G Halliday

Summary

Affiliation: University of New South Wales
Country: Australia

Publications

  1. ncbi request reprint Human-based studies on alpha-synuclein deposition and relationship to Parkinson's disease symptoms
    Glenda M Halliday
    Prince of Wales, Medical Research Institute, Randwick, NSW, Australia
    Exp Neurol 209:12-21. 2008
  2. ncbi request reprint A comparison of degeneration in motor thalamus and cortex between progressive supranuclear palsy and Parkinson's disease
    Glenda M Halliday
    Prince of Wales Medical Research Institute and University of New South Wales, Sydney, Australia
    Brain 128:2272-80. 2005
  3. ncbi request reprint Alpha-synuclein redistributes to neuromelanin lipid in the substantia nigra early in Parkinson's disease
    Glenda M Halliday
    Prince of Wales Medical Research Institute and the University of New South Wales, Sydney, Australia
    Brain 128:2654-64. 2005
  4. ncbi request reprint Pick bodies in a family with presenilin-1 Alzheimer's disease
    Glenda M Halliday
    Prince of Wales Medical Research Institute and the University of New South Wales, Barker Street, Randwick, Sydney, 2031 NSW, Australia
    Ann Neurol 57:139-43. 2005
  5. ncbi request reprint Consensus neuropathological diagnosis of common dementia syndromes: testing and standardising the use of multiple diagnostic criteria
    G Halliday
    Prince of Wales Medical Research Institute, High Street, Randwick, 2031 New South Wales, Australia
    Acta Neuropathol 104:72-8. 2002
  6. ncbi request reprint Identifying severely atrophic cortical subregions in Alzheimer's disease
    G M Halliday
    Prince of Wales Medical Research Institute, The University of New South Wales, Barker Street, Randwick 2031, Australia
    Neurobiol Aging 24:797-806. 2003
  7. ncbi request reprint Further evidence for an association between a mutation in the APP gene and Lewy body formation
    G Halliday
    Prince of Wales Medical Research Institute, Randwick, NSW, Australia
    Neurosci Lett 227:49-52. 1997
  8. ncbi request reprint Alzheimer's disease and inflammation: a review of cellular and therapeutic mechanisms
    G Halliday
    Prince of Wales Medical Research Institute, Randwick, Australia
    Clin Exp Pharmacol Physiol 27:1-8. 2000
  9. ncbi request reprint A role for the substantia nigra pars reticulata in the gaze palsy of progressive supranuclear palsy
    G M Halliday
    Prince of Wales Medical Research Institute, Randwick, Australia
    Brain 123:724-32. 2000
  10. ncbi request reprint A review of the neuropathology of schizophrenia
    G M Halliday
    The Prince of Wales Medical Research Institute, Randwick, New South Wales, Australia
    Clin Exp Pharmacol Physiol 28:64-5. 2001

Detail Information

Publications75

  1. ncbi request reprint Human-based studies on alpha-synuclein deposition and relationship to Parkinson's disease symptoms
    Glenda M Halliday
    Prince of Wales, Medical Research Institute, Randwick, NSW, Australia
    Exp Neurol 209:12-21. 2008
    ..Further correlation studies in prospectively-followed patients and, perhaps more importantly, controls are required in order to determine normal versus pathologic alpha-synuclein and how to detect such differences in clinical situations...
  2. ncbi request reprint A comparison of degeneration in motor thalamus and cortex between progressive supranuclear palsy and Parkinson's disease
    Glenda M Halliday
    Prince of Wales Medical Research Institute and University of New South Wales, Sydney, Australia
    Brain 128:2272-80. 2005
    ..The selective involvement of the VLp and primary motor cortex in PSP implicates these cerebellothalamocortical pathways as differentiating this disease, possibly contributing to the early falls...
  3. ncbi request reprint Alpha-synuclein redistributes to neuromelanin lipid in the substantia nigra early in Parkinson's disease
    Glenda M Halliday
    Prince of Wales Medical Research Institute and the University of New South Wales, Sydney, Australia
    Brain 128:2654-64. 2005
    ..Overall, these changes may trigger a cascade of events leading to larger intracellular aggregates of alpha-synuclein and the dispersement of protective pigment to precipitate cell death in Parkinson's disease...
