Abstract
Copper is an essential cofactor of proteins and enzymes involved in fundamental mechanisms like mitochondrial function, oxygen transportation, hematopoiesis, cellular metabolism and signal transduction. However, dysregulation of copper homeostasis is implicated in several neurodegenerative diseases, meaning drugs targeting copper availability could benefit millions of people.
Researchers at Florida Atlantic University have developed novel methods for modulating MBLAC1 (Metallo-Beta-Lactamase Domain Containing1) and its orthologs to treat copper-associated neurological conditions. MBLAC1 is a protein involved in histone mRNA processing that has been identified as a risk factor for Alzheimer's disease. Through several laboratory experiments, the researchers have shown that blocking MBLAC1 in an animal model influences both neurodegeneration and copper homeostasis.
FAU seeks to advance this technology into the marketplace through licensing or development partnerships.
Benefit
Novel Mechanism - MBLAC1 is a novel target for new drugs and a biomarker for diseaseEfficacious - Blocking MBLAC1 decreases clinical manifestations of neurological diseasesMarket Application
Treatment and diagnosis of neurological diseasesPublications
Glial swip-10 Controls Systemic Mitochondrial Function, Oxidative Stress, and Neuronal Viability via Copper Ion Homeostasis
Master Copper Regulator Discovery May Offer Alzheimer's Clues
Brochure
