This discovery recognizes the pro-inflammatory activity of a soluble molecule sAPP, which elicits discrete and specific responses from cells of the central nervous system. The pro-inflammatory activity of sAPP has demonstrated the potential to kill neurons. Reduction of this activity would shift the balance of sAPP effects toward greater neuronal viability.
Data indicate that this reduction can be achieved by binding sAPP to apolipoprotein E; design of simpler chemical structures that mimic this binding might have direct therapeutic potential. This shift would be of obvious benefit in conditions that involve accelerated neuron deaths, such as Alzheimer's disease.
The potential uses are in both basic research into the role of sAPP in nervous system functions, and clinical applications to Alzheimer's disease and other neurodegenerative conditions. The goal of this research is to both directly stimulate neuroprotection and dampening pro-inflammatory activity.
References: Neuron, Vol. 10 243 - 254, February 1993; J. of Neurochemistry, Vol. 69, No. I, 1997; J. of Neurochemistry, Vol. 63, No. 2, 1994.
Purification Facilitated Soluble Amyloid Precursor Protein (His6-APP) and Mutants A hybrid gene construct that 1) allows for the human sAPP protein sequence attached to a string of histidines, and 2) allows for controlled expression in Escherichia coli, and 3) include deletion mutants that differentially stimulate neuromodulatory or pro-inflammatory pathways.
Patent Status: Issued, License Status: Available for non-exclusive License
Additional Licensing Partner to further commercialize this technology
Mr. Christopher Fasel
Associate Director or Licensing
UAMS BioVentures - TLO
Medical School - Teaching Hospital - Research InstitutionView profile
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