ReviewCureus2022
Huntington's Disease: A Clinical Review.
Review in Cureus, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- In silico discovery of natural compound-derived multi-target inhibitor for Huntington's disease therapy.Scientific reports · 2026Article
- Pathological Insights into Neurodegenerative and Neurodevelopmental Disorders: Perspectives for the Development of Novel Treatment Approaches.CNS & neurological disorders drug targets · 2026Review
- Genetic Profiling of Huntington's Disease: Insights from CAG Repeat Analysis for Precision Diagnosis and Management.Noro psikiyatri arsivi · 2026Article
- Huntington's Disease Research Over Six Decades: Global Insights, Gaps, and Future Directions.Cureus · 2025Review
- Revolutionizing Huntington's Disease Treatment: Breakthroughs in AAV-Mediated Gene Therapy.Cells · 2025Review
- Article
- Mitochondrial Dysfunction in Neurodegenerative Diseases: Mechanisms and Corresponding Therapeutic Strategies.Biomedicines · 2025Review
- Recent Advancements in Lipid Nanoparticles-Based Phytoactives Delivery Systems for Neurodegenerative Diseases.International journal of nanomedicine · 2025Review
- Neurodegenerative diseases and neuroinflammation-induced apoptosis.Open life sciences · 2025Review
- Boosting the Therapeutic Potential of Extracellular Vesicles Derived From Mesenchymal Stem Cells via Advanced Preconditioning for Neurodegenerative Disorders.Stem cells international · 2025Review
- Evaluation of an Antisense Oligonucleotide Targeting CAG Repeats: A Patient-Customized Therapy Study for Huntington's Disease.Life (Basel, Switzerland) · 2024Article
- Therapeutic approaches targeting aging and cellular senescence in Huntington's disease.CNS neuroscience & therapeutics · 2024Review
- High-throughput virtual screening of potential inhibitors of GPR52 using docking and biased sampling method for Huntington's disease therapy.Molecular diversity · 2024Article
- Parthanatos: Mechanisms, modulation, and therapeutic prospects in neurodegenerative disease and stroke.Biochemical pharmacology · 2024Review
- Redox Homeostasis, Gut Microbiota, and Epigenetics in Neurodegenerative Diseases: A Systematic Review.Antioxidants (Basel, Switzerland) · 2024Review
- 3-Hydroxyanthranilic Acid Delays Paralysis inBiomolecules · 2024Article
- Induced Pluripotent Stem Cells and Organoids in Advancing Neuropathology Research and Therapies.Cells · 2024Review
- Childhood-onset Huntignton´s disease. A rare presentation.Revista de neurologia · 2024Article
- Article
- An Update on the Application of CRISPR Technology in Clinical Practice.Molecular biotechnology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Huntington's gene on chromosome 4 has a dominantly inherited CAG trinucleotide repeat expansion, ultimately resulting in Huntington's disease (HD), a completely penetrant neurological condition. The frequency is 10-100 times higher in the population descended from Europe than in East Asia. Through various processes, including impairment of proteostasis, transcription, and cell function, as well as direct toxicity of the mutant protein, mutated huntingtin triggers neuronal malfunction and loss at the cellular level. As the disease worsens, the brain becomes affected together with the striatum's initial macroscopic alterations. Since there are presently few medications that can change the course of the disease, palliative therapy, and symptom control are the cornerstone of treatment. Studying the cellular pathology and gross structural changes to the brain which occur as the illness advances have made enormous progress in recent years. There's been a substantial increase in medical studies and possible treatment options over the past ten years. The new treatments that aim to reduce amounts of mutant huntingtin are the most optimistic. However, one strategy is antisense oligonucleotide treatment, for which clinical trials are currently being conducted. These control trials might help us get another inch ahead of managing and perhaps even eliminating this nasty disease.
Indexed as
Identifiers
What OpenQuestion holds
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.