All Stories

  1. Artificial Intelligence in Transcriptomics: From Human-in-the-Loop to Agentic AI
  2. Multi‐Omics Integration for Advancing Glioma Precision Medicine
  3. Predicting amyotrophic lateral sclerosis in the pre-symptomatic phase: Insights from SOD1G93A mouse gene expression profiles
  4. Artificial Intelligence-Driven Multi-Omics Approaches in Glioblastoma
  5. Unraveling the missing heritability of amyotrophic lateral sclerosis: should we focus more on copy number variations?
  6. Dysregulated miRNAs in different tissues and circulating fluids of neurodegenerative diseases.
  7. Oligogenic background in SOD1 D91A south Italian ALS patients
  8. Transcriptional Profiles of Cell Fate Transitions Reveal Early Drivers of Neuronal Apoptosis and Survival
  9. Tumor Growth in the High Frequency Medulloblastoma Mouse Model Ptch1+/−/Tis21KO Has a Specific Activation Signature of the PI3K/AKT/mTOR Pathway and Is Counteracted by the PI3K Inhibitor MEN1611
  10. Strial Presbycusis in Cx30−/− Mice
  11. Genomic Portrait of a Sporadic Amyotrophic Lateral Sclerosis Case in a Large Spinocerebellar Ataxia Type 1 Family
  12. The contribution of CNVs to the most common aging-related neurodegenerative diseases
  13. Splicing Players Are Differently Expressed in Sporadic Amyotrophic Lateral Sclerosis Molecular Clusters and Brain Regions
  14. Translational Medicine in Neurological Disorders: A Genomic Perspective
  15. ALS and CHARGE syndrome: a clinical and genetic study
  16. Cx26 partial loss causes accelerated presbycusis by redox imbalance and dysregulation of Nfr2 pathway
  17. NeuroArray: A Customized aCGH for the Analysis of Copy Number Variations in Neurological Disorders
  18. Copy Number Variants in Neurological Disorder
  19. CXCL12 (chemokine (C-X-C motif) ligand 12)
  20. Functional Genomics Identifies Tis21-Dependent Mechanisms and Putative Cancer Drug Targets Underlying Medulloblastoma Shh-Type Development
  21. A customized high-resolution array-comparative genomic hybridization to explore copy number variations in Parkinson’s disease
  22. A neurocutaneous phenotype with paired hypo- and hyperpigmented macules, microcephaly and stunted growth as prominent features
  23. Whole exome sequencing reveals a MLL de novo mutation associated with mild developmental delay and without ‘hairy elbows’: expanding the phenotype of Wiedemann–Steiner syndrome
  24. Is this the real time for genomics?