Laura Ibáñez

This study integrates parietal cortex transcriptomics with GWAS data to refine Parkinson's disease risk gene nominations and identify STAT3 as a potential upstream glial regulator.

This study evaluates how biomarker variability affects individualized amyloid time estimation in Alzheimer's disease, finding that inter-individual variability is the main source of error.

This study shows hub disruption in ADAD follows a targeted attack pattern, detectable pre-clinically and linked to amyloid beta changes and neuronal activity.

This study identifies eight new genetic loci associated with cardioembolic stroke using multitrait analysis of GWAS data, revealing distinct genetic pathways from atrial fibrillation.

This study identifies increased circPSEN1 levels in ADAD brains compared to sporadic AD and controls, suggesting a potential role in neuroinflammatory processes.

This paper identifies seven genome-wide significant loci associated with early neurological instability after acute ischemic stroke, linking excitotoxic genes to poor outcomes.

The paper uses GWAS, PRS, and MR to show a genetic link between Parkinson's disease and CSF Aβ42 and APOE locus.

The paper integrates genomic and proteomic data across multiple tissues to identify protein quantitative loci (pQTL) and their implications for neurodegenerative diseases.

This study identifies a significant genetic correlation between Parkinson disease and melanoma, highlighting shared genes and pathways.

This study uses single-nuclei RNA-seq to compare cell proportions and gene expression in Mendelian and sporadic AD brains, identifying reduced excitatory neurons in a Mendelian carrier and proposing best practices for analysis.

The paper identifies a genetic variant in TMEM106B associated with increased neuronal proportion in neurodegenerative and cognitive normal cohorts, suggesting a role in neuronal protection.

This study evaluates gene-based methods for family-based analyses of familial late-onset Alzheimer disease, identifying novel candidate genes.

The paper constructs polygenic risk scores for sporadic late-onset Alzheimer's Disease and finds shared genetic architecture with familial and early-onset forms, showing varying odds ratios across cohorts.

This study identifies a haplotype lowering PU.1 expression in myeloid cells that delays Alzheimer’s disease onset by affecting gene expression and function.