  4. ncbi request reprint Pick bodies in a family with presenilin-1 Alzheimer's disease
    Glenda M Halliday
    Prince of Wales Medical Research Institute and the University of New South Wales, Barker Street, Randwick, Sydney, 2031 NSW, Australia
    Ann Neurol 57:139-43. 2005
    ..M146L mutant PS-1 may predispose to both Pick's disease and AD by affecting multiple intracellular pathways involving tau phosphorylation and amyloid metabolism...
  5. ncbi request reprint Consensus neuropathological diagnosis of common dementia syndromes: testing and standardising the use of multiple diagnostic criteria
    G Halliday
    Prince of Wales Medical Research Institute, High Street, Randwick, 2031 New South Wales, Australia
    Acta Neuropathol 104:72-8. 2002
    ..Further development of simple and accurate methods to identify small vessel lesions and diagnose frontotemporal dementia is warranted...
  6. ncbi request reprint Identifying severely atrophic cortical subregions in Alzheimer's disease
    G M Halliday
    Prince of Wales Medical Research Institute, The University of New South Wales, Barker Street, Randwick 2031, Australia
    Neurobiol Aging 24:797-806. 2003
    ..Our findings show that the fusiform gyrus is particularly affected by AD, and suggest two levels of atrophy that correspond with published neurofibrillary tangle (most atrophic) and senile plaque (less atrophic) densities...
  7. ncbi request reprint Further evidence for an association between a mutation in the APP gene and Lewy body formation
    G Halliday
    Prince of Wales Medical Research Institute, Randwick, NSW, Australia
    Neurosci Lett 227:49-52. 1997
    ..Some of these Lewy bodies had peripheral halos immunoreactive for beta-amyloid. These findings suggest a greater than chance link between genetic mutations for Alzheimer's disease and Lewy body formation...
  8. ncbi request reprint Alzheimer's disease and inflammation: a review of cellular and therapeutic mechanisms
    G Halliday
    Prince of Wales Medical Research Institute, Randwick, Australia
    Clin Exp Pharmacol Physiol 27:1-8. 2000
    ..Cerebral amyloidosis is highly prevalent in AD, compromising the BBB and vasoactivity. Anti-inflammatory medications may alleviate these problems...
  9. ncbi request reprint A role for the substantia nigra pars reticulata in the gaze palsy of progressive supranuclear palsy
    G M Halliday
    Prince of Wales Medical Research Institute, Randwick, Australia
    Brain 123:724-32. 2000
    ..This was the largest difference between these cases. As the SNr projects to the superior colliculus, degeneration of this basal ganglia structure may disrupt eye movements in progressive supranuclear palsy...
  10. ncbi request reprint A review of the neuropathology of schizophrenia
    G M Halliday
    The Prince of Wales Medical Research Institute, Randwick, New South Wales, Australia
    Clin Exp Pharmacol Physiol 28:64-5. 2001
    ....
  11. ncbi request reprint Effect of anti-inflammatory medications on neuropathological findings in Alzheimer disease
    G M Halliday
    Prince of Wales Medical Research Institute, High Street, Randwick, NSW 2031, Australia
    Arch Neurol 57:831-6. 2000
    ..There has been no analysis of brain tissue from longitudinally observed, cognitively tested patients to validate whether anti-inflammatory medications protect against the pathological changes of Alzheimer disease...
  12. pmc Pedigree with frontotemporal lobar degeneration--motor neuron disease and Tar DNA binding protein-43 positive neuropathology: genetic linkage to chromosome 9
    Agnes A Luty
    Prince of Wales Medical Research Institute, Sydney, NSW, Australia
    BMC Neurol 8:32. 2008
    ..The objective in this study is to identify the genetic locus in a multi-generational Australian family with FTLD-MND...
  13. doi request reprint Intralaminar nuclei of the thalamus in Lewy body diseases
    Daniel Brooks
    Prince of Wales Medical Research Institute and the University of New South Wales, Sydney, Australia
    Brain Res Bull 78:97-104. 2009
    ..The significant degeneration demonstrated in the intralaminar thalamus is likely to contribute to the movement and cognitive dysfunction observed in Lewy body disorders...
