ReviewLaboratory investigation; a journal of technical methods and pathology2019
MAPT mutations, tauopathy, and mechanisms of neurodegeneration.
Review in Laboratory investigation; a journal of technical methods and pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 245 papers, 3 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
245 citing papers in PubMed, 3 syntheses or guidelines pooled it, 390 citations in OpenAlex.
- The relationship between total tau protein, phosphorylated tau protein, schizophrenia and bipolar disorder: a systematic review and meta-analysis.Frontiers in psychiatry · 2026Pooled it
- Systematic Review on Neurotoxic Implications of Lead-Induced Gene Expression Alterations in the Etiology of Alzheimer's Disease.Cellular and molecular neurobiology · 2025Pooled it
- The Genetic Architecture of the Human Corpus Callosum and its Subregions.Nature communications · 2025Pooled it
- A frontotemporal dementia-like phenotype in schizophrenia: links to striatal dopamine and iron accumulation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Observational
- Structural Hierarchy and Maturation of Amyloid Fibrils Revealed by Interface Descriptor Analysis.Journal of chemical information and modeling · 2026Article
- Beyond Targeted Gene Panels: Whole-Exome Sequencing as a Strategic Platform for Precision Therapeutics in Alzheimer's Disease.Life (Basel, Switzerland) · 2026Review
- Genetic frontotemporal degeneration across the lifespan? A critical appraisal of the neurodevelopmental hypothesis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Neuroinflammation in Alzheimer's and Parkinson's diseases: pathogenic mechanisms and therapeutic strategies.Translational neurodegeneration · 2026Review
- MAPT-derived circTau6 induces tau pathogenesis and neurodegeneration by encoding Tau variants.Molecular psychiatry · 2026Article
- Microtubule-Associated Proteins: From Dynamic Regulation of Microtubules to Cellular Architecture.Cells · 2026Review
- Tau-mediated Mechanisms in Alzheimer's Disease Pathogenesis.Molecular neurobiology · 2026Review
- Patient-derived tau-seeded human neuronal chimeras recapitulate mature Alzheimer's tau pathology and uncover human-specific neuronal vulnerability.bioRxiv : the preprint server for biology · 2026Article
- Cholesterol at the Center of Alzheimer's Disease: A Unifying Hypothesis on the Pathogenic Mechanism.Molecules (Basel, Switzerland) · 2026Review
- Mutation-specific neuropathologic signatures in MAPT-associated frontotemporal lobar degeneration.Acta neuropathologica · 2026Article
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- Selection-guided discovery in South Asians implicates the MAPT locus in insulin resistance.medRxiv : the preprint server for health sciences · 2026Article
- iSCORE-PD: an isogenic stem cell collection to research Parkinson's disease.Nature communications · 2026Article
- Considerations for the selection and phenotyping of mouse models for the study of Alzheimer's disease.STAR protocols · 2026Review
- Shared genetic architecture of psychiatric disorders and ocular diseases: Evidence from genome-wide analyses.IBRO neuroscience reports · 2026Article
- Emerging directions in tauopathy research.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
185 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 at 1 institution in 1 country.
Funding
Abstract
In multiple neurodegenerative diseases, including Alzheimer's disease (AD), a prominent pathological feature is the aberrant aggregation and inclusion formation of the microtubule-associated protein tau. Because of the pathological association, these disorders are often referred to as tauopathies. Mutations in the MAPT gene that encodes tau can cause frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17), providing the clearest evidence that tauopathy plays a causal role in neurodegeneration. However, large gaps in our knowledge remain regarding how various FTDP-17-linked tau mutations promote tau aggregation and neurodegeneration, and, more generally, how the tauopathy is linked to neurodegeneration. Herein, we review what is known about how FTDP-17-linked pathogenic MAPT mutations cause disease, with a major focus on the prion-like properties of wild-type and mutant tau proteins. The hypothesized mechanisms by which mutations in the MAPT gene promote tauopathy are quite varied and may not provide definitive insights into how tauopathy arises in the absence of mutation. Further, differences in the ability of tau and mutant tau proteins to support prion-like propagation in various model systems raise questions about the generalizability of this mechanism in various tauopathies. Notably, understanding the mechanisms of tauopathy induction and spread and tau-induced neurodegeneration has important implications for tau-targeting therapeutics.
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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.