ReviewProgress in neurobiology2007
The corticostriatal pathway in Huntington's disease.
Review in Progress in neurobiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 174 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
174 citing papers in PubMed, 1 synthesis or guideline pooled it, 312 citations in OpenAlex.
- Chronic cholesterol administration to the brain supports complete and long-lasting cognitive and motor amelioration in Huntington's disease.Pharmacological research · 2023Pooled it
- A shared DNA-repeat toxicity threshold, reached somatically at cell-type-specific rates, unites cortical and striatal neurodegeneration in Huntington's disease.bioRxiv : the preprint server for biology · 2025Article
- BA9 Transcriptomics in Huntington's Disease 80-Gene Signature and MIR219A2-Linked Targets.International journal of molecular sciences · 2025Article
- Stage-Dependent Inhibitory Connectivity in Striatal-Motor Circuit in Huntington's Disease.Annals of clinical and translational neurology · 2025Article
- The regulation of rhythmic locomotion by motor cortical and dopaminergic inputs in the mouse striatum.Molecular brain · 2025Article
- Restoring endogenous Dlg4/PSD95 expression by an artificial transcription factor ameliorates cognitive and motor learning deficits in the R6/2 mouse model of Huntington's disease.Clinical epigenetics · 2025Article
- NMDA receptors in neurodegenerative diseases: mechanisms and emerging therapeutic strategies.Frontiers in aging neuroscience · 2025Review
- Restoring Compromised ClThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Modulation of SNARE-dependent exocytosis in astrocytes improves neuropathology in Huntington's disease.Disease models & mechanisms · 2024Article
- Break-up and recovery of harmony between direct and indirect pathways in the basal ganglia: Huntington's disease and treatment.Cognitive neurodynamics · 2024Article
- Neuroprotection by ADAM10 inhibition requires TrkB signaling in the Huntington's disease hippocampus.Cellular and molecular life sciences : CMLS · 2024Article
- Disentangling the neurobiological bases of temporal impulsivity in Huntington's disease.Brain and behavior · 2024Article
- Thalamic Foxp2 regulates output connectivity and sensory-motor impairments in a model of Huntington's Disease.Cellular and molecular life sciences : CMLS · 2023Article
- Microglia and complement mediate early corticostriatal synapse loss and cognitive dysfunction in Huntington's disease.Nature medicine · 2023Article
- M2 Cortex Circuitry and Sensory-Induced Behavioral Alterations in Huntington's Disease: Role of Superior Colliculus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- A Medicinal Chemistry Perspective on Excitatory Amino Acid Transporter 2 Dysfunction in Neurodegenerative Diseases.Journal of medicinal chemistry · 2023Review
- HSF1 and Its Role in Huntington's Disease Pathology.Advances in experimental medicine and biology · 2023Review
- Neurochemical correlates of synapse density in a Huntington's disease mouse model.Journal of neurochemistry · 2023Article
- Extracellular vesicles improve GABAergic transmission in Huntington's disease iPSC-derived neurons.Theranostics · 2023Article
- CNS Delivery of Nucleic Acid Therapeutics: Beyond the Blood-Brain Barrier and Towards Specific Cellular Targeting.Pharmaceutical research · 2023Review
114 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The corticostriatal pathway provides most of the excitatory glutamatergic input into the striatum and it plays an important role in the development of the phenotype of Huntington's disease (HD). This review summarizes results obtained from genetic HD mouse models concerning various alterations in this pathway. Evidence indicates that dysfunctions of striatal circuits and cortical neurons that make up the corticostriatal pathway occur during the development of the HD phenotype, well before there is significant neuronal cell loss. Morphological changes in the striatum are probably primed initially by alterations in the intrinsic functional properties of striatal medium-sized spiny neurons. Some of these alterations, including increased sensitivity of N-methyl-D-aspartate receptors in subpopulations of neurons, might be constitutively present but ultimately require abnormalities in the corticostriatal inputs for the phenotype to be expressed. Dysfunctions of the corticostriatal pathway are complex and there are multiple changes as demonstrated by significant age-related transient and more chronic interactions with the disease state. There also is growing evidence for changes in cortical microcircuits that interact to induce dysfunctions of the corticostriatal pathway. The conclusions of this review emphasize, first, the general role of neuronal circuits in the expression of the HD phenotype and, second, that both cortical and striatal circuits must be included in attempts to establish a framework for more rational therapeutic strategies in HD. Finally, as changes in cortical and striatal circuitry are complex and in some cases biphasic, therapeutic interventions should be regionally specific and take into account the temporal progression of the phenotype.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.