ReviewNature protocols2026
Three-dimensional direct neuronal reprogramming for modeling Alzheimer's disease neuropathology.
Review in Nature protocols, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed.
- Transcriptomic Challenges We Faced with Animal Models for Neurological Disorders.Current issues in molecular biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Late-onset Alzheimer's disease (LOAD) accounts for over 95% of Alzheimer's disease (AD) cases. However, modeling the age-dependent neuropathological hallmarks of LOAD has remained a major challenge. We recently developed a patient-based, three-dimensional (3D) neuronal culture system that endogenously recapitulates key neuropathological features of AD, including extracellular Aβ deposition, tau dysregulation and spontaneous neuronal death. This platform uses high-efficiency, microRNA- and chromatin-based direct somatic reprogramming of fibroblasts from patients with autosomal dominant AD or LOAD to cortical neurons in 3D thin gel (3D-CNs) or self-assembled neuronal spheroids. Here we provide stepwise instructions for generating 3D-CNs and cortical spheroids via neuronal reprogramming of patient fibroblasts, along with methods for analyzing downstream AD neuropathology. Within 3 weeks, fibroblasts are reprogrammed into neurons under either thin-gel or spheroid conditions. By 4 weeks, key AD neuropathology, such as Aβ deposition, tau dysregulation, and neuronal death, can be detected in AD neurons. This system provides an age-relevant, patient-specific neuronal model for investigating molecular events underlying AD-associated neurodegeneration and evaluating compounds or gene targets in the context of potential personalized therapeutic interventions. Successful implementation of this protocol requires prior experience in mammalian cell culture, plasmid preparation, lentiviral production and standard confocal imaging techniques.
Identifiers
42270887What 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.