Paul A Adlard

Summary

Affiliation: Mental Health Research Institute
Country: Australia

Publications

  1. pmc GSK-3 in Neurodegenerative Diseases
    Peng Lei
    Mental Health Research Institute, 155 Oak Street, Parkville, VIC 3052, Australia
    Int J Alzheimers Dis 2011:189246. 2011
  2. pmc Copper modulation as a therapy for Alzheimer's disease?
    Yasmina Manso
    Institute of Neurosciences and Department of Cellular Biology, Physiology and Immunology, Faculty of Biosciences, Autonomous University of Barcelona, Bellaterra, 08193 Barcelona, Spain
    Int J Alzheimers Dis 2011:370345. 2011
  3. doi request reprint Mild stress facilitates learning and exercise improves retention in aged mice
    Paul A Adlard
    Institute for Brain Aging and Dementia, University of California Irvine, 1226 Gillespie NRF, Irvine, CA 92697 4540, United States
    Exp Gerontol 46:53-9. 2011
  4. pmc Metal ionophore treatment restores dendritic spine density and synaptic protein levels in a mouse model of Alzheimer's disease
    Paul A Adlard
    Oxidation Biology Laboratory, The Mental Health Research Institute, Parkville, Victoria, Australia
    PLoS ONE 6:e17669. 2011
  5. doi request reprint Rapid restoration of cognition in Alzheimer's transgenic mice with 8-hydroxy quinoline analogs is associated with decreased interstitial Abeta
    Paul A Adlard
    Oxidation Biology Laboratory, The Mental Health Research Institute of Victoria, Parkville, Victoria 3052, Australia
    Neuron 59:43-55. 2008
  6. doi request reprint The Alzheimer's therapeutic PBT2 promotes amyloid-β degradation and GSK3 phosphorylation via a metal chaperone activity
    Peter J Crouch
    Department of Pathology, The University of Melbourne, Victoria, Australia
    J Neurochem 119:220-30. 2011
  7. doi request reprint Characterization of the role of metallothionein-3 in an animal model of Alzheimer's disease
    Yasmina Manso
    Unidad de Fisiologia Animal, Departamento de Biologia Celular, Fisiologia e Inmunologia, Facultad de Biociencias, Universidad Autonoma de Barcelona, Edificio C, Bellaterra, 08193 Barcelona, Spain
    Cell Mol Life Sci 69:3683-700. 2012
  8. doi request reprint Characterization of the role of the antioxidant proteins metallothioneins 1 and 2 in an animal model of Alzheimer's disease
    Yasmina Manso
    Animal Physiology Unit, Department of Cellular Biology, Physiology and Immunology, Faculty of Biosciences, Universitat Autonoma de Barcelona, Edificio C, Bellaterra, Barcelona 08193, Spain
    Cell Mol Life Sci 69:3665-81. 2012
  9. ncbi request reprint The exercise-induced expression of BDNF within the hippocampus varies across life-span
    Paul A Adlard
    Institute for Brain Aging and Dementia, University of California, 1125 Gillespie N R F, Irvine, CA 92697 4540, USA
    Neurobiol Aging 26:511-20. 2005
  10. doi request reprint Ceruloplasmin dysfunction and therapeutic potential for Parkinson disease
    Scott Ayton
    Oxidation Biology Laboratory, Florey Institute for Neuroscience and Mental Health, Parkville, Victoria, Australia
    Ann Neurol 73:554-9. 2013

Collaborators

Detail Information

Publications37

  1. pmc GSK-3 in Neurodegenerative Diseases
    Peng Lei
    Mental Health Research Institute, 155 Oak Street, Parkville, VIC 3052, Australia
    Int J Alzheimers Dis 2011:189246. 2011
    ..Thus, understanding the role of GSK-3 in neurodegenerative diseases will enhance our understanding of the basic mechanisms underlying the pathogenesis of these disorders and also facilitate the identification of new therapeutic avenues...
