SynthesisBMC neurology2017
Bapineuzumab for mild to moderate Alzheimer's disease: a meta-analysis of randomized controlled trials.
Synthesis in BMC neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 5 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
45 citing papers in PubMed, 5 syntheses or guidelines pooled it, 79 citations in OpenAlex.
- Efficacy of 5 and 10 mg donepezil in improving cognitive function in patients with dementia: a systematic review and meta-analysis.Frontiers in neuroscience · 2024Pooled it
- Safety and efficacy of lecanemab for Alzheimer's disease: a systematic review and meta-analysis of randomized clinical trials.Frontiers in aging neuroscience · 2023Pooled it
- Effect of reductions in amyloid levels on cognitive change in randomized trials: instrumental variable meta-analysis.BMJ (Clinical research ed.) · 2021Pooled it
- Intravenous Immunoglobulin for Patients With Alzheimer's Disease: A Systematic Review and Meta-Analysis.American journal of Alzheimer's disease and other dementias · 2019Pooled it
- The treatment of cognitive dysfunction in dementia: a multiple treatments meta-analysis.Psychopharmacology · 2018Pooled it
- Tau and β-Amyloid Relevant Pathology as a Central Therapeutic Target in Alzheimer's Disease.Biomolecules · 2026Review
- Monoclonal antibodies and small molecules: on the cutting edge of Alzheimer's disease therapy.Frontiers in cell and developmental biology · 2026Review
- Targeting Amyloid-β Proteins as Potential Alzheimer's Disease Therapeutics: Anti-Amyloid Drug Discovery, Emerging Therapeutics, Clinical Trials and Implications for Public Health.Pharmaceuticals (Basel, Switzerland) · 2025Review
- High-affinity transferrin receptor binding improves brain delivery of bispecific antibodies at tracer dose.Fluids and barriers of the CNS · 2025Article
- Recent Advances and Future Directions in Alzheimer's Disease Genetic Research.International journal of molecular sciences · 2025Review
- Advancing Alzheimer's Disease Modelling by Developing a Refined Biomimetic Brain Microenvironment for Facilitating High-Throughput Screening of Pharmacological Treatment Strategies.International journal of molecular sciences · 2024Review
- Targeting Beta-Amyloid Protein with Monoclonal Antibodies: A New Hope for Alzheimer's Treatment.Annals of neurosciences · 2024Article
- Engineered Antibodies to Improve Efficacy against Neurodegenerative Disorders.International journal of molecular sciences · 2024Review
- Innovative Therapeutic Strategies in Alzheimer's Disease: A Synergistic Approach to Neurodegenerative Disorders.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Passive Anti-Amyloid Beta Immunotherapies in Alzheimer's Disease: From Mechanisms to Therapeutic Impact.Biomedicines · 2024Review
- Review on anti-alzheimer drug development: approaches, challenges and perspectives.RSC advances · 2024Review
- Lecanemab: More Questions Than Answers!Clinical drug investigation · 2024Review
- Review
- Intranasal Drug Delivery by Nanotechnology: Advances in and Challenges for Alzheimer's Disease Management.Pharmaceutics · 2023Review
- ImmunoPET imaging of amyloid-beta in a rat model of Alzheimer's disease with a bispecific, brain-penetrating fusion protein.Translational neurodegeneration · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlzheimer's disease (AD) is a globally prevalent neurodegenerative condition, clinically characterized by progressive memory loss and gradual impairment of cognitive functions. Bapineuzumab is a fully humanized monoclonal antibody that binds to neurotoxic amyloid proteins in the brain, enhancing their clearance. We performed this systematic review and meta-analysis to evaluate the safety and efficacy of bapineuzumab in patients with mild to moderate Alzheimer's disease.
methodsWe performed a web-based literature search of PubMed, Ovid, EBSCO, Scopus, Embase, Cochrane CENTRAL, and web of science using the relevant keywords. Data were extracted from eligible records and pooled as mean difference (MD) or risk ratio (RR) values with their 95% confidence interval (CI), using Review Manager software (version 5.3 for windows). Heterogeneity was measured by Chi-square and I-square tests.
resultThe pooled effect estimate from six randomized clinical trials (n = 2380) showed that bapineuzumab significantly reduced the cerebrospinal fluid concentration of phosphorylated tau proteins (Standardized MD = -5.53, 95% CI [-8.29, -2.76]). However, the bapineuzumab group was not superior to the placebo group in terms of change from baseline in Alzheimer's disease assessment scale (ADAS)-Cog11 (MD = 0.14, 95% CI [-0.72, 0.99]), disability assessment for dementia (DAD) scale (MD = 1.35, 95% CI [-1.74, 4.43]), and mini-mental state examination (MMSE) scores (MD = 0.08, 95% CI [-0.31, 0.47]). Regarding safety, bapineuzumab increased the risk of serious treatment-emergent adverse events (RR = 1.18, 95% CI [1.02, 1.37]) and cerebral vasogenic edema (RR = 40.88, 95% CI [11.94, 135.95]). All bapineuzumab doses (0.15, 0.5, 1, and 2 mg/kg) were similar to placebo in terms of change from baseline in ADAS-cog11, DAD, and MMSE scores, except for the 0.15 mg/kg dose, which caused a significant worsening on the ADAS-cog11 scale (MD = 5.6, 95% CI [0.22, 10.98]).
conclusionsConsidering the lack of clinical efficacy, combined with the significant association with serious adverse events, bapineuzumab should not be used to treat patients with mild to moderate AD. Future studies should investigate the effect of combining bapineuzumab with other therapeutic strategies and reevaluate the efficacy of targeting amyloid β proteins in AD therapy.
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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.