  14. ncbi request reprint Differences in regional brain atrophy in genetic forms of Alzheimer's disease
    Gillian C Gregory
    Prince of Wales Medical Research Institute and the University of New South Wales, Barker Street, Randwick, Sydney, NSW 2031, Australia
    Neurobiol Aging 27:387-93. 2006
    ..This effect may be due to the influence of presenilin-1 on tau phosphorylation and metabolism. These differences may explain the earlier onset ages in these different forms of Alzheimer's disease...
  15. ncbi request reprint Distribution of brain atrophy in behavioral variant frontotemporal dementia
    Jillian J Kril
    Centre for Education and Research on Ageing, The University of Sydney, Concord Hospital, Concord 2139, Sydney, Australia
    J Neurol Sci 232:83-90. 2005
    ..This suggests that the regional pattern of neurodegeneration, rather than the type of histopathology influences the clinical syndrome in FTD...
  16. ncbi request reprint GSK3B polymorphisms alter transcription and splicing in Parkinson's disease
    John B J Kwok
    Garvan Institute of Medical Research, University of New South Wales, Barker Street, Randwick, Sydney NSW 2031, Australia
    Ann Neurol 58:829-39. 2005
    ..64; p = 0.007; (H1/H1 individuals: odds ratio, 0.68; p < 0.001). Ours results suggest GSK3B polymorphisms alter transcription and splicing and interact with Tau haplotypes to modify disease risk in PD...
  17. ncbi request reprint Comparison of motor, cognitive, and behavioral features in progressive supranuclear palsy and Parkinson's disease
    Nicholas J Cordato
    Department of Geriatric Medicine, Westmead Hospital and The University of Sydney, Westmead, New South Wales, Australia
    Mov Disord 21:632-8. 2006
    ..For PSP, behavioral changes related to severity of general disability, thereby challenging previous models of relationships between behavior, motor, and cognitive disturbance for this disorder...
  18. doi request reprint Degeneration in different parkinsonian syndromes relates to astrocyte type and astrocyte protein expression
    Yun Ju C Song
    Prince of Wales Medical Research Institute and the University of New South Wales, Barker Street, Randwick, Sydney, Australia
    J Neuropathol Exp Neurol 68:1073-83. 2009
    ..These heterogeneous astroglial responses in PD, MSA, PSP, and CBD indicate distinct underlying pathogenic mechanisms in each disorder...
  19. ncbi request reprint Prevalence and clinical features of common LRRK2 mutations in Australians with Parkinson's disease
    Yue Huang
    Prince of Wales Medical Research Institute, University of New South Wales, Australia
    Mov Disord 22:982-9. 2007
    ..Our results demonstrate that the G2019S mutation carriers share the same ancestors who migrated to Australia originally from Europe and that other LRRK2 mutations (R1441H and A1442P) can be found in this population...
  20. doi request reprint Relative preservation of thalamic centromedian nucleus in parkinsonian patients with dystonia
    Linda Truong
    Prince of Wales Medical Research Institute, University of New South Wales, Randwick, Australia
    Mov Disord 24:2128-35. 2009
    ..Overall this data provides evidence for pathway-specific neurodegeneration as an underlying feature of the clinical variability observed in patients with PD...
  21. doi request reprint Frontotemporal dementia and dementia with Lewy bodies in a case-control study of Alzheimer's disease
    Olivier Piguet
    Prince of Wales Medical Research Institute and University of New South Wales, Sydney, Australia
    Int Psychogeriatr 21:688-95. 2009
    ..We aimed to determine the frequency of clinical diagnosis of FTD and DLB and the underlying pathology in a well-characterized cohort of patients with a clinical diagnosis of probable or possible AD...
  22. doi request reprint Phosphorylation of soluble tau differs in Pick's disease and Alzheimer's disease brains
    Janet van Eersel
    Discipline of Pathology, The University of Sydney, Sydney, NSW, 2006, Australia
    J Neural Transm 116:1243-51. 2009
    ..Such differences in solubility and phosphorylation may contribute, at least in part, to the formation of distinct tau deposits, but may also have implications for the clinical differences between AD and PiD...
  23. ncbi request reprint Selective loss of pyramidal neurons in the pre-supplementary motor cortex in Parkinson's disease
    Virginia Macdonald
    Prince of Wales Medical Research Institute and the University of New South Wales, Sydney, Australia
    Mov Disord 17:1166-73. 2002
    ..Our results implicate the degeneration of the premotor projection from the pre-SMA, along with dopaminergic basal ganglia dysfunction, in the pathogenesis of Parkinson's disease...