  2. pmc Copper modulation as a therapy for Alzheimer's disease?
    Yasmina Manso
    Institute of Neurosciences and Department of Cellular Biology, Physiology and Immunology, Faculty of Biosciences, Autonomous University of Barcelona, Bellaterra, 08193 Barcelona, Spain
    Int J Alzheimers Dis 2011:370345. 2011
    ..These data support an interaction between copper/cholesterol and both Aβ and APP and further highlight the potential role of metal ion dyshomeostasis in AD...
  3. doi request reprint Mild stress facilitates learning and exercise improves retention in aged mice
    Paul A Adlard
    Institute for Brain Aging and Dementia, University of California Irvine, 1226 Gillespie NRF, Irvine, CA 92697 4540, United States
    Exp Gerontol 46:53-9. 2011
    ..In aged, but not young animals, all four genes increased significantly after exercise. Thus, in aged animals mild stress facilitates learning and the retention of this task is improved by voluntary exercise...
  4. pmc Metal ionophore treatment restores dendritic spine density and synaptic protein levels in a mouse model of Alzheimer's disease
    Paul A Adlard
    Oxidation Biology Laboratory, The Mental Health Research Institute, Parkville, Victoria, Australia
    PLoS ONE 6:e17669. 2011
    ..In Alzheimer's disease therefore, PBT2 may restore the uptake of physiological metal ions trapped within extracellular β-amyloid aggregates that then induce biochemical and anatomical changes to improve cognitive function...
  5. doi request reprint Rapid restoration of cognition in Alzheimer's transgenic mice with 8-hydroxy quinoline analogs is associated with decreased interstitial Abeta
    Paul A Adlard
    Oxidation Biology Laboratory, The Mental Health Research Institute of Victoria, Parkville, Victoria 3052, Australia
    Neuron 59:43-55. 2008
    ..The speed of recovery of the animals underscores the acutely reversible nature of the cognitive deficits associated with transgenic models of AD...
  6. doi request reprint The Alzheimer's therapeutic PBT2 promotes amyloid-β degradation and GSK3 phosphorylation via a metal chaperone activity
    Peter J Crouch
    Department of Pathology, The University of Melbourne, Victoria, Australia
    J Neurochem 119:220-30. 2011
    ..Intracellular translocation of Zn and Cu via the metal chaperone activity of PBT2 may be an important mechanism by which PBT2 improves cognitive function in people with AD...
  7. doi request reprint Characterization of the role of metallothionein-3 in an animal model of Alzheimer's disease
    Yasmina Manso
    Unidad de Fisiologia Animal, Departamento de Biologia Celular, Fisiologia e Inmunologia, Facultad de Biociencias, Universidad Autonoma de Barcelona, Edificio C, Bellaterra, 08193 Barcelona, Spain
    Cell Mol Life Sci 69:3683-700. 2012
    ..These results highlight that the control of the endogenous production and/or action of MT-3 could represent a powerful therapeutic target in AD...
  8. doi request reprint Characterization of the role of the antioxidant proteins metallothioneins 1 and 2 in an animal model of Alzheimer's disease
    Yasmina Manso
    Animal Physiology Unit, Department of Cellular Biology, Physiology and Immunology, Faculty of Biosciences, Universitat Autonoma de Barcelona, Edificio C, Bellaterra, Barcelona 08193, Spain
    Cell Mol Life Sci 69:3665-81. 2012
    ..These results highlight that the control of the endogenous production and/or action of MT1 + 2 could represent a powerful therapeutic target in AD...
  9. ncbi request reprint The exercise-induced expression of BDNF within the hippocampus varies across life-span
    Paul A Adlard
    Institute for Brain Aging and Dementia, University of California, 1125 Gillespie N R F, Irvine, CA 92697 4540, USA
    Neurobiol Aging 26:511-20. 2005
    ..BDNF protein induction may, therefore, not be directly correlated with significant mRNA changes. Exercise may represent a therapeutic tool for disorders which involve a decrease in BDNF...
