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

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

Publication date: Jan 16, 2025

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.

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Concepts Keywords
Alzheimer Aged
Atlas Alzheimer Disease
Healthy Atlases as Topic
Mice Brain
Neuroinflammation COVID-19
Female
Humans
Macrophages
Male
Microglia
Middle Aged
Multiple Sclerosis
Neurodegenerative Diseases
RNA-Seq
Single-Cell Analysis

Semantics

Type Source Name
disease MESH neuroinflammation
disease MESH neurodegenerative disease
disease MESH Alzheimer’s disease
disease MESH autism spectrum disorder
disease MESH epilepsy
disease MESH multiple sclerosis
disease MESH COVID-19
drug DRUGBANK Sulfasalazine
pathway REACTOME Neurodegenerative Diseases
drug DRUGBANK Ademetionine
pathway KEGG Alzheimer disease

Original Article

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