ArticleBrain : a journal of neurology2024
A cell autonomous regulator of neuronal excitability modulates tau in Alzheimer's disease vulnerable neurons.
Article in Brain : a journal of neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed.
- When Pathologies Collide: The Intersection of Tau and Alpha-Synuclein in Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- DEK Loss Induces Task-specific Deficits in Learning and Memory and Reprograms the Hippocampal Transcriptome in Mice.Molecular neurobiology · 2026Article
- Mapping cross-domain drivers of Alzheimer's disease risk through integrated network analysis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Optineurin is a gatekeeper of mitochondrial health and proteostasis in Alzheimer's disease vulnerable neurons.bioRxiv : the preprint server for biology · 2026Article
- All hands on DEK: structural insights into a unique histone modifier and chromatin remodeler.Epigenetics & chromatin · 2026Review
- Diverse Effects of Various Toll-Like Receptor 2 Ligands on Neuronal Activity and Cell Death.Cellular and molecular neurobiology · 2025Article
- Dek Loss Induces Sex-Dependent, Task-Specific Cognitive Deficits and Reprograms the Hippocampal Transcriptome in Mice.Research square · 2025Article
- Mapping cross-domain drivers of Alzheimer's disease risk through integrated network analysis.bioRxiv : the preprint server for biology · 2025Article
- Disentangling associations between complex traits and cell types with seismic.Nature communications · 2025Article
- DEK promotes mammary hyperplasia and is associated with H3K27me3 epigenetic modifications.Life science alliance · 2025Article
- DEK-nucleosome structure shows DEK modulates H3K27me3 and stem cell fate.Nature structural & molecular biology · 2025Article
- Cell-death pathways and tau-associated neuronal vulnerability in Alzheimer's disease.Cell reports · 2025Article
- Anterior-temporal network hyperconnectivity is key to Alzheimer's disease: from ageing to dementia.Brain : a journal of neurology · 2025Article
- Cell-type specific profiling of human entorhinal cortex at the onset of Alzheimer's disease neuropathology.bioRxiv : the preprint server for biology · 2025Article
- Central role of brain regulatory T cells in the inflammatory cascade in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Neurons from layer II of the entorhinal cortex (ECII) are the first to accumulate tau protein aggregates and degenerate during prodromal Alzheimer's disease. Gaining insight into the molecular mechanisms underlying this vulnerability will help reveal genes and pathways at play during incipient stages of the disease. Here, we use a data-driven functional genomics approach to model ECII neurons in silico and identify the proto-oncogene DEK as a regulator of tau pathology. We show that epigenetic changes caused by Dek silencing alter activity-induced transcription, with major effects on neuronal excitability. This is accompanied by the gradual accumulation of tau in the somatodendritic compartment of mouse ECII neurons in vivo, reactivity of surrounding microglia, and microglia-mediated neuron loss. These features are all characteristic of early Alzheimer's disease. The existence of a cell-autonomous mechanism linking Alzheimer's disease pathogenic mechanisms in the precise neuron type where the disease starts provides unique evidence that synaptic homeostasis dysregulation is of central importance in the onset of tau pathology in Alzheimer's disease.
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.