  10. doi request reprint Ceruloplasmin dysfunction and therapeutic potential for Parkinson disease
    Scott Ayton
    Oxidation Biology Laboratory, Florey Institute for Neuroscience and Mental Health, Parkville, Victoria, Australia
    Ann Neurol 73:554-9. 2013
    ..These findings show, in principle, that intravenous ceruloplasmin may have therapeutic potential in PD...
  11. doi request reprint Elevated labile Cu is associated with oxidative pathology in Alzheimer disease
    Simon A James
    The Mental Health Research Institute, The University of Melbourne, Melbourne, VIC 3010, Australia
    Free Radic Biol Med 52:298-302. 2012
    ..This deranged Cu homeostasis reflects the homeostatic breakdown of Cu observed in AD and supports biometal metabolism as a therapeutic target...
  12. doi request reprint High order W02-reactive stable oligomers of amyloid-β are produced in vivo and in vitro via dialysis and filtration of synthetic amyloid-β monomer
    Elysia Robb
    The Florey Institute of Neuroscience and Mental Health, Division of Mental Health, Parkville, Vic, Australia
    J Alzheimers Dis 44:69-78. 2015
    ..These data suggest that the experimental detection of higher order oligomers in tissues derived from Alzheimer's disease brains or from animal models of disease could, in some cases, be a product the method of analysis. ..
  13. doi request reprint Tau deficiency induces parkinsonism with dementia by impairing APP-mediated iron export
    Peng Lei
    Mental Health Research Institute, The University of Melbourne, Victoria, Australia
    Nat Med 18:291-5. 2012
    ..These data suggest that the loss of soluble tau could contribute to toxic neuronal iron accumulation in Alzheimer's disease, Parkinson's disease and tauopathies, and that it can be rescued pharmacologically...
  14. ncbi request reprint Voluntary exercise decreases amyloid load in a transgenic model of Alzheimer's disease
    Paul A Adlard
    Institute for Brain Aging and Dementia, University of California, Irvine, Irvine, California 92697 4540, USA
    J Neurosci 25:4217-21. 2005
    ..In support of existing epidemiological studies, this investigation demonstrates that exercise is a simple behavioral intervention sufficient to inhibit the normal progression of AD-like neuropathology in the TgCRND8 mouse model...
  15. doi request reprint Effects of Neonatal Iron Feeding and Chronic Clioquinol Administration on the Parkinsonian Human A53T Transgenic Mouse
    Jessica L Billings
    The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Victoria 3052, Australia
    ACS Chem Neurosci 7:360-6. 2016
    ..These data suggest that Fe exposure during a critical developmental window, combined with the overexpression mutant α-synuclein, presents a disease phenotype resistant to intervention using clioquinol later in life. ..
  16. doi request reprint Parkinson's disease iron deposition caused by nitric oxide-induced loss of β-amyloid precursor protein
    Scott Ayton
    Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Victoria 3010, Australia
    J Neurosci 35:3591-7. 2015
    ..Conversely, APP-overexpressing mice are protected in the MPTP PD model. NO suppresses APP translation in mouse MPTP models, explaining how elevated NO causes iron-dependent neurodegeneration in PD. ..
  17. ncbi request reprint Exercise-induced gene expression changes in the rat spinal cord
    Victoria M Perreau
    Institute for Brain Aging and Dementia, 1113 Gillespie N R F, University of California Irvine, Irvine, CA 92697, USA
    Gene Expr 12:107-21. 2005
    ..Taken together these data suggest cellular pathways through which exercise may promote recovery in the SCI population...
  18. doi request reprint Cognitive loss in zinc transporter-3 knock-out mice: a phenocopy for the synaptic and memory deficits of Alzheimer's disease?
    Paul A Adlard
    Oxidation Biology Laboratory, The Mental Health Research Institute, Parkville, Victoria 3052, Australia
    J Neurosci 30:1631-6. 2010
    ....
