ArticleBrain communications2022
The long and the short of Huntington's disease: how the sphingolipid profile is shifted in the caudate of advanced clinical cases.
Article in Brain communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
The trial behind it
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
20 citing papers in PubMed, 31 citations in OpenAlex.
- An exploratory metabolomic comparison of participants with fast or absent functional progression from 2CARE, a randomized, double-blind clinical trial in Huntington's disease.Scientific reports · 2024Trial
- The lipidomic atlas for cellular organelles to reveal the central role of mitochondria in organelle communication.Science China. Life sciences · 2026Article
- Article
- Lipid Messengers: Mechanisms and Clinical Applications of Exosomal Lipids in Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- The physiological and pathological effects of sphingolipid metabolism and signaling in the central nervous system.Brain pathology (Zurich, Switzerland) · 2026Review
- Glycosphingolipids in Dementia: Insights from Mass Spectrometry and Systems Biology Approaches.Biomedicines · 2025Review
- Cerebellar lipid dysregulation in SCA3: A comparative study in patients and mice.Neurobiology of disease · 2025Article
- Lipidomics of Huntington's Disease: A Comprehensive Review of Current Status and Future Directions.Metabolites · 2025Review
- Red blood cell lipid distribution in the pathophysiology and laboratory evaluation of chorea-acanthocytosis and McLeod syndrome patients.Frontiers in physiology · 2025Article
- Myelin Lipid Alterations in Neurodegenerative Diseases: Landscape and Pathogenic Implications.Antioxidants & redox signaling · 2024Review
- Nutritional roles and therapeutic potentials of dietary sphingomyelin in brain diseases.Journal of clinical biochemistry and nutrition · 2024Article
- Circulating sphingolipids and subclinical brain pathology: the cardiovascular health study.Frontiers in neurology · 2024Article
- Mutant-Huntingtin Molecular Pathways Elucidate New Targets for Drug Repurposing.International journal of molecular sciences · 2023Review
- Early whole-body mutant huntingtin lowering averts changes in proteins and lipids important for synapse function and white matter maintenance in the LacQ140 mouse model.Neurobiology of disease · 2023Article
- Early whole-body mutant huntingtin lowering averts changes in proteins and lipids important for synapse function and white matter maintenance in the LacQ140 mouse model.bioRxiv : the preprint server for biology · 2023Article
- Treatment with the Glycosphingolipid Modulator THI Rescues Myelin Integrity in the Striatum of R6/2 HD Mice.International journal of molecular sciences · 2023Article
- Involvement of Lipids in the Pathogenesis of Amyotrophic Lateral Sclerosis.Life (Basel, Switzerland) · 2023Review
- Aberrant Ganglioside Functions to Underpin Dysregulated Myelination, Insulin Signalling, and Cytokine Expression: Is There a Link and a Room for Therapy?Biomolecules · 2022Review
- Phospholipid Profiles Are Selectively Altered in the Putamen and White Frontal Cortex of Huntington's Disease.Nutrients · 2022Article
- Circulating sphingolipids in relation to cognitive decline and incident dementia: The Cardiovascular Health Study.Alzheimer's & dementia (Amsterdam, Netherlands)Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease is a devastating neurodegenerative disorder that onsets in late adulthood as progressive and terminal cognitive, psychiatric and motor deficits. The disease is genetic, triggered by a CAG repeat (polyQ) expansion mutation in the Huntingtin gene and resultant huntingtin protein. Although the mutant huntingtin protein is ubiquitously expressed, the striatum degenerates early and consistently in the disease. The polyQ mutation at the N-terminus of the huntingtin protein alters its natural interactions with neural phospholipids
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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.