ReviewCurrent opinion in neurobiology2018
Molecular insights into cortico-striatal miscommunications in Huntington's disease.
Review in Current opinion in neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed.
- Article
- UBL3 Interacts with PolyQ-Expanded Huntingtin Fragments and Modifies Their Intracellular Sorting.Neurology international · 2024Article
- Why Is Arginine the Only Amino Acid That Inhibits Polyglutamine Monomers from Taking on Toxic Conformations?ACS chemical neuroscience · 2024Article
- Neuroprotection by ADAM10 inhibition requires TrkB signaling in the Huntington's disease hippocampus.Cellular and molecular life sciences : CMLS · 2024Article
- Huntington's disease cellular phenotypes are rescued non-cell autonomously by healthy cells in mosaic telencephalic organoids.Nature communications · 2024Article
- BDNF and TRiC-inspired reagent rescue cortical synaptic deficits in a mouse model of Huntington's disease.Neurobiology of disease · 2024Article
- Fatigue and perceived energy in a sample of older adults over 10 years: A resting state functional connectivity study of neural correlates.Experimental gerontology · 2024Article
- Innate immune mechanisms mediate loss of corticostriatal synapses in Huntington's disease.Nature medicine · 2023Article
- Regulation of one-carbon metabolism may open new avenues to slow down the initiation and progression of Huntington's disease.Neural regeneration research · 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
- Noninvasive modulation of human corticostriatal activity.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Failure to Thrive: Impaired BDNF Transport along the Cortical-Striatal Axis in Mouse Q140 Neurons of Huntington's Disease.Biology · 2023Article
- A plant-based mutant huntingtin model-driven discovery of impaired expression of GTPCH and DHFR.Cellular and molecular life sciences : CMLS · 2022Article
- Molecular Pathophysiological Mechanisms in Huntington's Disease.Biomedicines · 2022Review
- Dynamics of huntingtin protein interactions in the striatum identifies candidate modifiers of Huntington disease.Cell systems · 2022Article
- Article
- Synaptic Dysfunction in Huntington's Disease: Lessons from Genetic Animal Models.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022Article
- Early impairment of thalamocortical circuit activity and coherence in a mouse model of Huntington's disease.Neurobiology of disease · 2021Article
- Spatiotemporal analysis of soluble aggregates and autophagy markers in the R6/2 mouse model.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Huntington's disease (HD), a dominantly inherited neurodegenerative disease, is defined by its genetic cause, a CAG-repeat expansion in the HTT gene, its motor and psychiatric symptomology and primary loss of striatal medium spiny neurons (MSNs). However, the molecular mechanisms from genetic lesion to disease phenotype remain largely unclear. Mouse models of HD have been created that exhibit phenotypes partially recapitulating those in the patient, and specifically, cortico-striatal disconnectivity appears to be a shared pathogenic event shared by HD mouse models and patients. Molecular studies have begun to unveil converging molecular and cellular pathogenic mechanisms that may account for cortico-striatal miscommunication in various HD mouse models. Systems biological approaches help to illuminate synaptic molecular networks as a nexus for HD cortio-striatal pathogenesis, and may offer new candidate targets to modify the disease.
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Registered trials
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