ArticleAlzheimer's & dementia (New York, N. Y.)2016
NPT088 reduces both amyloid-β and tau pathologies in transgenic mice.
Article in Alzheimer's & dementia (New York, N. Y.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03008161 (A Phase 1 Randomized, Double-Blind, Placebo-Controlled, Multiple Dose, Dose Escalation Study of NPT088 in Patients With Probable Alzheimer's Disease), which is not on this 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.
A Phase 1 Randomized, Double-Blind, Placebo-Controlled, Multiple Dose, Dose Escalation Study of NPT088 in Patients With Probable Alzheimer's Disease
Who cites it
20 citing papers in PubMed, 45 citations in OpenAlex.
- Targeting protein aggregate co-pathologies in neurodegeneration: a viable therapeutic strategy?Molecular neurodegeneration advances · 2026Review
- Alpha-Synuclein Neurobiology in Parkinson's Disease: A Comprehensive Review of Its Role, Mechanisms, and Therapeutic Perspectives.Brain sciences · 2025Review
- Differential roles of human tau isoforms in the modulation of inflammation and development of neuropathology.Neurobiology of disease · 2025Article
- Immunization targeting diseased proteins in synucleinopathy and tauopathy: insights from clinical trials.Translational neurodegeneration · 2025Review
- Emerging perspectives on precision therapy for Parkinson's disease: multidimensional evidence leading to a new breakthrough in personalized medicine.Frontiers in aging neuroscience · 2024Review
- Testing the amyloid cascade hypothesis: Prevention trials in autosomal dominant Alzheimer disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- Alpha-Synuclein Aggregation Pathway in Parkinson's Disease: Current Status and Novel Therapeutic Approaches.Cells · 2022Review
- Emerging Therapeutic Strategies for Parkinson's Disease and Future Prospects: A 2021 Update.Biomedicines · 2022Review
- Therapeutics in the Pipeline TargetingPharmacological reviews · 2022Review
- Small molecules to perform big roles: The search for Parkinson's and Huntington's disease therapeutics.Frontiers in neuroscience · 2022Review
- Feasibility of short imaging protocols for [European journal of nuclear medicine and molecular imaging · 2021Article
- Tau in Alzheimer's Disease: Pathological Alterations and an Attractive Therapeutic Target.Current medical science · 2020Review
- Passive immunotherapies targeting Aβ and tau in Alzheimer's disease.Neurobiology of disease · 2020Review
- Advances and considerations in AD tau-targeted immunotherapy.Neurobiology of disease · 2020Review
- Current and Future Treatments in Alzheimer Disease: An Update.Journal of central nervous system disease · 2020Review
- Novel approaches to counter protein aggregation pathology in Parkinson's disease.Progress in brain research · 2020Review
- Modulation of Disordered Proteins with a Focus on Neurodegenerative Diseases and Other Pathologies.International journal of molecular sciences · 2019Review
- Emerging disease-modifying strategies targeting α-synuclein for the treatment of Parkinson's disease.British journal of pharmacology · 2018Review
- Precision pharmacology for Alzheimer's disease.Pharmacological research · 2018Review
- Designer protein disaggregases to counter neurodegenerative disease.Current opinion in genetics & development · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAlzheimer's disease (AD) is characterized by appearance of both extracellular senile plaques and intracellular neurofibrillary tangles, comprised of aggregates of misfolded amyloid-β (Aβ) and hyper-phosphorylated tau, respectively. In a previous study, we demonstrated that g3p, a capsid protein from bacteriophage M13, binds to and remodels misfolded aggregates of proteins that assume an amyloid conformation. We engineered a fusion protein ("NPT088") consisting of the active fragment of g3p and human-IgG
methodsAged Tg2576 mice or rTg4510 mice received NPT088 weekly via IP injection. Cognitive and/or functional motor endpoints were monitored during dosing. Pathology was quantified biochemically and immunohistochemically.
resultsNPT088-lowered Aβ plaque and improved cognitive performance of aged Tg2576 mice. Moreover, NPT088 reduced phospho-tau pathology, reduced brain atrophy, and improved cognition in rTg4510 mice. DISCUSSION: These observations establish NPT088 as a novel therapeutic approach and potential drug class that targets both Aβ and tau, the hallmark pathologies of AD.
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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.