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Your search keyword '"Karolina Deleva"' showing total 2 results
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2 results on '"Karolina Deleva"'

1. O3‐05–04: The 8‐hydroxyquinoline analog PBT2 rapidly restores cognition and reduces soluble Abeta in Alzheimer transgenic mice

Author

Joseph A. Nicolazzo, David Finkelstein, Qiao-Xin Li, Roberto Cappai, Karolina Deleva, Craig W. Ritchie, Mikhalina Cortes, Colin L. Masters, Simon Wilkins, Penny Huggins, Elysia Robb, Gaik Beng Kok, Elisabeth Gautier, Ashley I. Bush, Robert A. Cherny, Irene Volitakis, Paul A. Adlard, Susan A. Charman, Xiang Liu, Kevin J. Barnham, Katrina M. Laughton, Keyla Perez, Rudi E. Tanzi, Jack Gordon Parsons, and Jeffrey P. Smith

Subjects
Psychiatry and Mental health, Cellular and Molecular Neuroscience, Developmental Neuroscience, Epidemiology, Drug candidate, Health Policy, media_common.quotation_subject, Neurology (clinical), Art, Geriatrics and Gerontology, Humanities, media_common
Abstract

Robert A. Cherny, Paul A. Adlard, David I. Finkelstein, Elisabeth Gautier, Penny Huggins, Jack Parsons, Craig W. Ritchie, Elysia Robb, Mikhalina Cortes, Irene Volitakis, Xiang Liu, Jeffrey P. Smith, Keyla Perez, Katrina Laughton, Qiao-Xin Li, Susan A. Charman, Joseph A. Nicolazzo, Simon Wilkins, Karolina Deleva, Gaik Kok, Roberto Cappai, Rudi E. Tanzi, Colin L. Masters, Kevin J. Barnham, Ashley I. Bush, The Mental Health Research Institute of Victoria & The University of Melbourne, Parkville, VIC, Australia; MHRI & The University of Melbourne, Parkville, Australia; Prana Biotechnology Ltd, Parkville, Australia; Imperial College London, London, United Kingdom; MHRI, Parkville, Australia; The University of Melbourne, Parkville, Australia; Centre for Drug Candidate Optimisation, Parkville, Australia; Bio 21 Institute, The University of Melbourne, Parkville, Australia; Genetics & Aging Research Unit, MGH, Boston, MA, USA. Contact e-mail: rcherny@mhri.edu.au

Published
2008
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2. Rapid restoration of cognition in alzheimer's transgenic mice with 8-hydroxy quinoline analogs is associated with decreased interstitial Abeta

Author

Roberto Cappai, Joseph A. Nicolazzo, Ashley I. Bush, Jeffrey P. Smith, Robert A. Cherny, Paul A. Adlard, Katrina M. Laughton, Elisabeth Gautier, Mikhalina Cortes, Toni Lynch, Qiao-Xin Li, Elysia Robb, David Finkelstein, Xiang Liu, Colin L. Masters, Keyla Perez, Irene Volitakis, Kevin J. Barnham, Simon Wilkins, Susan A. Charman, Gaik Beng Kok, Karolina Deleva, Craig W. Ritchie, and Rudolph E. Tanzi

Subjects
Genetically modified mouse, Amyloid beta, Neuroscience(all), Long-Term Potentiation, HUMDISEASE, Mice, Transgenic, Pharmacology, In Vitro Techniques, Hippocampus, Presenilin, MOLNEURO, Amyloid beta-Protein Precursor, Mice, Neuroblastoma, Cognition, Alzheimer Disease, Cell Line, Tumor, medicine, Presenilin-1, Animals, Humans, Maze Learning, Analysis of Variance, Amyloid beta-Peptides, biology, Behavior, Animal, Chemistry, General Neuroscience, Clioquinol, Long-term potentiation, Quinoline analog, medicine.disease, Peptide Fragments, Mice, Inbred C57BL, Disease Models, Animal, Zinc, Immunology, biology.protein, Hydroxyquinolines, CELLBIO, PBT2, Alzheimer's disease, Copper, medicine.drug
Abstract

As a disease-modifying approach for Alzheimer's disease (AD), clioquinol (CQ) targets beta-amyloid (Abeta) reactions with synaptic Zn and Cu yet promotes metal uptake. Here we characterize the second-generation 8-hydroxy quinoline analog PBT2, which also targets metal-induced aggregation of Abeta, but is more effective as a Zn/Cu ionophore and has greater blood-brain barrier permeability. Given orally to two types of amyloid-bearing transgenic mouse models of AD, PBT2 outperformed CQ by markedly decreasing soluble interstitial brain Abeta within hours and improving cognitive performance to exceed that of normal littermate controls within days. Nontransgenic mice were unaffected by PBT2. The current data demonstrate that ionophore activity, inhibition of in vitro metal-mediated Abeta reactions, and blood-brain barrier permeability are indices that predict a potential disease-modifying drug for AD. The speed of recovery of the animals underscores the acutely reversible nature of the cognitive deficits associated with transgenic models of AD.

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