  24. ncbi request reprint Neuromelanin in human dopamine neurons: comparison with peripheral melanins and relevance to Parkinson's disease
    H Fedorow
    Prince of Wales Medical Research Institute, Barker St, Randwick, Sydney, NSW 2031, Australia
    Prog Neurobiol 75:109-24. 2005
    ..Recent data from neuromelanin in the Parkinson's disease brain suggests that this proposed function may be compromised, thus rendering pigmented neurons vulnerable to oxidative damage in this disorder...
  25. doi request reprint Excessive dopamine neuron loss in progressive supranuclear palsy
    Karen E Murphy
    Prince of Wales Medical Research Institute, Randwick, Australia
    Mov Disord 23:607-10. 2008
    ..These cell groups innervate subcortical and cortical regions and may be required for adequate response to levodopa therapy...
  26. doi request reprint Mitochondrial DNA haplogroups J and K are not protective for Parkinson's disease in the Australian community
    Prachi Mehta
    Department of Neurology and Neurogenetics, Kolling Institute, Royal North Shore Hospital and University of Sydney, Sydney, Australia
    Mov Disord 24:290-2. 2009
    ..There was no significant difference in the prevalence of mtDNA haplogroup J or K in PD patients compared to population-based controls. Our findings indicate that mtDNA haplogroups J and K are not associated with a lower risk of PD...
  27. doi request reprint The Sydney multicenter study of Parkinson's disease: the inevitability of dementia at 20 years
    Mariese A Hely
    Department of Neurology, Westmead Hospital, Westmead, New South Wales, Australia
    Mov Disord 23:837-44. 2008
    ..The challenge is to understand the cellular mechanisms underlying the diverse features of advanced PD that go far beyond a lack of dopamine...
  28. ncbi request reprint A possible role for humoral immunity in the pathogenesis of Parkinson's disease
    Carolyn F Orr
    Prince of Wales Medical Research Institute, University of New South Wales, Randwick, Sydney, Australia
    Brain 128:2665-74. 2005
    ..This pattern of humoral immune reactivity is consistent with an immune activation of microglia leading to the targeting of dopamine nigral neurons for destruction in both idiopathic and genetic cases of Parkinson's disease...
  29. ncbi request reprint Cognitive, extrapyramidal, and magnetic resonance imaging predictors of functional impairment in nondemented older community dwellers: the Sydney Older Person Study
    Hayley P Bennett
    Prince of Wales Medical Research Institute and University of New South Wales, Sydney, Australia
    J Am Geriatr Soc 54:3-10. 2006
    ..To identify the clinical correlates of functional incapacity in the community living "old-old."..
  30. ncbi request reprint Preserved cognition and functional independence after a large right posterior cerebral artery infarct: longitudinal clinical and neuropathological findings
    Olivier Piguet
    Prince of Wales Medical Research Institute and the University of New South Wales, Sydney, Australia
    Neurocase 12:81-90. 2006
    ..Postmortem investigations revealed additional recent vascular lesions in the occipital region. This case study underscores the importance of comprehensive assessment methods combining neurological, neuroimaging and cognitive tools...
  31. ncbi request reprint Clinical correlates of selective pathology in the amygdala of patients with Parkinson's disease
    Antony J Harding
    Prince of Wales Medical Research Institute and University of New South Wales, Sydney, NSW, Australia
    Brain 125:2431-45. 2002
    ..Thus, the impact of Parkinson's disease on the amygdala is highly selective and correlates with both early and late clinical features...
  32. ncbi request reprint Positional effects of presenilin-1 mutations on tau phosphorylation in cortical plaques
    Claire E Shepherd
    Prince of Wales Medical Research Institute, Randwick, 2031 Sydney, Australia
    Neurobiol Dis 15:115-9. 2004
    ..These findings suggest that PS-1 mutations increase tau deposition while mutation-specific cellular responses determine phosphorylation events and may influence cell death mechanisms...
  33. ncbi request reprint Postmortem analysis of bilateral subthalamic electrode implants in Parkinson's disease
    Jasmine M Henderson
    Prince of Wales Medical Research Institute, Sydney, NSW, Australia
    Mov Disord 17:133-7. 2002
    ..Tissue changes associated with the subthalamic electrode tracts included mild cell loss, astrogliosis, and some tissue vacuolation. Our postmortem analysis indicates little tissue damage associated with STN stimulation for PD...
