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Genomes and Genes | Judith MiklossySummaryAffiliation: University Hospital Country: Switzerland Publications
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Publications
Beta-amyloid deposition and Alzheimer's type changes induced by Borrelia spirochetesJudith Miklossy
Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3
Neurobiol Aging 27:228-36. 2006..These observations indicate that, by exposure to bacteria or to their toxic products, host responses similar in nature to those observed in AD may be induced...
Emerging roles of pathogens in Alzheimer diseaseJudith Miklossy
International Alzheimer Research Centre, Prevention Alzheimer Foundation, Martigny Combe, Switzerland
Expert Rev Mol Med 13:e30. 2011..Global attention and action is needed to support this emerging field of research because dementia might be prevented by combined antibiotic, antiviral and anti-inflammatory therapy...
Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteriaJudith Miklossy
International Alzheimer Research Center, Prevention Alzheimer Foundation, Martigny Combe, Switzerland
J Neuroinflammation 8:90. 2011..Spirochetal infection occurs years or decades before the manifestation of dementia. As adequate antibiotic and anti-inflammatory therapies are available, as in syphilis, one might prevent and eradicate dementia...
Beta amyloid and hyperphosphorylated tau deposits in the pancreas in type 2 diabetesJudith Miklossy
Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, BC, Canada
Neurobiol Aging 31:1503-15. 2010....
Persisting atypical and cystic forms of Borrelia burgdorferi and local inflammation in Lyme neuroborreliosisJudith Miklossy
Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, BC, Canada
J Neuroinflammation 5:40. 2008..We investigated whether a similar situation may occur in Lyme neuroborreliosis...
Chronic inflammation and amyloidogenesis in Alzheimer's disease -- role of SpirochetesJudith Miklossy
University of British Columbia, Kinsmen Laboratory of Neurological Research, Vancouver, BC, Canada
J Alzheimers Dis 13:381-91. 2008....
Lrrk2 and chronic inflammation are linked to pallido-ponto-nigral degeneration caused by the N279K tau mutationJudith Miklossy
Kinsmen Laboratory of Neurological Research, The University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada, V6T 1Z3
Acta Neuropathol 114:243-54. 2007..The results indicate that Lrrk2 is linked to frontotemporal atrophy of PPND type caused by N279K tau mutation. They also show that chronic inflammation is involved in the pathogenesis of N279K/FTDP-17/PPND...
Enduring involvement of tau, beta-amyloid, alpha-synuclein, ubiquitin and TDP-43 pathology in the amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam (ALS/PDC)Judith Miklossy
Kinsmen Laboratory of Neurological Research, The University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, V6T 1Z3, Canada
Acta Neuropathol 116:625-37. 2008..The results obtained may help to define the commonality of the Guam disease with other tangle forming disorders and may help in monitoring the epidemiological changes that are taking place...
LRRK2 expression in normal and pathologic human brain and in human cell linesJudith Miklossy
Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, BC, Canada
J Neuropathol Exp Neurol 65:953-63. 2006..In summary, LRRK2 is constitutively expressed in neurons and also in glial cells of human brain. It strongly associates with pathological inclusions in several neurodegenerative disorders...
Thrombin and prothrombin are expressed by neurons and glial cells and accumulate in neurofibrillary tangles in Alzheimer disease brainTetsuaki Arai
Department of Psychiatry, Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, BC, Canada
J Neuropathol Exp Neurol 65:19-25. 2006..The accumulation of thrombin and prothrombin in NFTs supports the hypothesis that thrombin may be involved in tau proteolysis and that failure to metabolize tau may lead to its aggregation in neurodegenerative diseases...
Adhesion of exogenous human microglia and THP-1 cells to amyloid plaques of postmortem Alzheimer's disease brainSadayuki Hashioka
Kinsmen Laboratory of Neurological Research, Department of Psychiatry, The University of British Columbia, Vancouver, BC, Canada
J Alzheimers Dis 14:345-52. 2008..These results suggest that human microglial cells are capable of adhering to and phagocytosing post mortem AD plaque material but activation may be necessary. Astrocytes may further enhance the process...
Negative regulation of AbetaPP gene expression by pur-alphaNune Darbinian
Department of Neuroscience and Center for Neurovirology, Temple University School of Medicine, Philadelphia, PA 19122, USA
J Alzheimers Dis 15:71-82. 2008..These data point to a novel mechanism of controlling AbetaPP levels by the transcriptional regulatory protein, Pur-alpha, and suggest that Pur-alpha may be involved in the dysregulation of AbetaPP in Alzheimer's disease...
Borrelia burgdorferi persists in the brain in chronic lyme neuroborreliosis and may be associated with Alzheimer diseaseJudith Miklossy
University Institute of Pathology, Division of Neuropathology, University Medical School CHUV, 1011, Lausanne, Switzerland
J Alzheimers Dis 6:639-49; discussion 673-81. 2004..Further in vitro and in vivo studies may bring more insight into the potential role of spirochetes in AD...
Two novel presenilin-1 mutations (Y256S and Q222H) are associated with early-onset Alzheimer's diseaseJudith Miklossy
Centre for Neurovirology and Cancer Biology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA
Neurobiol Aging 24:655-62. 2003....
Cerebrospinal fluid antimicroglial antibodies in Alzheimer disease: a putative marker of an ongoing inflammatory processAmanda McRae
University of the West Indies, Faculty of Medical Sciences, Preclinical Sciences, Uriah Butler Highway, Champs Fleurs Trinidad and Tobago, WI, USA
Exp Gerontol 42:355-63. 2007..They may also indicate dysregulation of microglial function. Together with previous observations, these findings indicate that compromised immune defense mechanisms play an important role in the pathogenesis of AD...
Cerebral hypoperfusion induces cortical watershed microinfarcts which may further aggravate cognitive decline in Alzheimer's diseaseJudith Miklossy
University Institute of Pathology, Division of Neuropathology, CHUV, Lausanne, Switzerland
Neurol Res 25:605-10. 2003..Therefore, to treat and prevent arterial hypotension and maintain cerebral perfusion at an appropriate level in AD is essential...
Association of alleles carried at TNFA -850 and BAT1 -22 with Alzheimer's diseaseAnastazija Gnjec
Centre of Excellence for Alzheimer s Disease Research and Care, Faculty of Computing, Health and Science, School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Joondalup, 6027, WA, Australia
J Neuroinflammation 5:36. 2008..In the current study TNFA and BAT1 promoter polymorphisms were analysed in AD and control cases and BAT1 mRNA levels were investigated in brain tissue from AD and control cases...
Iron withholding: a defense against diseaseEugene D Weinberg
Department of Biology and Program in Medical Sciences, Indiana University, Bloomington, Indiana 47405, USA
J Alzheimers Dis 13:451-63. 2008....
Interferon regulatory factor 4 is involved in Epstein-Barr virus-mediated transformation of human B lymphocytesDongsheng Xu
Nebraska Center for Virology, School of Biological Sciences, University of Nebraska, Lincoln, Nebraska 68588, USA
J Virol 82:6251-8. 2008..011) in these CNS lymphomas. Our data suggest that IRF-4 may be a critical factor in EBV transformation and a useful target in the therapy of EBV-mediated neoplasia...
Cerebral hypoperfusion generates cortical watershed microinfarcts in Alzheimer diseaseOda-Christina Suter
University Institute of Pathology, Division of Neuropathology, University Medical School, University of Lausanne, Lausanne, Switzerland
Stroke 33:1986-92. 2002..To prevent the formation of watershed cortical microinfarcts in AD, monitoring blood pressure and treating arterial hypotension are essential...
