ReviewBrain sciences2020
The Significance of Tau Aggregates in the Human Brain.
Review in Brain sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed, 25 citations in OpenAlex.
- Comparing Gallyas and AT8 staining for quantification of tau pathology in subregions of the human hippocampus.Journal of neuropathology and experimental neurology · 2026Article
- Exploring the PLD1-tau interaction in Frontotemporal Dementia.bioRxiv : the preprint server for biology · 2026Article
- Chronic traumatic encephalopathy neuropathologic change in the Late Effects of Traumatic Brain Injury project: Findings in a community autopsy cohort.Journal of neuropathology and experimental neurology · 2025Article
- Interplay Between Aging and Tau Pathology in Alzheimer's Disease: Mechanisms and Translational Perspectives.Antioxidants (Basel, Switzerland) · 2025Review
- Review
- LncRNA ENST00000440246.1 Promotes Alzheimer's Disease Progression by Targeting PP2A.Biochemical genetics · 2024Article
- Effect of the ROCK inhibitor fasudil on the brain proteomic profile in the tau transgenic mouse model of Alzheimer's disease.Frontiers in aging neuroscience · 2024Article
- Brain pathology and symptoms linked to concussion history: beyond chronic traumatic encephalopathy.Brain communications · 2024Article
- Tau pathology in neurodegenerative disease: disease mechanisms and therapeutic avenues.The Journal of clinical investigation · 2023Review
- Longevity, Centenarians and Modified Cellular Proteodynamics.International journal of molecular sciences · 2023Review
- Regulation of Tau Expression in Superior Cervical Ganglion (SCG) Neurons In Vivo and In Vitro.Cells · 2023Article
- Is Pathology Always the Diagnostic Gold Standard in Neurodegeneration?Movement disorders clinical practice · 2022Article
- Article
- Synaptopathy Mechanisms in ALS Caused by C9orf72 Repeat Expansion.Frontiers in cellular neuroscience · 2021Article
- Cognitive Decline Assessment: A Review From Medical Imaging Perspective.Frontiers in aging neuroscience · 2021Review
- Unraveling the molecular links: Alzheimer's disease-induced mechanisms of memory impairment: A narrative review.Journal of Alzheimer's disease reportsReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurofibrillary degeneration has attracted the attention of neuroscientists as both a hallmark of the disease and a subject for experimentation for more than a century. Recent studies implicate phosphorylated tau (p-tau) directly in neurodegenerative disease pathogenesis, although the human data continue to raise questions. P-tau accumulates with age in a roughly hierarchical manner, but avoids abundance in the neocortex unless co-occurring with amyloid-β. Neurodegenerative tauopathies tend to have p-tau morphologies that differ from aging and Alzheimer's disease. Tau isoforms (3R vs. 4R) have a tendency to vary with tauopathy phenotype for unknown reasons. Selective vulnerability to p-tau and spatial-temporal disconnect from amyloid-β are evident in aging. P-tau assessment at autopsy involves tissue decomposition, which may skew microanatomical observations toward limited biological meaning. Two major consensus guidelines for interpreting p-tau at autopsy emphasize the challenges of clinicopathologic correlation, and reinforce the observation that regional neurodegeneration is a better correlate of clinical signs than is proteinopathy. Despite the proliferation of interesting and novel theories related to tau-mediated pathogenesis, the weight of the human observations suggests that neurofibrillary degeneration is an epiphenomenal hallmark of aging and disease rather than an epicenter of neurotoxicity. This is consistent with numerous tau-targeted therapeutic strategies that have been unsuccessful to date.
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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.