Abstract
More than one billion people worldwide suffer from a neurological disorder. Cholinergic circuits have been implicated in abnormal cognitive functioning and are involved in cognitive impairments observed in these disorders. Choline transport via the neuronal high-affinity choline transporter (CHT) is essential for cholinergic terminals to synthesize and release acetylcholine (ACh). Mutations in a gene called Val89 lead to loss of function of CHT in many neurological diseases.
Researchers at Florida Atlantic University have developed a CRISPR generated mouse model where animals express a Val89 substitution for studying neurogenerative diseases. Val89 mice exhibit up to an 80% reduction in CHT clearance and experience deficits in attentional control mechanisms when challenged with a visual disruptor.
FAU seeks partners to advance this technology into the marketplace through licensing or development partnerships.
Benefit
Disease Research - A mouse model to determine the underlying mechanisms of neurological diseasesDrug Development - Novel compounds can be evaluated in mice with neurological impairmentMarket Application
Neurological ResearchDrug ScreeningAnimal ModelsPublications
Disrupted Choline Clearance and Sustained Acetylcholine Release In Vivo by a Common Choline Transporter Coding Variant Associated with Poor Attentional Control in Humans
Brochure
