ReviewCNS drugs2015
Alzheimer's Disease: Lessons Learned from Amyloidocentric Clinical Trials.
Review in CNS drugs, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed.
- Short-chain fatty acid-producing commensals: Key modulators of AD neuroinflammation via the microbiota-gut-brain axis.Current research in microbial sciences · 2026Review
- Transcriptomic and glycomic analyses highlight pathway-specific glycosylation alterations unique to Alzheimer's disease.Scientific reports · 2023Article
- Next-generation antibody-based therapies in neurology.Brain : a journal of neurology · 2022Review
- Retinal arteriolar parameters as a surrogate marker of intracranial vascular pathology.Alzheimer's & dementia (Amsterdam, Netherlands) · 2022Article
- MMP9 modulation improves specific neurobehavioral deficits in a mouse model of Alzheimer's disease.BMC neuroscience · 2021Article
- Integrative glycoproteomics reveals protein N-glycosylation aberrations and glycoproteomic network alterations in Alzheimer's disease.Science advances · 2020Article
- β-Asarone improves learning and memory in AβMetabolic brain disease · 2020Article
- Augmentation of Bri2 molecular chaperone activity against amyloid-β reduces neurotoxicity in mouse hippocampus in vitro.Communications biology · 2020Article
- Early Preclinical Changes in Hippocampal CREB-Binding Protein Expression in a Mouse Model of Familial Alzheimer's Disease.Molecular neurobiology · 2018Article
- Integrated proteomics and network analysis identifies protein hubs and network alterations in Alzheimer's disease.Acta neuropathologica communications · 2018Article
- Memantine for the Treatment of Dementia: A Review on its Current and Future Applications.Journal of Alzheimer's disease : JAD · 2018Review
- Drug discovery effectiveness from the standpoint of therapeutic mechanisms and indications.Nature reviews. Drug discovery · 2018Review
- Antibody Engineering for Optimized Immunotherapy in Alzheimer's Disease.Frontiers in neuroscience · 2018Review
- Article
- Tracking progressive pathological and functional decline in the rTg4510 mouse model of tauopathy.Alzheimer's research & therapy · 2017Article
- Evidence that the Human Innate Immune Peptide LL-37 may be a Binding Partner of Amyloid-β and Inhibitor of Fibril Assembly.Journal of Alzheimer's disease : JAD · 2017Article
- Antioxidants and Dementia Risk: Consideration through a Cerebrovascular Perspective.Nutrients · 2016Review
- Tau downregulates BDNF expression in animal and cellular models of Alzheimer's disease.Neurobiology of aging · 2016Article
- Deletion of Neurotrophin Signaling through the Glucocorticoid Receptor Pathway Causes Tau Neuropathology.Scientific reports · 2016Article
- Defective Transcytosis of APP and Lipoproteins in Human iPSC-Derived Neurons with Familial Alzheimer's Disease Mutations.Cell reports · 2016Article
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
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is one of the most debilitating neurodegenerative diseases and is predicted to affect 1 in 85 people by 2050. Despite much effort to discover a therapeutic strategy to prevent progression or to cure AD, to date no effective disease-modifying agent is available that can prevent, halt, or reverse the cognitive and functional decline of patients with AD. Several underlying etiologies to this failure are proposed. First, accumulating evidence from past trials suggests a preventive as opposed to therapeutic paradigm, and the precise temporal and mechanistic relationship of β-amyloid (Aβ) and tau protein should be elucidated to confirm this hypothesis. Second, we are in urgent need of revised diagnostic criteria to support future trials. Third, various technical and methodological improvements are required, based on the lessons learned from previous failed trials.
Indexed as
Identifiers
26187557What 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.