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Single-cell atlas of transcriptomic vulnerability across brain disorders

Donghoon Lee, Mikaela Koutrouli, Nicolas Y. Masse, Gabriel E. Hoffman, Seon Kinrot, Xinyi Wang, N. M. Prashant, Milos Pjanic, Tereza Clarence, Fotis Tsetsos, Deepika Dayal Mathur, David Burstein, Karen Therrien, Aram Hong, Clara Casey, Zhiping Shao, Marcela Alvia, Stathis Argyriou, Jennifer Monteiro Fortes, Sarah E. Murphy, Pavel Katsel, Pavan Kumar Auluck, Lisa L. Barnes, Stefano Marenco, David Alan Bennett, Athan Z. Li, Biao Zeng, Chenfeng He, Chirag Gupta, Christian Dillard, Christian Porras, Colleen A. McClung, Collin Spencer, Daifeng Wang, Gennadi Ryan, Hui Yang, Jerome J. Choi, Kalpana H. Arachchilage, Lars J. Jensen, Logan C. Dumitrescu, Lyra Sheu, Madeline R. Scott, Marios Anyfantakis, Maxim Signaevsky, Monika Ahirwar, Noah Cohen Kalafut, Pengfei Dong, Pramod B. Chandrashekar, Rachel Bercovitch, Roman Kosoy y 10 más

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En palabras de los autores

. Here, to gain deeper insights into the aetiology of different brain diseases, we used specimens from 1,494 unique donors to generate a population-scale single-cell transcriptomic atlas of the human dorsolateral prefrontal cortex, comprising over 6.3 million individual nuclei. The cohort includes neurotypical controls, as well as donors affected by eight common and complex brain disorders: Alzheimer's disease (AD), diffuse Lewy body disease (DLBD), vascular dementia (Vas), Parkinson's disease (PD), tauopathy, frontotemporal dementia, schizophrenia, and bipolar disorder. We show that interindividual variation accounts for a substantial portion of gene expression variation. By comparing transcriptomic variation across diseases, we reveal universal signatures enriched in basic cellular functions such as mRNA processing and protein localization. After discounting these cross-disease signatures, we show stronger genetic and transcriptomic concordance among AD, DLBD, Vas and PD. Furthermore, we characterize transcriptomic variation among different AD phenotypes, distinct from those observed in healthy ageing, revealing a reduction in neuronal abundance in individuals with more severe AD, coupled with an increase in immune and vascular cell populations. Exploring the neuropsychiatric symptoms (NPSs) that frequently accompany AD, we find an increased abundance of deep-layer excitatory neurons associated with a broad range of NPSs. By constructing transcriptome trajectories that capture AD progression, we implicate cell-type-specific responses in the early and late stages of AD. Our disease atlas provides a perspective of the transcriptomic landscape in neurodegenerative and neuropsychiatric disorders, shedding light on shared and distinct processes involving the neurological-immune-vascular systems, and identifying potential targets for therapeutic intervention.

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Apareció: viernes, 25 de septiembre. Nature. Revista con revisión por pares.

DOI: 10.1038/s41586-025-09573-z