  34. ncbi request reprint Identification of families with cortical Lewy body disease
    Antony J Harding
    Prince of Wales Medical Research Institute, Barker Street, Randwick, Sydney, NSW 2031, Australia
    Am J Med Genet B Neuropsychiatr Genet 128:118-22. 2004
    ....
  35. ncbi request reprint Identifying the pattern of olfactory deficits in Parkinson disease using the brief smell identification test
    Kay L Double
    Prince of Wales Medical Research Institute, University of New South Wales, Sydney, Australia
    Arch Neurol 60:545-9. 2003
    ..Olfactory testing may be a useful diagnostic aid for Parkinson disease, but the types of odors most commonly affected need to be identified...
  36. ncbi request reprint Selective hippocampal neuron loss in dementia with Lewy bodies
    Antony J Harding
    Prince of Wales Medical Research Institute and University of New South Wales, Sydney, Australia
    Ann Neurol 51:125-8. 2002
    ..These findings suggest a selective loss of frontally projecting hippocampal neurons in dementia with Lewy bodies versus those projecting to temporal lobe regions in Alzheimer's disease...
  37. ncbi request reprint Mutations in the tau gene that cause an increase in three repeat tau and frontotemporal dementia
    Prudence M Stanford
    Garvan Institute of Medical Research, Sydney, NSW, Australia
    Brain 126:814-26. 2003
    ..The increase in tau proteolysis was associated with increased evidence of apoptosis. This mechanism of neurodegeneration may be more applicable to the majority of FTD cases, which do not accumulate insoluble tau deposits...
  38. ncbi request reprint Variable phenotype of Alzheimer's disease with spastic paraparesis
    Helena Karlstrom
    Garvan Institute of Medical Research, Sydney, Australia, and Karolinska Institutet, Stockholm, Sweden
    J Neurochem 104:573-83. 2008
    ..Variations in neuropathology and neurological symptoms in PSEN1 AD raise the prospect that modifier genes may underlie this phenotypic heterogeneity...
  39. ncbi request reprint Neurofilament-immunoreactive neurons in Alzheimer's disease and dementia with Lewy bodies
    Claire E Shepherd
    Prince of Wales Medical Research Institute, University of New South Wales, Barker Street, Randwick, Sydney 2031, Australia
    Neurobiol Dis 9:249-57. 2002
    ..This increased number of cortical NF-containing neurons reveal novel widespread cortical changes, beyond those explained by Lewy body formation, that are specific for DLB...
  40. ncbi request reprint Severity of gliosis in Pick's disease and frontotemporal lobar degeneration: tau-positive glia differentiate these disorders
    Emma Schofield
    Prince of Wales Medical Research Institute and University of New South Wales, Sydney, Australia
    Brain 126:827-40. 2003
    ..In frontotemporal lobar degeneration, a significant proportion of the activated white matter microglia were tau-2-immunoreactive, suggesting direct involvement in axonal degeneration, possibly via immune processes...
  41. ncbi request reprint Anticipation of onset age in familial Parkinson's disease without SCA gene mutations
    Yue Huang
    Prince of Wales Medical Research Institute, University of New South Wales, Barker Street, Randwick, NSW 2031, Australia
    Parkinsonism Relat Disord 12:309-13. 2006
    ....
  42. ncbi request reprint Neuron loss from the hippocampus of Alzheimer's disease exceeds extracellular neurofibrillary tangle formation
    Jillian J Kril
    Department of Pathology, The University of Sydney, Sydney, Australia
    Acta Neuropathol 103:370-6. 2002
    ..2-17.2%, mean 8.1%). Analysis of NFT accumulation with duration of dementia showed a linear relationship, supporting the belief that NFTs progressively accumulate with time...
  43. ncbi request reprint Clinicopathological staging of frontotemporal dementia severity: correlation with regional atrophy
    Jillian J Kril
    Centre for Education and Research on Ageing, The University of Sydney, Sydney, Australia
    Dement Geriatr Cogn Disord 17:311-5. 2004
    ..Much of the frontal lobe, the amygdala and hippocampus are severely atrophic by stage 2, suggesting that they are some of the earliest areas affected in FTD...
