ReviewNature reviews. Neurology2018
Tau-targeting therapies for Alzheimer disease.
Review in Nature reviews. Neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 562 papers, 2 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
562 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,090 citations in OpenAlex.
- Evaluating computational and experimental approaches in early-stage Alzheimer's drug discovery: a systematic review.Journal of computer-aided molecular design · 2025Pooled it
- Targeting Protein Aggregates with Natural Products: An Optional Strategy for Neurodegenerative Diseases.International journal of molecular sciences · 2023Pooled it
- Systemic davunetide provides sex-specific neuroprotection during Coronary Artery Bypass Grafting (CABG).Translational psychiatry · 2025Trial
- Inhibition of FAM19A5 reverses synaptic loss and cognitive decline in mouse models of Alzheimer's disease.Alzheimer's research & therapy · 2025Trial
- Review
- Advances in Alzheimer's disease: mechanistic insights and therapeutic targets.Science China. Life sciences · 2026Review
- Passive amyloid-β immunotherapy in Alzheimer's disease: a multicellular clearance system beyond plaque removal.Molecular neurodegeneration · 2026Review
- Functional Implications of Marine Biosurfactants and Their Therapeutic Potential Against Alzheimer's Disease.Food science & nutrition · 2026Review
- Association of dietary copper intake with Alzheimer's disease, brain structure and cognitive function.The journal of nutrition, health & aging · 2026Article
- Article
- Dysregulation of the Tau-Microtubule-End-Binding Protein Axis in Alzheimer's Disease and Related Tauopathies.International journal of molecular sciences · 2026Review
- Review
- CMV-GLA: contrastive multi-view graph layer attention for predicting phosphorylation site-disease associations.BMC bioinformatics · 2026Article
- Targeting of kinases to treat neurodegenerative diseases.Pharmacological reviews · 2026Review
- TNMD BRICHOS domain attenuates tau pathology and memory deficits in a mouse model of tauopathy.Cell death & disease · 2026Article
- Alzheimer's disease: from molecular pathways to therapies.Molecular biomedicine · 2026Review
- Injectable anti-inflammatory, antioxidant supramolecular nanofiber hydrogel for peripheral nerve injury repair and neuropathic pain relief.Materials today. Bio · 2026Article
- Inhaled General Anesthetics in Alzheimer's Disease Progression: Divergent Effects, Underlying Mechanisms, and Future Perspectives.Molecular neurobiology · 2026Review
- Engineering a dimeric single-domain antibody for improved detection and neutralization of amyloid-β oligomers.Communications biology · 2026Article
- Brain network dynamics determine tau presence while regional vulnerability governs tau load in Alzheimer's disease.Research square · 2026Article
502 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 at 1 institution in 1 country.
Funding
Abstract
Alzheimer disease (AD) is the most common form of dementia. Pathologically, AD is characterized by amyloid plaques and neurofibrillary tangles in the brain, with associated loss of synapses and neurons, resulting in cognitive deficits and eventually dementia. Amyloid-β (Aβ) peptide and tau protein are the primary components of the plaques and tangles, respectively. In the decades since Aβ and tau were identified, development of therapies for AD has primarily focused on Aβ, but tau has received more attention in recent years, in part because of the failure of various Aβ-targeting treatments in clinical trials. In this article, we review the current status of tau-targeting therapies for AD. Initially, potential anti-tau therapies were based mainly on inhibition of kinases or tau aggregation, or on stabilization of microtubules, but most of these approaches have been discontinued because of toxicity and/or lack of efficacy. Currently, the majority of tau-targeting therapies in clinical trials are immunotherapies, which have shown promise in numerous preclinical studies. Given that tau pathology correlates better with cognitive impairments than do Aβ lesions, targeting of tau is expected to be more effective than Aβ clearance once the clinical symptoms are evident. With future improvements in diagnostics, these two hallmarks of the disease might be targeted prophylactically.
Indexed as
Identifiers
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.