Paul A Adlard
Affiliation: Mental Health Research Institute
- Metal ionophore treatment restores dendritic spine density and synaptic protein levels in a mouse model of Alzheimer's diseasePaul 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...
- Mild stress facilitates learning and exercise improves retention in aged micePaul 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...
- Rapid restoration of cognition in Alzheimer's transgenic mice with 8-hydroxy quinoline analogs is associated with decreased interstitial AbetaPaul 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...
- The Alzheimer's therapeutic PBT2 promotes amyloid-β degradation and GSK3 phosphorylation via a metal chaperone activityPeter 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...
- The exercise-induced expression of BDNF within the hippocampus varies across life-spanPaul 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...
- Elevated labile Cu is associated with oxidative pathology in Alzheimer diseaseSimon 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...
- Tau deficiency induces parkinsonism with dementia by impairing APP-mediated iron exportPeng 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...
- Voluntary exercise decreases amyloid load in a transgenic model of Alzheimer's diseasePaul 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...
- Exercise-induced gene expression changes in the rat spinal cordVictoria 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...
- 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....
- Pharmacotherapeutic targets in Alzheimer's diseaseYif 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...
- The effect of dopamine on MPTP-induced rotarod disabilityScott Ayton
Florey Institute for Neuroscience and Mental Health, Kenneth Myer Building, University of Melbourne, Parkville, Australia
Neurosci Lett 543:105-9. 2013..Conclusion: dopamine restoration, not depletion, precipitates rotarod disability after MPTP intoxication, and caution should be applied when using this assay for MPTP...
- A domain level interaction network of amyloid precursor protein and Abeta of Alzheimer's diseaseVictoria 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...
- Amyloid imaging in Alzheimer's disease and other dementiasMichelle T Fodero-Tavoletti
Department of Pathology, The University of Melbourne, Melbourne, Victoria, 3010, Australia
Brain Imaging Behav 3:246-61. 2009....
- Metals and Alzheimer's diseasePaul 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...
- Tau protein: relevance to Parkinson's diseasePeng 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...
- beta-Amyloid as a molecular therapeutic target in Alzheimer's diseasePaul 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...
- GSK-3 in Neurodegenerative DiseasesPeng 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...
- 18F-THK523: a novel in vivo tau imaging ligand for Alzheimer's diseaseMichelle 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...
- Development of a Platinum Complex as an anti-Amyloid Agent for the Therapy of Alzheimer's DiseaseVijaya 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...
- The timecourse of induction of brain-derived neurotrophic factor mRNA and protein in the rat hippocampus following voluntary exercisePaul 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...
- 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