ArticleBMC neurology2014
Moving beyond anti-amyloid therapy for the prevention and treatment of Alzheimer's disease.
Article in BMC neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed.
- A phase II randomized trial of sodium oligomannate in Alzheimer's dementia.Alzheimer's research & therapy · 2020Trial
- Newer Therapeutic Approaches in Treating Alzheimer's Disease: A Comprehensive Review.ACS omega · 2025Review
- AD and non-AD mediators of the pathway between the APOE genotype and cognition.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- Transcriptional changes in the rat brain induced by repetitive transcranial magnetic stimulation.Frontiers in human neuroscience · 2023Article
- Neuroprotection ofFrontiers in pharmacology · 2022Article
- Multifaceted Alzheimer's Disease: Building a Roadmap for Advancement of Novel Therapies.Neurochemical research · 2021Review
- Loss of APP in mice increases thigmotaxis and is associated with elevated brain expression of IL-13 and IP-10/CXCL10.Physiology & behavior · 2021Article
- Article
- Reciprocal Predictive Relationships between Amyloid and Tau Biomarkers in Alzheimer's Disease Progression: An Empirical Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Relation of Serum Plasmalogens andBrain sciences · 2019Article
- Exploiting microglial and peripheral immune cell crosstalk to treat Alzheimer's disease.Journal of neuroinflammation · 2019Review
- Questions concerning the role of amyloid-β in the definition, aetiology and diagnosis of Alzheimer's disease.Acta neuropathologica · 2018Review
- Association between Alzheimer's disease pathogenesis and early demyelination and oligodendrocyte dysfunction.Neural regeneration research · 2018Article
- PSEN1 Mutant iPSC-Derived Model Reveals Severe Astrocyte Pathology in Alzheimer's Disease.Stem cell reports · 2017Article
- Development of proteolytically stable N-methylated peptide inhibitors of aggregation of the amylin peptide implicated in type 2 diabetes.Interface focus · 2017Article
- Inhibition of IKKβ by celastrol and its analogues - an in silico and in vitro approach.Pharmaceutical biology · 2017Article
- Increased localization of APP-C99 in mitochondria-associated ER membranes causes mitochondrial dysfunction in Alzheimer disease.The EMBO journal · 2017Article
- Cellular hormetic response to 27-hydroxycholesterol promotes neuroprotection through AICD induction of MAST4 abundance and kinase activity.Scientific reports · 2017Article
- Dihydropyrimidine-Thiones and Clioquinol Synergize To Target β-Amyloid Cellular Pathologies through a Metal-Dependent Mechanism.ACS chemical neuroscience · 2017Article
- Aging alters mRNA expression of amyloid transporter genes at the blood-brain barrier.Neurobiology of aging · 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
No grant is acknowledged in the PubMed record.
Abstract
backgroundHigh-profile Phase 3 clinical trials of bapineuzumab and solanezumab, antibodies targeted at amyloid-beta (Aβ) removal, have failed to meet their primary endpoints. Neither drug improves clinical outcomes in patients with late onset AD, joining a long list of unsuccessful attempts to treat AD with anti-amyloid therapies. DISCUSSION: These therapies are based on the assumption that Aβ accumulation is the primary pathogenic trigger of AD. Current evidence suggests that Aβ may actually accumulate as part of an adaptive response to long-term chronic brain stress stimuli that would make more suitable candidates for therapeutic intervention. SUMMARY: At this juncture it is no longer unreasonable to suggest that further iterations of anti-Aβ therapies should be halted. Clinicians and researchers should instead direct their attention toward greater understanding of the biological function of Aβ both in healthy and demented brains, as well as the involvement of long-term chronic exposure to stress in the etiology 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.