  44. ncbi request reprint Staging disease severity in movement disorder tauopathies: brain atrophy separates progressive supranuclear palsy from corticobasal degeneration
    Emma C Schofield
    Prince of Wales Medical Research Institute and the University of New South Wales, Randwick, Australia
    Mov Disord 20:34-9. 2005
    ..86; P = 0.03). The degree of global atrophy in PSP appears to be distinct from other tauopathies, while CBD fits the same pattern as other pathological forms of frontotemporal dementia...
  45. doi request reprint Increased ATP-binding cassette transporter A1 expression in Alzheimer's disease hippocampal neurons
    Woojin Scott Kim
    Prince of Wales Medical Research Institute, Randwick, NSW, Australia
    J Alzheimers Dis 21:193-205. 2010
    ..However, hippocampal Apoe and Puma gene expression were not correlated with increased Abca1 expression in mice. Our data indicate that ABCA1 is upregulated in AD hippocampal neurons potentially via an amyloid-beta-mediated pathway...
  46. doi request reprint Monocyte chemoattractant protein-1 plays a dominant role in the chronic inflammation observed in Alzheimer's disease
    Anna Sokolova
    Prince of Wales Medical Research Institute, Barker Street, Randwick, Sydney, Australia
    Brain Pathol 19:392-8. 2009
    ..Our data support previous work on significant increases in IL-6 and IL-8 in AD but indicate that MCP-1 may play a more dominant role in chronic inflammation in AD...
  47. ncbi request reprint What is the dominant Abeta species in human brain tissue? A review
    Gillian C Gregory
    Prince of Wales Medical Research Institute and the University of New South Wales, Sydney, Australia
    Neurotox Res 7:29-41. 2005
    ..These findings are discussed in association with Abeta peptide function and a model of toxicity developed...
  48. ncbi request reprint Pallidal stimulation reduces treatment-induced dyskinesias in "minimal-change" multiple system atrophy
    Yue Huang
    Prince of Wales Medical Research Institute and University of New South Wales, Randwick, Australia
    Mov Disord 20:1042-7. 2005
    ..Here, we present an autopsy-confirmed case of "minimal-change" multiple system atrophy in whom pallidal stimulation surgery was effective in abolishing severe levodopa-induced dyskinesia...
  49. ncbi request reprint Insoluble alpha-synuclein in Alzheimer's disease without Lewy body formation
    Melissa Broe
    Prince of Wales Medical Research Institute, Sydney, 2031 Australia
    Neurotox Res 7:69-76. 2005
    ..This lipid-association of alpha-synuclein in mature AD plaques links this protein with other lipid changes thought to be important in disease pathogenesis...
  50. doi request reprint Thalamic changes in Parkinson's disease
    Glenda M Halliday
    Prince of Wales Medical Research Institute and University of New South Wales, Sydney, Australia
    Parkinsonism Relat Disord 15:S152-5. 2009
    ..Damage to these regions appears to impact on cognition, awareness and perception. These studies suggest that direct thalamic pathology contributes to the symptoms of Parkinson's disease...
  51. ncbi request reprint Frequency of tau mutations in familial and sporadic frontotemporal dementia and other tauopathies
    Prudence M Stanford
    Garvan Institute for Medical Research, 384 Victoria Street, Sydney, 2010, Australia
    J Neurol 251:1098-104. 2004
    ..Although tauopathies have been considered to result from genetic defects, screening for tau gene mutations in sporadic cases is not likely to identify pathogenic mutations...
  52. ncbi request reprint Regional and cellular pathology in frontotemporal dementia: relationship to stage of disease in cases with and without Pick bodies
    Cindy Kersaitis
    Centre for Education and Research on Ageing, The University of Sydney, Concord Hospital, 2139 Concord, NSW, Australia
    Acta Neuropathol 108:515-23. 2004
    ..These results show that the earliest cellular changes in FTD occur in glia, and that disease stage rather than FTD subtype determines the pattern and extent of neuronal degeneration...
  53. pmc Apolipoprotein-E forms dimers in human frontal cortex and hippocampus
    David A Elliott
    Prince of Wales Medical Research Institute, Randwick NSW 2031, Australia
    BMC Neurosci 11:23. 2010
    ..Human frontal cortex and hippocampus from control and AD post-mortem samples were homogenised and analysed for apoE by western blotting under both reducing and non-reducing conditions...
