ReviewNature reviews. Neuroscience2020
Amyloid-β-independent regulators of tau pathology in Alzheimer disease.
Review in Nature reviews. Neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 324 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
324 citing papers in PubMed, 5 syntheses or guidelines pooled it.
- Cognitive Intra-individual Variability in Cognitively Healthy APOE ε4 Carriers, Mild Cognitive Impairment, and Alzheimer's Disease: a Meta-analysis.Neuropsychology review · 2025Pooled it
- Repetitive transcranial magnetic stimulation for Alzheimer's disease: an overview of systematic reviews and meta-analysis.Frontiers in aging neuroscience · 2024Pooled it
- Pooled it
- The efficacy and safety of anti-Aβ agents for delaying cognitive decline in Alzheimer's disease: a meta-analysis.Frontiers in aging neuroscience · 2023Pooled it
- Genome-wide meta-analysis for Alzheimer's disease cerebrospinal fluid biomarkers.Acta neuropathologica · 2022Pooled it
- Plasma P-tau217 for detecting amyloid clearance after donanemab in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Trial
- Association between lower body temperature and increased tau pathology in cognitively normal older adults.Neurobiology of disease · 2022Trial
- Molecular Pathogenesis of Cerebral Amyloid Angiopathy in Alzheimer's Disease: The Role of the Central Fibrinolytic Cascade at the Neurovascular Unit.Molecular neurobiology · 2026Review
- Global and regional amyloid-β in explaining APOE-ε4 and sex associations with medial temporal tau: a neuropathology study.Acta neuropathologica · 2026Article
- Engineered mesenchymal stem cell-derived extracellular vesicles overexpressing miR-146a alleviate neuroinflammation in Alzheimer's disease.Neural regeneration research · 2026Article
- Prospect in Alzheimer's disease integrative therapy targeting both amyloid-beta and tau.Neural regeneration research · 2026Article
- Artificial intelligence in biomarker discovery for diseases: diagnostic and therapeutic prospects.Signal transduction and targeted therapy · 2026Review
- Virobiome-mediated regulation of microbiota-gut-brain axis signaling and neuroimmune homeostasis.Cell communication and signaling : CCS · 2026Review
- Prediction of mild cognitive impairment progression using time-sensitive multimodal biomarkers.Science advances · 2026Article
- When myelin breaks, tau aggregates - a new perspective on Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Classification of tau status with machine learning models in amyloid-positive cohorts.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- The mitochondrial unfolded protein response in human microglia disrupts neuronal-glial communication and promotes senescence.Nature neuroscience · 2026Article
- Higher baseline CSF cortisol is associated with adverse 24-month tau-related, neuroimaging, and cognitive outcomes across the Alzheimer's disease continuum.European geriatric medicine · 2026Article
- Distinct factors drive the progression of tau pathology in Alzheimer's disease.Fundamental research · 2026Review
- Choroid plexus remodeling linked to impaired CSF-mediated clearance and Alzheimer's disease progression.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
264 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
3 authors.
Funding
Abstract
The global epidemic of Alzheimer disease (AD) is worsening, and no approved treatment can revert or arrest progression of this disease. AD pathology is characterized by the accumulation of amyloid-β (Aβ) plaques and tau neurofibrillary tangles in the brain. Genetic data, as well as autopsy and neuroimaging studies in patients with AD, indicate that Aβ plaque deposition precedes cortical tau pathology. Because Aβ accumulation has been considered the initial insult that drives both the accumulation of tau pathology and tau-mediated neurodegeneration in AD, the development of AD therapeutics has focused mostly on removing Aβ from the brain. However, striking preclinical evidence from AD mouse models and patient-derived human induced pluripotent stem cell models indicates that tau pathology can progress independently of Aβ accumulation and arises downstream of genetic risk factors for AD and aberrant metabolic pathways. This Review outlines novel insights from preclinical research that implicate apolipoprotein E, the endocytic system, cholesterol metabolism and microglial activation as Aβ-independent regulators of tau pathology. These factors are discussed in the context of emerging findings from clinical pathology, functional neuroimaging and other approaches in humans. Finally, we discuss the implications of these new insights for current Aβ-targeted strategies and highlight the emergence of novel therapeutic strategies that target processes upstream of both Aβ and tau.
Indexed as
Identifiers
31780819What 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.