferred← citeshttps://doi.org/10.2174/1389200223666220321103942openalex-snapshot
A Review On Huntington Protein: Insight Into Protein Aggregation and Therapeutic Interventions
inferred← citeshttps://doi.org/10.2174/1570159x19666211201094608openalex-snapshot
Neuroinflammation in Huntington’s Disease: A Starring Role for Astrocyte and Microglia
inferred← citeshttps://doi.org/10.3233/jhd-200395openalex-snapshot
Biological Aging and the Cellular Pathogenesis of Huntington’s Disease
inferred← citeshttps://doi.org/10.3233/jhd-210502openalex-snapshot
Diminished LC3-Associated Phagocytosis by Huntington’s Disease Striatal Astrocytes
inferred← citeshttps://doi.org/10.3389/fimmu.2021.644294openalex-snapshot
Neuro-Immune Cross-Talk in the Striatum: From Basal Ganglia Physiology to Circuit Dysfunction
inferred← citeshttps://doi.org/10.3389/fimmu.2023.1283331openalex-snapshot
Blockade of mGluR5 in astrocytes derived from human iPSCs modulates astrocytic function and increases phagocytosis
inferred← citeshttps://doi.org/10.3389/fnagi.2023.1190563openalex-snapshot
Pain in Huntington’s disease and its potential mechanisms
inferred← citeshttps://doi.org/10.3389/fnana.2021.673177openalex-snapshot
BACHD Mice Recapitulate the Striatal Parvalbuminergic Interneuron Loss Found in Huntington’s Disease
inferred← citeshttps://doi.org/10.3389/fncel.2021.689332openalex-snapshot
Huntingtin and the Synapse
inferred← citeshttps://doi.org/10.3389/fncel.2023.1094503openalex-snapshot
Striatal spatial heterogeneity, clustering, and white matter association of GFAP+ astrocytes in a mouse model of Huntington’s disease
inferred← citeshttps://doi.org/10.3389/fnetp.2023.1205544openalex-snapshot
Astrocytic modulation of neuronal signalling
inferred← citeshttps://doi.org/10.3389/fnins.2021.736888openalex-snapshot
Primary Cilia in Glial Cells: An Oasis in the Journey to Overcoming Neurodegenerative Diseases
inferred← citeshttps://doi.org/10.3389/fnins.2022.946822openalex-snapshot
Hunting for the cause: Evidence for prion-like mechanisms in Huntington’s disease
inferred← citeshttps://doi.org/10.3389/fnmol.2019.00258openalex-snapshot
The Role of Microglia and Astrocytes in Huntington’s Disease
inferred← citeshttps://doi.org/10.3390/biom12010034openalex-snapshot
RTP801/REDD1 Is Involved in Neuroinflammation and Modulates Cognitive Dysfunction in Huntington’s Disease
inferred← citeshttps://doi.org/10.3390/biomedicines10061432openalex-snapshot
Molecular Pathophysiological Mechanisms in Huntington’s Disease
inferred← citeshttps://doi.org/10.3390/cells10071565openalex-snapshot
Cell Reprogramming to Model Huntington’s Disease: A Comprehensive Review
inferred← citeshttps://doi.org/10.3390/ijms21145149openalex-snapshot
Endosomal-Lysosomal Processing of Neurodegeneration-Associated Proteins in Astrocytes
inferred← citeshttps://doi.org/10.3390/ijms21239188openalex-snapshot
Glia in Neurodegeneration: The Housekeeper, the Defender and the Perpetrator
inferred← citeshttps://doi.org/10.3390/ijms22083884openalex-snapshot
Genetic Screen in Adult Drosophila Reveals That dCBP Depletion in Glial Cells Mitigates Huntington Disease Pathology through a Foxo-Dependent Pathway
inferred← citeshttps://doi.org/10.3390/ijms222212499openalex-snapshot
Non-Cell Autonomous and Epigenetic Mechanisms of Huntington’s Disease
inferred← citeshttps://doi.org/10.3390/ijms252111787openalex-snapshot
Neuroinflammatory Proteins in Huntington’s Disease: Insights into Mechanisms, Diagnosis, and Therapeutic Implications
inferred← citeshttps://doi.org/10.3390/pharmaceutics17060726openalex-snapshot
In Vitro Efficacy of PEI-Derived Lipopolymers in Silencing of Toxic Proteins in a Neuronal Model of Huntington’s Disease
inferred← citeshttps://doi.org/10.4103/1673-5374.265541openalex-snapshot
Genetic targeting of astrocytes to combat neurodegenerative disease
inferred← citeshttps://doi.org/10.6084/m9.figshare.20003491openalex-snapshot
Additional file 10 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.6084/m9.figshare.20003494openalex-snapshot
Additional file 11 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.6084/m9.figshare.20003497openalex-snapshot
Additional file 12 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.6084/m9.figshare.20003500openalex-snapshot
Additional file 13 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.6084/m9.figshare.20003503openalex-snapshot
Additional file 14 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.6084/m9.figshare.20003506openalex-snapshot
Additional file 15 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.6084/m9.figshare.20003509openalex-snapshot
Additional file 16 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.6084/m9.figshare.20003512openalex-snapshot
Additional file 18 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.6084/m9.figshare.20003515openalex-snapshot
Additional file 1 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.6084/m9.figshare.20003521openalex-snapshot
Additional file 2 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.6084/m9.figshare.20003524openalex-snapshot
Additional file 3 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.6084/m9.figshare.20003527openalex-snapshot
Additional file 4 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.6084/m9.figshare.20003530openalex-snapshot
Additional file 5 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.6084/m9.figshare.20003533openalex-snapshot
Additional file 6 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.6084/m9.figshare.20003539openalex-snapshot
Additional file 7 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.6084/m9.figshare.20003542openalex-snapshot
Additional file 8 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.6084/m9.figshare.20003545openalex-snapshot
Additional file 9 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease
inferred← citeshttps://doi.org/10.70675/f664e003zf93fz467eza6a3z3d953eaffe4eopenalex-snapshot
Les astrocytes réactifs, des partenaires anti-agrégants dans la maladie de Huntington : identification des mécanismes impliqués dans le dialogue neurone-astrocyte
inferred← citeshttps://doi.org/10.7554/elife.64564openalex-snapshot
Downregulation of glial genes involved in synaptic function mitigates Huntington's disease pathogenesis
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