Fabiola Galiana-Melendez

ORCID: 0009-0006-8926-496X
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neurological Disease Mechanisms and Treatments
  • Single-cell and spatial transcriptomics
  • Management of metastatic bone disease
  • Ferroptosis and cancer prognosis
  • Circadian rhythm and melatonin
  • Tryptophan and brain disorders
  • Cancer Diagnosis and Treatment
  • Fetal and Pediatric Neurological Disorders
  • Neonatal Respiratory Health Research
  • Neurogenesis and neuroplasticity mechanisms
  • Orthopaedic implants and arthroplasty
  • Stress Responses and Cortisol
  • Cerebrospinal fluid and hydrocephalus

Massachusetts Institute of Technology
2023-2024

Abstract The glymphatic movement of fluid through the brain removes metabolic waste 1–4 . Noninvasive 40 Hz stimulation promotes neural activity in multiple regions and attenuates pathology mouse models Alzheimer’s disease 5–8 Here we show that multisensory gamma influx cerebrospinal efflux interstitial cortex 5XFAD model disease. Influx was associated with increased aquaporin-4 polarization along astrocytic endfeet dilated meningeal lymphatic vessels. Inhibiting clearance abolished removal...

10.1038/s41586-024-07132-6 article EN cc-by Nature 2024-02-28

Abstract Alzheimer’s disease is the leading cause of dementia worldwide, but cellular pathways that underlie its pathological progression across brain regions remain poorly understood 1–3 . Here we report a single-cell transcriptomic atlas six different in aged human brain, covering 1.3 million cells from 283 post-mortem samples 48 individuals with and without disease. We identify 76 cell types, including region-specific subtypes astrocytes excitatory neurons an inhibitory interneuron...

10.1038/s41586-024-07606-7 article EN cc-by Nature 2024-07-24

Demyelination is a common pathological feature in wide range of diseases, characterized by the loss myelin sheath and myelin-supporting oligodendrocytes. These losses lead to impaired axonal function, increased vulnerability axons damage, result significant brain atrophy neuro-axonal degeneration. Multiple pathomolecular processes contribute neuroinflammation, oligodendrocyte cell death, progressive neuronal dysfunction. In this study, we use cuprizone mouse model demyelination investigate...

10.1038/s41467-024-51003-7 article EN cc-by-nc-nd Nature Communications 2024-08-08
Coming Soon ...