Jurgen Gotz and Lars Ittner report from a recent IBRO Satellite Symposium.

On the occasion of the IBRO World Congress of Neuroscience, held last month in Melbourne, Australia, a total of 20 satellite symposia all across the country and even in Taiwan attracted speakers and researchers to the fifth continent, many of them for the first time. The Alzheimer’s and Parkinson’s Disease Laboratory at the newly established Brain & Mind Research Institute (BMRI) of the University of Sydney hosted the Satellite Symposium on Protein Aggregation in Neurodegeneration, a one-day event that preceded the main conference. Speakers from Europe and Australia presented mostly unpublished research findings covering AD, PD, frontotemporal dementia (FTD), and prion diseases (PrP). Here’s a brief summary.

Wei Ping Gai of Flinders University, Adelaide, Australia, presented new data on the role of truncated α-synuclein in diseases with Lewy bodies. These truncated forms have been identified by mass spectrometry using Lewy bodies as starting material. David Small of Monash University, Australia, highlighted the role of proteoglycans in regulating the activity of BACE1. Small described evidence from in vitro and cell culture studies suggesting that proteoglycans regulate BACE1 activity and Aβ production. Gerald Muench of James Cook University, Townsville, Australia, spoke about reactive carbonyl compounds (RCCs) as physiological protein cross-linkers in pathological protein deposits, particularly neurofibrillary tangles and amyloid plaques. Furthermore, Muench introduced lipoic acid as an anti-inflammatory antioxidant with possible therapeutic potential. Muench presented clinical indications that lipoic acid might be particularly potent in MCI and early stage AD patients (MMSE >25), where the average progression was slowed to 0.6 MMSE points per year over a 4-year period. Muench cautioned, however, that these data were derived from an open trial of only 43 patients in Hannover, Germany.

Novel data on the tau kinase MARK and its role in axonal outgrowth and growth cone formation were presented by Eva-Maria Mandelkow, Max Planck Unit for Structural Molecular Biology, Hamburg, Germany. Roland Brandt from the University of Osnabrueck, Germany, applied a photoactivation approach to GFP-tagged tau to determine tau dynamics and to show where tau is localized within the cell. The data indicate that trapping of tau by microtubule interaction, and flux to the distal neurite, mediate the distribution of tau in neurons. Dysregulation of tau phosphorylation causes a redistribution of tau similar to what has been described in tauopathies. Jillian Kril, of the University of Sydney, presented her neuropathological findings of different subtypes of frontotemporal dementia and also discussed the role of astrocytes in FTD. Simon Hawke of the BMRI discussed the role of subcellular compartments of PrP conversion. Ralph Martins, Centre of Excellence for Alzheimer’s Disease Research and Care at Edith Cowan University in Western Australia, presented data on novel peptides that selectively neutralized Aβ toxicity in vitro and in vivo. The specificity of these peptides to human Aβ has resulted in their evaluation as potential PET amyloid plaque imaging agents. Claire Shepherd of the Prince of Wales Medical Research Institute, University of New South Wales, Sydney, presented her new data on inflammation in AD, using a multiplex approach to compare sporadic AD with familial cases carrying PS1 mutations. The data demonstrate that monocyte chemotactic protein-1 (MCP-1) plays a dominant role in the chronic inflammation in AD.

A novel transgenic mouse model of parkinsonism in frontotemporal dementia was the focus of Lars Ittner’s presentation. Ittner is at BMRI, Sydney. These mice express the K369I mutation of tau that has been previously identified in Pick’s disease. The mice faithfully model the histopathology of Pick’s disease. They further display early onset memory impairment, parkinsonism, and amyotrophy. Importantly, the transgenic mice respond to L-dopa (see also Salzburg conference story). Eckhard Mandelkow, Max Planck Unit for Structural Molecular Biology, Hamburg, Germany, showed new data of anti-aggregation and pro-aggregation tau mutant mice, the latter forming mixed aggregates of human and mouse tau. Finally, Richard Banati of the BMRI spoke about microglial activation and novel kinetic studies using the PK11195 ligand for the peripheral-type benzodiazepine receptor. This receptor has a regulatory influence on several immune functions, and for this reason is under investigation as a potential therapeutic target using novel specific drugs.

The atmosphere at the symposium was convivial. Meals served in the meeting room allowed for time to mingle and talk. The symposium concluded with an Australian dinner in the historic quarter, The Rocks, complete with a resplendent view of the Sydney Opera House.—Jurgen Gotz and Lars Ittner.

Jurgen Gotz and Lars Ittner are both at the Alzheimer’s and Parkinson’s Disease Laboratory, BMRI, University of Sydney.


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News Citations

  1. Salzburg: Like PD, Like AD—New Tau Mice Draw Notice

Other Citations

  1. K369I mutation

External Citations

  1. IBRO World Congress of Neuroscience
  2. The Rocks

Further Reading

No Available Further Reading