  54. pmc Genetically confirmed clinical Huntington's disease with no observable cell loss
    M Caramins
    Department of Molecular and Clinical Genetics, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia
    J Neurol Neurosurg Psychiatry 74:968-70. 2003
    ..The potential to miss other HD cases at post-mortem examination, and the implications of this for family members, are discussed...
  55. ncbi request reprint Tau isoform expression in frontotemporal dementia without tau deposition
    Greg T Sutherland
    Centre for Education and Research on Ageing, The University of Sydney, Sydney, 2006, New South Wales, Australia
    J Clin Neurosci 14:1182-5. 2007
    ..There were no differences in total tau mRNA or 4R versus 3R isoform expression. Our study suggests that perturbed tau mRNA expression is unlikely to be involved in the pathogenesis of tau-negative FTD...
  56. ncbi request reprint Clinicopathological correlates in frontotemporal dementia
    John R Hodges
    Prince of Wales Medical Research Institute, The University of New South Wales, Randwick, New South Wales, Australia
    Ann Neurol 56:399-406. 2004
    ..Therefore, the pathological substrate can be predicted in a significant proportion of FTD patients, which has important implications for studies targeting mechanistic treatments...
  57. ncbi request reprint Dolichol is the major lipid component of human substantia nigra neuromelanin
    Heidi Fedorow
    Centre for Vascular Research, University of New South Wales, Sydney, New South Wales, Australia
    J Neurochem 92:990-5. 2005
    ..Furthermore, these studies identify a potential novel role for the isoprenoid pathway in the regulation of neuromelanin function and neurodegeneration within the SN...
  58. pmc p25alpha relocalizes in oligodendroglia from myelin to cytoplasmic inclusions in multiple system atrophy
    Yun Ju C Song
    Prince of Wales Medical Research Institute, Randwick, New South Wales, Australia
    Am J Pathol 171:1291-303. 2007
    ....
  59. doi request reprint Sigma nonopioid intracellular receptor 1 mutations cause frontotemporal lobar degeneration-motor neuron disease
    Agnes A Luty
    Neuroscience Research Australia, Randwick, Sydney, New South Wales, Australia
    Ann Neurol 68:639-49. 2010
    ..Our objective was to identify the causative gene in an FTLD-MND pedigree with no mutations in known dementia genes...
  60. doi request reprint The case of a 48 year-old woman with bizarre and complex delusions
    Clement T Loy
    Prince of Wales Medical Research Institute, Barker Street, Randwick, Sydney, NSW 2031, Australia
    Nat Rev Neurol 6:175-9. 2010
    ..Her psychosis progressed despite receiving high doses of antipsychotics. The patient's father also had a psychotic episode in his 40s. He subsequently developed motor neuron disease, which caused his death at 68 years of age...
  61. doi request reprint Neuropathologic correlates of white matter hyperintensities
    Vanessa G Young
    Discipline of Medicine, University of Sydney, Sydney, Australia
    Neurology 71:804-11. 2008
    ..Study 2 compared the histopathology of WMH with normal WM...
  62. doi request reprint Effect of age on proliferation-regulating factors in human adult neurogenic regions
    Eryn L Werry
    Brain Sciences University of New South Wales, Randwick, NSW, Australia
    J Neurochem 115:956-64. 2010
    ..These findings suggest regulation of the adult neurogenic environment in the human brain may differ over time from that in other species...
  63. ncbi request reprint Phosphorylation of apolipoprotein-E at an atypical protein kinase CK2 PSD/E site in vitro
    Mark Raftery
    Bioanalytical Mass Spectrometry Facility, University of New South Wales, Sydney NSW 2052, Australia
    Biochemistry 44:7346-53. 2005
    ..The phosphorylation of apoE by CK2 as well as the activation of CK2 by apoE may be relevant in vivo where apoE, CK2, and tau are co-localized with additional CK2 targets on neuronal microtubules...