  19. pmc Iron accumulation confers neurotoxicity to a vulnerable population of nigral neurons: implications for Parkinson's disease
    Scott Ayton
    Florey Institute for Neuroscience and Mental Health, The University of Melbourne, Melbourne, Victoria, Australia
    Mol Neurodegener 9:27. 2014
    ..Here, we explored whether known iron-stressors of the SN (1) aging and (2) MPTP, would exaggerate the lesion severity of CP KO mice...
  20. doi request reprint Tau protein: relevance to Parkinson's disease
    Peng Lei
    Oxidation Biology Laboratory, Mental Health Research Institute, Parkville, Victoria, Australia
    Int J Biochem Cell Biol 42:1775-8. 2010
    ..Toxic interactions with alpha synuclein may lead to hyperphosphorylation of tau and eventually to the deposition of both proteins in the disease...
  21. pmc Pharmacotherapeutic targets in Alzheimer's disease
    Yif at Biran
    The Oxidation Biology Laboratory, The Mental Health Research Institute, Parkville, Victoria, Australia
    J Cell Mol Med 13:61-86. 2009
    ..We will review the way these pharmacological strategies target the biochemical and clinical features of the disease and the investigational drugs for each category...
  22. doi request reprint Clioquinol Improves Cognitive, Motor Function, and Microanatomy of the Alpha-Synuclein hA53T Transgenic Mice
    David I Finkelstein
    The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Victoria 3052, Australia
    ACS Chem Neurosci 7:119-29. 2016
    ..In conclusion, our data suggests that CQ is capable of mitigating the pathological metal/α-syn interactions, suggesting that the modulation of metal ions warrants further study as a therapeutic approach for the synucleinopathies. ..
  23. doi request reprint A comparison of ceruloplasmin to biological polyanions in promoting the oxidation of Fe(2+) under physiologically relevant conditions
    Bruce X Wong
    Oxidation Biology Unit, The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Victoria, Australia
    Biochim Biophys Acta 1840:3299-310. 2014
    ..This process may be impaired in disease, and requires more accurate analytical assays to interrogate enzymatic- and auto-oxidation within a physiologically relevant environment...
  24. doi request reprint The effect of dopamine on MPTP-induced rotarod disability
    Scott Ayton
    Florey Institute for Neuroscience and Mental Health, Kenneth Myer Building, University of Melbourne, Parkville, Australia
    Neurosci Lett 543:105-9. 2013
    ..Paradoxically, rotarod disability coincided with gradual striatal dopamine restoration. l-Dopa supplementation exacerbated rotarod disability, whereas dopamine antagonism restored performance...
  25. ncbi request reprint Amyloid imaging in Alzheimer's disease and other dementias
    Michelle T Fodero-Tavoletti
    Department of Pathology, The University of Melbourne, Melbourne, Victoria, 3010, Australia
    Brain Imaging Behav 3:246-61. 2009
    ....
  26. ncbi request reprint Metals and Alzheimer's disease
    Paul A Adlard
    The Oxidation Disorders Laboratory, The Mental Health Research Institute, Parkville, Victoria, 3052, Australia
    J Alzheimers Dis 10:145-63. 2006
    ..This offers a broad biochemical front for novel therapeutic interventions...
  27. doi request reprint A domain level interaction network of amyloid precursor protein and Abeta of Alzheimer's disease
    Victoria M Perreau
    Neuroproteomics and Neurogenomics Platform, National Neurosciences Facility, The University of Melbourne, Parkville, Vic, Australia
    Proteomics 10:2377-95. 2010
    ..Gene ontology and network analysis were used to identify potentially novel functional relationships among interacting proteins...
  28. doi request reprint Overexpression of Metallothionein-1 Modulates the Phenotype of the Tg2576 Mouse Model of Alzheimer's Disease
    Yasmina Manso
    Animal Physiology Unit, Department of Cellular Biology, Physiology and Immunology, Faculty of Biosciences Bellaterra, Barcelona, Spain
    J Alzheimers Dis 51:81-95. 2016
    ..These results clearly suggest that MT-1 may be involved in AD pathogenesis. ..
