November 12-16, 2011: Dr. Greg Hook of ALSP Inc. and his colleagues Dr. Vivian Hook of UCSD and Dr. Mark Kindy of the Medical University of South Carolina, presented at Neuroscience 2011 in San Diego, November 12-16, 2011. Presented data suggest that both cathepsin B and BACE-1 are true beta-secretases but that they function at different levels in the generation of Abeta peptides. These data strongly suggest that a therapeutically acceptable method of inhibiting Cat B can be developed to reduce brain Abeta in AD patients.
>Cathepsin B has wild-type beta-secretase activity relevant to Alzheimer's disease drug development by Hook, G., Yu, J., Hong, Z, El- Amouri, S., Hook, V., and Kindy, M.
>The cysteine protease inhibitor, E64d, reduces brain amyloid-beta and improves memory deficits Alzheimer's disease animal models by inhibiting cathepsin B, but not BACE1, beta-secretase activity by Hook, G., Hook, V., and Kindy, M
October 16-29, 2011: Presentations at the INTERNATIONAL PROTEOLYSIS SOCIETY meeting in San Diego, CA.
>Cathepsin B knockout improves memory and reduces beta-amyloid in Alzheimer's disease mice expressing APP with the wild-type beta-secretase site by Kindy, M., Yu, J., El-Amouri, S.S., Hook, G. and Hook, V.
>The cysteine protease inhibitor, E64d, reduces brain amyloid-beta and improves memory deficits in Alzheimer's disease animal models by inhibiting cathepsin B, but not BACE1, beta-secretase activity by Hook, G., Hook, V., and Kindy, M.
September 8, 2011: Researchers from University of California, San Diego, ALSP Inc., and the Medical University of South Carolina published in the Biochimica et Biophysica Acta data discovering biological roles of Cathepsin L and B which indicate their significance in human health and disease. Recent new findings indicate significant biological roles of cysteine cathepsin proteases in secretory vesicles for production of biologically active peptides. Notably, cathepsin L in secretory vesicles has been demonstrated as a key protease for proteolytic processing of proneuropeptides (and prohormones) into active neuropeptides that are released to mediate cell-cell communication in the nervous system for neurotransmission. Moreover, cathepsin B in secretory vesicles has been recently identified as a beta-secretase for production of neurotoxic beta-amyloid (Abeta) peptides that accumulate in Alzheimer's disease (AD), participating as a notable factor in the severe memory loss in AD. Read More...
May 25, 2011: Researchers from ALSP Inc., the Medical University of South Carolina and the University of California, San Diego, published in the Journal of Alzheimer's disease data showing that the cysteine protease inhibitor E64d is efficacious in Alzheimer's disease animal models when orally administered. Importantly, the data show that feeding E64d to transgenic mice restores the memory deficits and reduces the brain amyloid plaque, which occurs in those animals and mimics the behavior and pathology seen in Alzheimer's disease patients. Dr. Gregory Hook, VP Research at ALSP, said that "these data are particularly exciting because E64d has previously been shown safe to use in man and thus this compound, or a derivative of it, have real clinical potential for Alzheimer's disease treatment." Read More..
February 6-8, 2011: Dr. James Hogan, post-doctoral fellow at ALSP Inc. receives "ADDF Young Investigator Scholarship". The award was presented at the "5th Drug Discovery for Neurodegeneration" meeting in San Diego, February 6-8, 2011. Read More...
>Discovery and development work toward a cathepsin B inhibitor for treatment of Alzheimer's disease by Hogan, J., Allan, A., Marakovits, J., Ternansky, R., Willette, J., Hook, V., Kindy, M., and Hook, G.