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Masrori, P.

Publications and source records attributed to Masrori, P..

2 recordsLinked to original sources

Motor System Oligodendroglia Atlas Reveals Activation States Associated with Region-Specific Vulnerability in ALS

Oligodendrocytes, the second most abundant cell type in the motor cortex and the most abundant in the spinal cord--are increasingly recognized as active contributors to neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). Yet their diversity and disease relevance in the central nervous system remain incompletely defined. Here, we generate a comprehensive single-nucleus transcriptomic atlas of 176 samples, integrating 2 in-house and 16 publicly available datasets. It encompasses more than 1,000,000 cells (350,000 oligodendrocytes and oligodendrocyte precursors) from the human motor cortex and spinal cord in non-neurological controls and ALS patients. We identify a previously unrecognized oligodendrocyte subpopulation--marked by PPEF1--and uncover regional differences, with distinct OPALIN+ and RBFOX1+ oligodendrocyte proportions between cortex and spinal cord. Importantly, we demonstrate that "disease-associated oligodendrocytes" (DAOs) represent a distinct activation state, rather than a distinct subpopulation. In ALS, spinal cord oligodendrocytes selectively shift toward reactive states, characterized by JUND-enriched regulon activity, heightened metabolic demand, increased intercellular signaling, and activation of cell-death pathways. Finally, we identify LRP2 as a novel transcriptional oligodendrocyte marker and find LRP2 and MBP proteins to be elevated in ALS cerebrospinal fluid (CSF), offering a potential biomarker of oligodendrocyte dysfunction. Our study provides a systems-level framework to interpret oligodendrocyte and OPC changes in ALS, linking cell state shifts to molecular alterations that can guide biomarker and therapeutic strategies.

neuroscience↗

Hexanucleotide repeat expansions in C9orf72 alter microglial responses and prevent a coordinated glial reaction in ALS

Neuroinflammation is an important hallmark in amyotrophic lateral sclerosis (ALS). Experimental evidence has highlighted a role of microglia in the modulation of motor neuron degeneration. However, the exact contribution of microglia to both sporadic and genetic forms of ALS is still unclear. We generated single nuclei profiles of spinal cord and motor cortex from sporadic and C9orf72 ALS patients, as well as controls. We particularly focused on the transcriptomic responses of both microglia and astrocytes. We confirmed that C9orf72 is highly expressed in microglia and shows a diminished expression in carriers of the hexanucleotide repeat expansion (HRE). This resulted in an impaired response to disease, with specific deficits in phagocytic and lysosomal transcriptional pathways. Astrocytes also displayed a dysregulated response in C9orf72 ALS patients, remaining in a homeostatic state. This suggests that C9orf72 HRE alters a coordinated glial response, which ultimately would increase the risk for developing ALS. Our results indicate that C9orf72 HRE results in a selective microglial loss-of-function, likely impairing microglial-astrocyte communication and preventing a global glial response. This is relevant as it indicates that sporadic and familial forms of ALS may present a different cellular substrate, which is of great importance for patient stratification and treatment.

neuroscience↗