Francisco Javier Lopera

The paper identifies astrocyte-driven small vessel disease as an early, amyloid-independent feature of PSEN1 E280A familial Alzheimer's disease through proteomic and transcriptomic analyses.

This study identifies genetic variants associated with Alzheimer's disease and frontotemporal dementia in admixed Latin American populations using whole-genome sequencing and ancestry analysis.

The paper identifies a serum lipidomic signature in asymptomatic Alzheimer's disease mutation carriers that differentiates them from non-carriers and correlates with dementia risk factors.

The paper identifies plasma proteomic signatures associated with CADASIL stages, revealing fibrosis, angiogenesis, and metabolic alterations.

The paper evaluates the reliability of neural components from resting-state EEG data using group ICA and identifies reproducible components across multiple datasets.

The paper conducts an X-chromosome association study in Latin American cohorts, identifying new loci linked to Parkinson Disease and replicating previous findings.

The paper identifies viral infection and inflammation signatures in the olfactory system of familial Alzheimer's disease patients, suggesting their role in disease progression.

The paper constructs and validates a polygenic risk score for Parkinson's disease in a Latino cohort, finding ancestry-related biases and haplotype associations at the SNCA locus.

This study examines how amyloid-β and tau pathologies affect brain functional connectivity in preclinical Alzheimer's disease carriers, finding distinct dysconnectivity patterns in specific brain regions.

This study conducts the first GWAS of Parkinson's disease in Latinos, identifies SNCA as significant, and finds genetic overlap with Europeans.

The paper analyzes copy number variants in Latin American Parkinson's disease patients and finds enrichment of variants overlapping known Parkinson's genes, particularly PARK2, associated with early-onset disease.

The paper models familial Alzheimer's disease using MSC-derived cholinergic-like neurons with PSEN1 E280A mutation, revealing key pathological features and potential therapeutic targets.