ReviewNature reviews. Neurology2023
Neural cell state shifts and fate loss in ageing and age-related diseases.
Review in Nature reviews. Neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 27 citations in OpenAlex.
- Global StationaryOT: trajectory inference for aging time courses of single-cell snapshots.Bioinformatics (Oxford, England) · 2026Article
- Coordinated transcriptional shifts in microglia and oligodendrocytes from neurodevelopment to inflammaging.npj aging · 2026Article
- PCSK9 in bridging metabolism and neurodegeneration: a new paradigm for alzheimer's treatment.Metabolic brain disease · 2026Review
- C1q drives neural stem cell quiescence by regulating cell cycle and metabolism through BAI1.Nature communications · 2025Article
- Exploring the pharmacological mechanisms and therapeutic implications of galangin against neurological disorders.Pharmacological reports : PR · 2025Review
- Zebrafish optic nerve injury results in systemic retinal ganglion cell dedifferentiation.PLoS genetics · 2025Article
- Systematic transcriptomics analysis of calorie restriction and rapamycin unveils their synergistic interaction in prolonging cellular lifespan.Communications biology · 2025Article
- Ferroptosis in neurodegenerative diseases: mechanisms and therapeutic potential of stem cell derivatives.Frontiers in cell and developmental biology · 2025Review
- A cellular identity crisis? Plasticity changes during aging and rejuvenation.Genes & development · 2024Review
- The role of cellular senescence in neurodegenerative diseases.Archives of toxicology · 2024Review
- Canalizing cell fate by transcriptional repression.Molecular systems biology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Most age-related neurodegenerative diseases remain incurable owing to an incomplete understanding of the disease mechanisms. Several environmental and genetic factors contribute to disease onset, with human biological ageing being the primary risk factor. In response to acute cellular damage and external stimuli, somatic cells undergo state shifts characterized by temporal changes in their structure and function that increase their resilience, repair cellular damage, and lead to their mobilization to counteract the pathology. This basic cell biological principle also applies to human brain cells, including mature neurons that upregulate developmental features such as cell cycle markers or glycolytic reprogramming in response to stress. Although such temporary state shifts are required to sustain the function and resilience of the young human brain, excessive state shifts in the aged brain might result in terminal fate loss of neurons and glia, characterized by a permanent change in cell identity. Here, we offer a new perspective on the roles of cell states in sustaining health and counteracting disease, and we examine how cellular ageing might set the stage for pathological fate loss and neurodegeneration. A better understanding of neuronal state and fate shifts might provide the means for a controlled manipulation of cell fate to promote brain resilience and repair.
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.