The Human Microglia Atlas (HuMicA) unravels changes in disease-associated microglia subsets across neurodegenerative conditions

Ricardo Martins-Ferreira, Josep Calafell-Segura, Bárbara Leal, Javier Rodríguez-Ubreva, Elena Martínez-Saez, Elisabetta Mereu, Paulo Pinho E Costa, Ariadna Laguna and Esteban Ballestar ()
Additional contact information
Ricardo Martins-Ferreira: 08916 Badalona
Josep Calafell-Segura: 08916 Badalona
Bárbara Leal: 4050-313
Javier Rodríguez-Ubreva: 08916 Badalona
Elena Martínez-Saez: Universitat Autònoma de Barcelona
Elisabetta Mereu: 08916 Badalona
Paulo Pinho E Costa: 4050-313
Ariadna Laguna: Vall d’Hebron Research Institute (VHIR)-Network Center for Biomedical Research in Neurodegenerative Diseases (CIBERNED)
Esteban Ballestar: 08916 Badalona

Nature Communications, 2025, vol. 16, issue 1, 1-15

Abstract: Abstract Dysregulated microglia activation, leading to neuroinflammation, is crucial in neurodegenerative disease development and progression. We constructed an atlas of human brain immune cells by integrating nineteen single-nucleus RNA-seq and single-cell RNA-seq datasets from multiple neurodegenerative conditions, comprising 241 samples from patients with Alzheimer’s disease, autism spectrum disorder, epilepsy, multiple sclerosis, Lewy body diseases, COVID-19, and healthy controls. The integrated Human Microglia Atlas (HuMicA) included 90,716 nuclei/cells and revealed nine populations distributed across all conditions. We identified four subtypes of disease-associated microglia and disease-inflammatory macrophages, recently described in mice, and shown here to be prevalent in human tissue. The high versatility of microglia is evident through changes in subset distribution across various pathologies, suggesting their contribution in shaping pathological phenotypes. A GPNMB-high subpopulation was expanded in AD and MS. In situ hybridization corroborated this increase in AD, opening the question on the relevance of this population in other pathologies.

Date: 2025
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DOI: 10.1038/s41467-025-56124-1

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