ReviewNature reviews. Neurology2024
Is Alzheimer disease a disease?
Review in Nature reviews. Neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis 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
95 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Sleep characteristics and risk of Alzheimer's disease: a systematic review and meta-analysis of longitudinal studies.Journal of neurology · 2024Pooled it
- Atypical Alzheimer disease: a multi-axis framework toward defining heterogeneity.Nature reviews. Neurology · 2026Review
- Data-driven modeling of spatiotemporal dynamics using multimodal imaging data.PLoS computational biology · 2026Article
- Circadian rhythms and chronotherapy in Alzheimer's disease: Mechanisms and therapeutic implications.Neuroprotection (Chichester, England) · 2026Review
- Integrated multi-omics analysis identifies potential therapeutic targets for Alzheimer's disease.Neural regeneration research · 2026Article
- Single-cell multiomics connects 3D genome and transcriptome alterations in Alzheimer's disease.Science (New York, N.Y.) · 2026Article
- Development of a Novel AAV-Mediated microRNA Gene Therapy for Spatial Suppression of BACE1 to Improve Cognitive Function in Alzheimer's Disease Model Mice.Biomolecules · 2026Article
- Translational potential of medicinal plants for Alzheimer's disease: integrated evidence from molecular mechanisms to preclinical and clinical findings.Natural products and bioprospecting · 2026Review
- Regional mapping of CSF1R-positive microglia in neurodegenerative diseases and progressive MS, with exploratory presynaptic marker analyses.Journal of neuroinflammation · 2026Article
- Proteomics of post mortem brains in early- and late-onset Alzheimer's disease: Unraveling differential Aβ effects and potential AD biomarkers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- The Monomeric Conformational Ensembles of Aβ40 and Aβ42 Encode Their Differential Amyloid Aggregation Propensity.The journal of physical chemistry. B · 2026Article
- Retrospective case-control study of pre-diagnosis observational and prescription data in Parkinson's disease.Scientific reports · 2026Observational
- The past, present, and future of Alzheimer's disease-part 3: the future.Arquivos de neuro-psiquiatria · 2026Review
- Provider and patient perspectives on the diagnosis and treatment of Alzheimer's disease: A global perspective from the Global Alzheimer's Leadership Series (GoALS).Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Rhamnazin attenuates Amyloid β-Peptide (1-42) induced spatial memory impairments by modulation of BDNF-ERK signaling pathway.3 Biotech · 2026Article
- Plant-mediated green nanoparticles: combining nanometal and biometabolite potential for Alzheimer's treatment.Biomedical engineering online · 2026Review
- Molecular Mechanisms Underlying Alzheimer's Disease Pathogenesis: Comprehensive Overview.International journal of molecular sciences · 2026Review
- Pooling Alzheimer's disease: when methodological rigor risks obscuring biological complexity.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
- L-Leucine Upregulates Lysosomal Biogenesis and Autophagy to Lower Plaques in 5XFAD Mouse Model of Alzheimer's Disease.Journal of neurochemistry · 2026Article
- Modulation of Tau Protein Neurotoxic Hallmarks by Novel σChemMedChem · 2026Article
35 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Dementia, a prevalent condition among older individuals, has profound societal implications. Extensive research has resulted in no cure for what is perceived as the most common dementing illness: Alzheimer disease (AD). AD is defined by specific brain abnormalities - amyloid-β plaques and tau protein neurofibrillary tangles - that are proposed to actively influence the neurodegenerative process. However, conclusive evidence of amyloid-β toxicity is lacking, the mechanisms leading to the accumulation of plaques and tangles are unknown, and removing amyloid-β has not halted neurodegeneration. So, the question remains, are we making progress towards a solution? The complexity of AD is underscored by numerous genetic and environmental risk factors, and diverse clinical presentations, suggesting that AD is more akin to a syndrome than to a traditional disease, with its pathological manifestation representing a convergence of pathogenic pathways. Therefore, a solution requires a multifaceted approach over a single 'silver bullet'. Improved recognition and classification of conditions that converge in plaques and tangle accumulation and their treatment requires the use of multiple strategies simultaneously.
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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.