Inma Cobos

This study shows that tau regulates mitochondrial reverse electron transport, leading to ROS production and neurodegeneration, and identifies potential therapeutic targets.

This study uses somatic mutations to track marrow-derived cell infiltration into the human brain, finding widespread microglia replenishment and a protective link between clonal hematopoiesis and Alzheimer's disease.

This study shows that blocking fibrin-microglia interactions reduces AD-related brain network dysfunction and behavioral issues in mice.

The paper identifies molecular signatures of resilience in neocortical layer 4 neurons in Alzheimer's disease using single-cell and spatial transcriptomics.

This study investigates how APOE4 and Aβ interact in preclinical Alzheimer's disease, finding their synergistic effects on neuronal proteostasis and network dysfunction.

This paper develops a pipeline for precise MRI-histology coregistration using blockface imaging, achieving high alignment accuracy for neurodegenerative disease research.

The paper identifies cell type-specific molecular changes in ALS patients, showing enrichment of genetic risk factors in extratelencephalic neurons and altered responses in oligodendrocytes and microglia.

The paper develops 3D genome atlases for human and mouse cerebellar granule cells across lifespan, revealing non-neuronal 3D genome architecture remodeling.

The paper identifies gene expression signatures in Alzheimer's disease neurons with tau aggregates, revealing shared and subtype-specific molecular changes related to synaptic function and metabolism.

This study identifies transcriptomic signatures of human astrocytes across age, sex, and disease states, revealing changes in synaptic function, ionic homeostasis, and tumor microenvironment interactions.

This study identifies JADE1 as a novel genetic factor in tauopathy through genome-wide association and functional validation in human and Drosophila models.

The paper analyzes single-nucleus transcriptomes from brain and choroid plexus tissues of COVID-19 and influenza patients, identifying broad transcriptional dysregulation in multiple cell types and linking these changes to neurological symptoms.