ReviewInternational journal of molecular sciences2023
New Pathways Identify Novel Drug Targets for the Prevention and Treatment of Alzheimer's Disease.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 35 citations in OpenAlex.
- Proteomics research in aging: a bibliometric and visualized analysis of evolution and emerging trends (1998-2024 and early 2025).Biogerontology · 2025Article
- Adenylate kinase 5, a novel genetic risk factor for Alzheimer's disease, regulates microglial inflammatory activation.Molecular brain · 2025Article
- Multi-omics exploration of chaperone-mediated immune-proteostasis crosstalk in vascular dementia and identification of diagnostic biomarkers.Frontiers in immunology · 2025Article
- New Sulfonate Ester-Linked Fluorinated Hydrazone Derivatives as Multitarget Carbonic Anhydrase and Cholinesterase Inhibitors: Design, Synthesis, Biological Evaluation, Molecular Docking and ADME Analysis.Chemistry & biodiversity · 2024Article
- Recent advances in therapeutic strategies for Alzheimer's and Parkinson's disease using protein/peptide co-modified polymer nanoparticles.Neuroprotection (Chichester, England) · 2024Review
- Novel Therapeutic Strategies in Alzheimer's Disease: Pitfalls and Challenges of Anti-Amyloid Therapies and Beyond.Journal of clinical medicine · 2024Review
- CoQAntioxidants (Basel, Switzerland) · 2024Review
- Genetic Predisposition for White Matter Hyperintensities and Risk of Mild Cognitive Impairment and Alzheimer's Disease: Results from the HELIAD Study.Current issues in molecular biology · 2024Article
- Neurodegenerative Disease: From Molecular Basis to Therapy.International journal of molecular sciences · 2024Article
- Artificial Intelligence in Eye Movements Analysis for Alzheimer's Disease Early Diagnosis.Current Alzheimer research · 2024Review
- Recombinant Antibody Fragments for Neurological Disorders: An Update.Current neuropharmacology · 2024Review
- Role of oxidative stress in neurodegenerative disorders: a review of reactive oxygen species and prevention by antioxidants.Brain communications · 2024Review
- Stem cell therapy in Alzheimer's disease: current status and perspectives.Frontiers in neuroscience · 2024Review
- Effectiveness and Safety of Shenxiong Huanglian Detoxification Granule Combined with Donepezil for the Treatment of Alzheimer's Disease: Study Protocol for a Multicenter, Pragmatic, Randomized Controlled Clinical Trial.International journal of general medicine · 2024Article
- Neuroprotective Effects of N-methyl-(2S, 4R)-trans-4-hydroxy-L-proline (NMP) against Amyloid-β-Induced Alzheimer's Disease Mouse Model.Nutrients · 2023Article
- Genome-Wide Epistasis Study of Cerebrospinal Fluid Hyperphosphorylated Tau in ADNI Cohort.Genes · 2023Article
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 at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is an incurable, progressive neurodegenerative disorder. AD is a complex and multifactorial disease that is responsible for 60-80% of dementia cases. Aging, genetic factors, and epigenetic changes are the main risk factors for AD. Two aggregation-prone proteins play a decisive role in AD pathogenesis: β-amyloid (Aβ) and hyperphosphorylated tau (pTau). Both of them form deposits and diffusible toxic aggregates in the brain. These proteins are the biomarkers of AD. Different hypotheses have tried to explain AD pathogenesis and served as platforms for AD drug research. Experiments demonstrated that both Aβ and pTau might start neurodegenerative processes and are necessary for cognitive decline. The two pathologies act in synergy. Inhibition of the formation of toxic Aβ and pTau aggregates has been an old drug target. Recently, successful Aβ clearance by monoclonal antibodies has raised new hopes for AD treatments if the disease is detected at early stages. More recently, novel targets, e.g., improvements in amyloid clearance from the brain, application of small heat shock proteins (Hsps), modulation of chronic neuroinflammation by different receptor ligands, modulation of microglial phagocytosis, and increase in myelination have been revealed in AD research.
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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.