ArticleThe American journal of pathology1998
Identification of septins in neurofibrillary tangles in Alzheimer's disease.
Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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
69 citing papers in PubMed, 158 citations in OpenAlex.
- A functional role for Septin-2 in the maintenance of the axon initial segment and in human cognitive development.Brain : a journal of neurology · 2026Article
- RNA isoform diversity, splicing variants and switching in single cells of the Alzheimer's disease brain.Communications biology · 2026Article
- Localization and function of septins are susceptible to epitope tagging.Molecular biology of the cell · 2025Article
- RNA isoform diversity, splicing variants, and switching in single cells of the Alzheimer's disease brain.Research square · 2025Article
- Localization and function of septins are susceptible to epitope tagging.bioRxiv : the preprint server for biology · 2025Article
- Pharmacological modulation of septins restores calcium homeostasis and is neuroprotective in models of Alzheimer's disease.Science (New York, N.Y.) · 2024Article
- Investigation of the shared biological mechanisms and common biomarker APTAF1 of sleep deprivation and mild cognitive impairment using integrated bioinformatics analysis.Frontiers in pharmacology · 2024Article
- Review
- Molecular Pathways Involved in Frontotemporal Lobar Degeneration with TDP-43 Proteinopathy: What Can We Learn from Proteomics?International journal of molecular sciences · 2021Review
- Synaptic tau: A pathological or physiological phenomenon?Acta neuropathologica communications · 2021Review
- Septins, a cytoskeletal protein family, with emerging role in striated muscle.Journal of muscle research and cell motility · 2021Review
- Article
- The Structural Biology of Septins and Their Filaments: An Update.Frontiers in cell and developmental biology · 2021Review
- Biochemical and morphological characterization of SEPT1 in mouse brain.Medical molecular morphology · 2020Article
- Synaptic mitochondrial dysfunction and septin accumulation are linked to complement-mediated synapse loss in an Alzheimer's disease animal model.Cellular and molecular life sciences : CMLS · 2020Article
- Septin 2/6/7 complexes tune microtubule plus-end growth and EB1 binding in a concentration- and filament-dependent manner.Molecular biology of the cell · 2019Article
- coMethDMR: accurate identification of co-methylated and differentially methylated regions in epigenome-wide association studies with continuous phenotypes.Nucleic acids research · 2019Article
- A blueprint of septin expression in human tissues.Functional & integrative genomics · 2019Article
- Proteomic analysis of the effect of the polyphenol pentagalloyl glucose on proteins involved in neurodegenerative diseases in activated BV‑2 microglial cells.Molecular medicine reports · 2019Article
- Septin-2 is overexpressed in epithelial ovarian cancer and mediates proliferation via regulation of cellular metabolic proteins.Oncotarget · 2019Article
9 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
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Septins are evolutionarily conserved cytoskeletal GTPases that can form heteropolymer complexes involved in cytokinesis and other cellular processes. We detected expression of the human septin genes Nedd5, H5, Diff6, and hCDC100 in postmortem brain tissues using the reverse transcription-coupled polymerase chain reaction and their products by immunoblot analysis. Four antibodies directed against three septins, Nedd5, H5, and Diff6, consistently labeled neurofibrillary tangles, neuropil threads, and dystrophic neurites in the senile plaques in brains affected by Alzheimer's disease but did not label obvious structures in young control brains. Immunoelectron microscopy revealed that Nedd5 localized to the paired helical filaments. Pre-tangles, the precursory granular deposits that accumulate in the neuronal cytoplasm, also were labeled with the antibodies. These findings suggest that at least the three septins are associated with tau-based paired helical filament core, and may contribute to the formation of neurofibrillary tangle as integral constituents of paired helical filaments.
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.