ReviewNature reviews. Drug discovery2011
Convergent pathogenic pathways in Alzheimer's and Huntington's diseases: shared targets for drug development.
Review in Nature reviews. Drug discovery, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.
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
34 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- GSMA: an approach to identify robust global and test Gene Signatures using Meta-Analysis.Bioinformatics (Oxford, England) · 2020Pooled it
- Common transcriptional signatures in brain tissue from patients with HIV-associated neurocognitive disorders, Alzheimer's disease, and Multiple Sclerosis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2012Pooled it
- Neurological Effects ofNutrients · 2026Article
- Therapeutic approaches targeting aging and cellular senescence in Huntington's disease.CNS neuroscience & therapeutics · 2024Review
- Carboxymethylcellulose encapsulated fingolimod, siRNA@ZnO hybrid nanocomposite as a new anti-Alzheimer's material.RSC advances · 2024Article
- Oligodendrocyte progenitor cells in Alzheimer's disease: from physiology to pathology.Translational neurodegeneration · 2023Review
- A Nanoenzyme Constructed from Manganese and Strandberg-Type Phosphomolybdate with Versatility in Antioxidant and Modulating Conformation of AInternational journal of molecular sciences · 2023Article
- Nucleic acid drug vectors for diagnosis and treatment of brain diseases.Signal transduction and targeted therapy · 2023Review
- WNT/β-catenin Pathway: a Possible Link Between Hypertension and Alzheimer's Disease.Current hypertension reports · 2022Review
- The Common Cellular Events in the Neurodegenerative Diseases and the Associated Role of Endoplasmic Reticulum Stress.International journal of molecular sciences · 2022Review
- Therapeutic drug repositioning with special emphasis on neurodegenerative diseases: Threats and issues.Frontiers in pharmacology · 2022Review
- Label-free photothermal disruption of cytotoxic aggregates rescues pathology in a C. elegans model of Huntington's disease.Scientific reports · 2021Article
- A Novel NMDA Receptor Antagonist Protects against Cognitive Decline Presented by Senescent Mice.Pharmaceutics · 2020Article
- Riluzole: a therapeutic strategy in Alzheimer's disease by targeting the WNT/β-catenin pathway.Aging · 2020Article
- An "Amyloid-β Cleaner" for the Treatment of Alzheimer's Disease by Normalizing Microglial Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Insights into Computational Drug Repurposing for Neurodegenerative Disease.Trends in pharmacological sciences · 2019Review
- Therapeutic approaches to Huntington disease: from the bench to the clinic.Nature reviews. Drug discovery · 2018Review
- Thermodynamics in Neurodegenerative Diseases: Interplay Between Canonical WNT/Beta-Catenin Pathway-PPAR Gamma, Energy Metabolism and Circadian Rhythms.Neuromolecular medicine · 2018Review
- Mitochondrial bioenergetics decay in aging: beneficial effect of melatonin.Cellular and molecular life sciences : CMLS · 2017Review
- The stress response factor daf-16/FOXO is required for multiple compound families to prolong the function of neurons with Huntington's disease.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Neurodegenerative diseases, exemplified by Alzheimer's disease and Huntington's disease, are characterized by progressive neuropsychiatric dysfunction and loss of specific neuronal subtypes. Although there are differences in the exact sites of pathology, and the clinical profiles of these two conditions only partially overlap, considerable similarities in disease mechanisms and pathogenic pathways can be observed. These shared mechanisms raise the possibility of exploiting common therapeutic targets for drug development. As Huntington's disease has a monogenic cause, it is possible to accurately identify individuals who carry the Huntington's disease mutation but do not yet manifest symptoms. These individuals could act as a model for Alzheimer's disease to test therapeutic interventions that target shared pathogenic pathways.
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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.