  29. doi request reprint beta-Amyloid as a molecular therapeutic target in Alzheimer's disease
    Paul A Adlard
    The Oxidation Disorders Laboratory, The Mental Health Research Institute of Victoria, Parkville, Victoria, Australia
    Drugs Today (Barc) 45:293-304. 2009
    ..It will become clear that beta-amyloid represents a potent molecular target for pharmacological manipulation to perhaps prevent the onset and progression of Alzheimer's disease...
  30. doi request reprint Iron Regulates Apolipoprotein E Expression and Secretion in Neurons and Astrocytes
    He Xu
    The Florey Institute of Neuroscience and Mental Health, Melbourne, Victoria, Australia
    J Alzheimers Dis 51:471-87. 2016
    ..Apolipoprotein E (APOE) has been identified as the strongest genetic risk factor for AD. However, the interaction between the two has yet to be fully explored...
  31. pmc β-Amyloid precursor protein does not possess ferroxidase activity but does stabilize the cell surface ferrous iron exporter ferroportin
    Bruce X Wong
    Oxidation Biology Unit, The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Victoria, Australia
    PLoS ONE 9:e114174. 2014
    ..Therefore, despite lacking ferroxidase activity, APP still supports iron export from neurons. ..
  32. doi request reprint Metallothionein and brain inflammation
    Yasmina Manso
    Animal Physiology Unit, Department of Cellular Biology, Physiology and Immunology, Faculty of Biosciences, Institute of Neurosciences, Universitat Autonoma Barcelona, Bellaterra, 08193, Barcelona, Spain
    J Biol Inorg Chem 16:1103-13. 2011
    ....
  33. doi request reprint 18F-THK523: a novel in vivo tau imaging ligand for Alzheimer's disease
    Michelle T Fodero-Tavoletti
    Department of Pathology, The University of Melbourne, Victoria, 3010, Australia
    Brain 134:1089-100. 2011
    ..The preclinical examination of THK523 has demonstrated its high affinity and selectivity for tau pathology both in vitro and in vivo, indicating that (18)F-THK523 fulfils ligand criteria for human imaging trials...
  34. doi request reprint A time-course analysis of changes in cerebral metal levels following a controlled cortical impact
    Stuart D Portbury
    The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Kenneth Myer Building, 30 Royal Parade, Parkville, Victoria 3052, Australia
    Metallomics 8:193-200. 2016
    ..Such alterations are likely to play a role in both the short- and long-term consequences of head trauma and suggest that pharmacological modulation to normalize these metal levels may be efficacious in improving functional outcome. ..
  35. doi request reprint Development of a Platinum Complex as an anti-Amyloid Agent for the Therapy of Alzheimer's Disease
    Vijaya B Kenche
    The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Victoria, 3010 Australia Bio21 Molecular Science and Biotechnology Institute, The University of Melbourne, Parkville, Victoria, 3010 Australia
    Angew Chem Int Ed Engl 52:3374-8. 2013
    ..Analyses of brain tissues showed that treatment with the Pt compound led to a 26 % decrease in the number of amyloid β-peptide plaques...
  36. ncbi request reprint The timecourse of induction of brain-derived neurotrophic factor mRNA and protein in the rat hippocampus following voluntary exercise
    Paul A Adlard
    Institute for Brain Aging and Dementia, University of California, Irvine, CA 92697 4540, USA
    Neurosci Lett 363:43-8. 2004
    ..Exercise, therefore, was shown to modulate BDNF induction in a time-dependent manner, and this may translate to improvements in neurotrophin-mediated tasks within the CNS...
  37. ncbi request reprint Alzheimer's disease--a sum greater than its parts?
    Paul A Adlard
    Institute for Brain Aging and Dementia, University of California, 1113 Gillespie N R F, Irvine, CA 92697 4540, USA
    Neurobiol Aging 25:725-33; discussion 743-6. 2004