ArticleCell2024
Single-cell dissection of the human motor and prefrontal cortices in ALS and FTLD.
Article in Cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
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Who cites it
63 citing papers in PubMed, 82 citations in OpenAlex.
- Vascular profiling of the spinal cord and cortex reveals region-specific endothelial dysfunction and fibroblast remodeling in human ALS.Acta neuropathologica communications · 2026Article
- Distinct cellular phenotypes of language and executive decline in amyotrophic lateral sclerosis.Cell · 2026Article
- Motor dysfunction phenotypes in a drosophila model validate DAO as an ALS gene.Human molecular genetics · 2026Article
- Selective vulnerability and resilience of thalamic neuronal populations in Frontotemporal Dementia.Research square · 2026Article
- Developmental and cellular vulnerabilities underlie genetic architecture of schizophrenia.Molecular psychiatry · 2026Article
- Single-cell transcriptomics of human brain disorders.Molecular psychiatry · 2026Review
- Proteomic profile of CSF obtained at the time of diagnosis determines amyotrophic lateral sclerosis progression and survival: CXCL7 levels in disease prognosis and survival.Brain pathology (Zurich, Switzerland) · 2026Article
- Revisiting oligodendrocytes in amyotrophic lateral sclerosis using human multicellular stem cell models.Trends in cell biology · 2026Review
- Single-cell transcriptomic atlas of frontoinsular cortex reveals molecular correlates of selective neuronal vulnerability in FTD.bioRxiv : the preprint server for biology · 2026Article
- Multi-hit genetic lesions and a stress-imprinted immune transcriptome define the inflammatory pathology in ALS patients.Research square · 2026Article
- Single-nucleus multiome shows motor neuron glutamate overactivation in amyotrophic lateral sclerosis.Brain : a journal of neurology · 2026Article
- Integrated single-cell and spatial transcriptomic profiling in ALS uncovers peripheral-to-central immune infiltration and reprogramming.Nature neuroscience · 2026Article
- Reactive OPCs in CNS Injury: From Functional Diversity to Therapeutic Translation.Neuroscience bulletin · 2026Review
- Neural Organoid Models as a Platform for Studying Disease Mechanisms in Amyotrophic Lateral Sclerosis.Journal of neurochemistry · 2026Review
- An expanded cortical map of von Economo neurons in the human medial prefrontal cortex.Cerebral cortex (New York, N.Y. : 1991) · 2026Article
- Single-nucleus multiomic atlas of ALS primary motor cortex nominates neuroprotective WDR49-expressing astrocytes.Research square · 2026Article
- ALS mutations do not alter perineuronal net formation in human stem cell-derived motor neurons.Communications biology · 2026Article
- Spindle neurons in human cortex possess distinctive firing properties and transcriptomic signatures.Nature communications · 2026Article
- A stereotyped glial attachment determines the morphology and function of neuronal cilia.bioRxiv : the preprint server for biology · 2026Article
- Modeling spastic paraplegia 4 with corticospinal motor neuron-enriched cortical organoids reveals genotype-phenotype and HDAC6-targetable pathology.Cell reports · 2026Article
3 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
20 authors at 4 institutions in 1 country.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) share many clinical, pathological, and genetic features, but a detailed understanding of their associated transcriptional alterations across vulnerable cortical cell types is lacking. Here, we report a high-resolution, comparative single-cell molecular atlas of the human primary motor and dorsolateral prefrontal cortices and their transcriptional alterations in sporadic and familial ALS and FTLD. By integrating transcriptional and genetic information, we identify known and previously unidentified vulnerable populations in cortical layer 5 and show that ALS- and FTLD-implicated motor and spindle neurons possess a virtually indistinguishable molecular identity. We implicate potential disease mechanisms affecting these cell types as well as non-neuronal drivers of pathogenesis. Finally, we show that neuron loss in cortical layer 5 tracks more closely with transcriptional identity rather than cellular morphology and extends beyond previously reported vulnerable cell types.
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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.