  64. ncbi request reprint Presenilin-1 mutation L271V results in altered exon 8 splicing and Alzheimer's disease with non-cored plaques and no neuritic dystrophy
    John B J Kwok
    Garvan Institute of Medical Research, Darlinghurst, Sydney 2010, Australia
    J Biol Chem 278:6748-54. 2003
    ..We postulate that variant plaques observed in this family are due in part to the effects of PS-1deltaexon8 and that interaction between PS-1 and various protein complexes are necessary for neuritic plaque formation...
  65. ncbi request reprint Astrocytic degeneration relates to the severity of disease in frontotemporal dementia
    Melissa Broe
    Centre for Education and Research on Ageing, The University of Sydney, Concord, Australia
    Brain 127:2214-20. 2004
    ..Furthermore, this astrocytic apoptosis directly relates to the degree of degeneration in FTD, and becomes the overwhelming pathological feature as the disease progresses...
  66. ncbi request reprint Neuropathology in the S305S tau gene mutation
    Glenda M Halliday
    Brain 129:E40. 2006
  67. ncbi request reprint Mutations in progranulin explain atypical phenotypes with variants in MAPT
    Stuart M Pickering-Brown
    Brain 129:3124-6. 2006
    ..Here, we demonstrate that the MAPT variants are almost certainly rare benign polymorphisms as all of these cases harbour mutations in Progranulin (PGRN). Mutations in PGRN were recently shown to cause ubiquitin-positive FTDP-17...
  68. ncbi request reprint Progression in frontotemporal dementia: identifying a benign behavioral variant by magnetic resonance imaging
    Rhys R Davies
    Department of Clinical Neurosciences, University of Cambridge, Addenbrooke s Hospital, Cambridge, England
    Arch Neurol 63:1627-31. 2006
    ..To assess the clinical course and prognosis in patients with behavioral-variant frontotemporal dementia (FTD) lacking evidence of brain atrophy on magnetic resonance imaging (MRI)...
  69. ncbi request reprint Intraneuronal advanced glycation endproducts in presenilin-1 Alzheimer's disease
    Gerald Munch
    Neuroimmunological Cell Biology IZKF, Leipzig, Germany
    Neuroreport 13:601-4. 2002
    ..These conditions of carbonyl stress may contribute to increased neuronal dysfunction and vulnerability leading to the early disease onset...
  70. ncbi request reprint Parkin Co-Regulated Gene (PACRG) is regulated by the ubiquitin-proteasomal system and is present in the pathological features of Parkinsonian diseases
    Juliet M Taylor
    Bruce Lefroy Centre for Genetic Health Research, Murdoch Children s Research Institute, Melbourne, Victoria 3052, Australia
    Neurobiol Dis 27:238-47. 2007
    ..Together, these results demonstrate that PACRG is regulated by the ubiquitin-proteasomal system and may play a role in the pathogenesis of Parkinson's disease...
  71. ncbi request reprint The pathological basis of semantic dementia
    R Rhys Davies
    Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK
    Brain 128:1984-95. 2005
    ....
  72. ncbi request reprint Clinical significance of lobar atrophy in frontotemporal dementia: application of an MRI visual rating scale
    Christopher M Kipps
    Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK
    Dement Geriatr Cogn Disord 23:334-42. 2007
    ....
  73. ncbi request reprint P25alpha immunoreactive but alpha-synuclein immunonegative neuronal inclusions in multiple system atrophy
    Kerry G Baker
    Acta Neuropathol 111:193-5. 2006
  74. ncbi request reprint A critical review of the development and importance of proteinaceous aggregates in animal models of Parkinson's disease: new insights into Lewy body formation
    Gloria E Meredith
    Department of Cellular and Molecular Pharmacology, Chicago Medical School, Finch University of Health Sciences, 3333 Green Bay Road, North Chicago, IL 60054, USA
    Parkinsonism Relat Disord 10:191-202. 2004
    ..Elucidating the common mechanisms in animal models is a first step towards understanding the role of Lewy bodies and their formation in Parkinson's disease...
  75. ncbi request reprint Haplotype analysis of the IGF2-INS-TH gene cluster in Parkinson's disease
    Greg Sutherland
    School of Biomolecular and Biomedical Sciences, Eskitis Institute, Griffith University, Brisbane, Australia
    Am J Med Genet B Neuropsychiatr Genet 147:495-9. 2008
    ..Our findings suggest that common genetic variants in the IGF2-INS-TH cluster modify susceptibility to idiopathic Parkinson's disease...