ArticleMolecular psychiatry2021
Shedding a new light on Huntington's disease: how blood can both propagate and ameliorate disease pathology.
Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- SIRT1 in Neurodegenerative Diseases: Molecular Mechanisms, Disease Relevance, and Therapeutic Potential.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Psychosis in Huntington disease: a short update.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Concomitant pathologies and their impact on Huntington's disease. A brief review of current evidence.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Brain-derived extracellular vesicles potentially mediate crosstalk with peripheral organs in neurodegenerative diseases.Frontiers in cell and developmental biology · 2025Review
- Review
- Effectiveness of Flavonoid-Rich Diet in Alleviating Symptoms of Neurodegenerative Diseases.Foods (Basel, Switzerland) · 2024Review
- Healthy blood, healthy brain: a window into understanding and treating neurodegenerative diseases.Journal of neurology · 2024Review
- Brain-Periphery Interactions in Huntington's Disease: Mediators and Lifestyle Interventions.International journal of molecular sciences · 2024Review
- Mutant huntingtin protein induces MLH1 degradation, DNA hyperexcision, and cGAS-STING-dependent apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Widespread alterations in microRNA biogenesis in human Huntington's disease putamen.Acta neuropathologica communications · 2022Article
- A New Perspective on Huntington's Disease: How a Neurological Disorder Influences the Peripheral Tissues.International journal of molecular sciences · 2022Review
- Hunting for the cause: Evidence for prion-like mechanisms in Huntington's disease.Frontiers in neuroscience · 2022Review
- Prion-like properties of the mutant huntingtin protein in living organisms: the evidence and the relevance.Molecular psychiatry · 2022Review
- Huntingtin silencing delays onset and slows progression of Huntington's disease: a biomarker study.Brain : a journal of neurology · 2021Article
- Myelinosome Organelles in the Retina of R6/1 Huntington Disease (HD) Mice: Ubiquitous Distribution and Possible Role in Disease Spreading.International journal of molecular sciences · 2021Article
- Non-Cell Autonomous and Epigenetic Mechanisms of Huntington's Disease.International journal of molecular sciences · 2021Review
- Systemic manifestation and contribution of peripheral tissues to Huntington's disease pathogenesis.Ageing research reviews · 2021Review
- Targeting Tau to Treat Clinical Features of Huntington's Disease.Frontiers in neurology · 2020Review
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 6 institutions in 2 countries.
Funding
Abstract
Huntington's disease (HD) is a monogenic neurodegenerative disorder resulting from a mutation in the huntingtin gene. This leads to the expression of the mutant huntingtin protein (mHTT) which provokes pathological changes in both the central nervous system (CNS) and periphery. Accumulating evidence suggests that mHTT can spread between cells of the CNS but here, we explored the possibility that mHTT could also propagate and cause pathology via the bloodstream. For this, we used a parabiosis approach to join the circulatory systems of wild-type (WT) and zQ175 mice. After surgery, we observed mHTT in the plasma and circulating blood cells of WT mice and post-mortem analyses revealed the presence of mHTT aggregates in several organs including the liver, kidney, muscle and brain. The presence of mHTT in the brain was accompanied by vascular abnormalities, such as a reduction of Collagen IV signal intensity and altered vessel diameter in the striatum, and changes in expression of Glutamic acid decarboxylase 65/67 (GAD65-67) in the cortex. Conversely, we measured reduced pathology in zQ175 mice by decreased mitochondrial impairments in peripheral organs, restored vessel diameter in the cortex and improved expression of Dopamine- and cAMP-regulated phosphoprotein 32 (DARPP32) in striatal neurons. Collectively, these results demonstrate that circulating mHTT can disseminate disease, but importantly, that healthy blood can dilute pathology. These findings have significant implications for the development of therapies in HD.
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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.