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Valor, L. M.

Publications and source records attributed to Valor, L. M..

3 recordsLinked to original sources

Single-cell transcriptomics and mouse model phenotyping for biomarker screen of peripheral blood biomarkers in Huntington disease

Transcriptional dysregulation is among the most prominent molecular alterations in Huntingtons disease (HD). It is not confined to brain but is also extended to peripheral tissues and cells, enabling minimally invasive screens aimed at identifying transcriptional surrogates of the health status in HD mutation carriers. Nonetheless, transcriptomics approaches have failed to identify consistent candidates from peripheral blood, probably due to the low impact of the HD mutation in the transcriptional profiles of circulating cells that can be masked by the high cellular complexity of this biofluid. In this study, we applied for the first time single-cell RNA-seq in peripheral blood mononuclear cells (PBMCs) to determine those cells that accumulate the most prominent gene expression changes as potential sources of reliable biomarkers. We observed both specific and common transcriptional alterations across different blood cell subtypes, justifying partial overlapping of our results with published bulk transcriptomics datasets. To relate these gene expression patterns with disease progression in the absence of a large cohort of patients, we examined selected candidates in a phenotypically characterized cohort of transgenic R6/1 mice. Of the tested genes, only the changes in the interferon related gene Irf7 in blood were correlated with motor coordination performance in mutant mice. Notably, this gene was significantly upregulated in the striatum of these animals. Overall, transcriptional-based changes in peripheral blood can be linked to HD although dissection of individual blood cells in combination with subsequent validation in mouse models emphasizes the challenges in obtaining clinically relevant biomarkers in HD.

neuroscience↗

Cell-type Specific Extracellular Vesicles in Mouse Brain: Proteomic Signatures Highlight Astrocytic GlialCAM Network and GPCR Enrichment

Extracellular vesicles (EVs) mediate intercellular communication in the central nervous system (CNS) and are emerging as biomarkers of brain health and disease. However, the molecular composition of cell type-specific brain EVs, particularly astrocyte-derived EVs (ADEVs), remains poorly defined. We performed comparative proteomic analysis of neuronal (NDEVs), microglial (MDEVs), and astrocytic (ADEVs) from mouse brain using magnetic immunocapture and LC-MS/MS proteomic profiling. Each EV subtype displayed distinct molecular fingerprints. NDEVs were enriched in synaptic and neurogenesis-related proteins (e.g., APP, SNAP25, GPR158 and BDNF), whereas MDEVs contained immune and phagocytic markers (e.g., TMEM119, CX3CR1, CD11B). Strikingly, the ADEV proteome closely mirrored the recently characterized GlialCAM interactome from leukodystrophy research, encompassing GlialCAM/MLC1 and associated partners involved in ion and water homeostasis (EAAT1/2, AQP4, GJA1), together with GPCRs such as GPRC5B. This overlap suggests that ADEVs encapsulate a molecular scaffold characteristic of astrocytic endfeet, potentially extending their signaling functions to the extracellular space. In conclusion, our study provides a detailed comparative proteomic characterization of brain cell type-specific EVs, revealing that ADEVs contain the GlialCAM/MLC1 network and GPCRs. These findings highlight ADEVs as promising candidates for biomarker development and mechanistic studies of blood-brain barrier integrity and neurodegenerative disorders.

neuroscience↗

Retinal affectation in Huntington's disease mouse models concurs with a local innate immune response

Huntingtons disease (HD) is a devastating disorder caused by aberrant expansion of CAG repeats in the HTT gene. Striatal dysfunction has been widely studied in HD mouse models. However, cumulative evidence indicates that the retina can also be functionally altered with consequences for visual function and circadian rhythms. The retina is the most exposed part of the central nervous system that can be used for monitoring the health status of patients using noninvasive techniques. To establish the retina as an appropriate tissue for HD studies, we linked the retinal alterations with those in the inner brain. We confirmed the malfunction of the R6/1 retinas, which underwent a rearrangement of their transcriptome as extensive as in the striatum, indicating a profound retinal affectation in HD. Tissue-enriched genes were downregulated in both areas, but a neuroinflammation signature was specifically induced in the R6/1 retina due to glial activation that was reminiscent of the situation in HD patients brains. These phenomena were confirmed in the zQ175 strain, and were accompanied by a differential impairment of the autophagy system between both tissues. Overall, these results demonstrated the suitability of the mouse retina as a research model for HD.

neuroscience↗