The joint PSP (Europe) Association/Alzheimer's Society International Medical Workshop took place on the 22nd and 23rd of October, 2001, in the state rooms at Stowe School, previously the ancestral residence of the Dukes of Buckingham in Buckinghamshire, United Kingdom. This was the third in a series of successful workshops organised by Brigadier Michael Koe, Chief Executive of the PSP (Europe) Association and Professor Andrew Lees, Chairman of the Medical Advisory Panel of the PSP Association. The two-day workshop, jointly sponsored by the PSP Association and the Alzheimer's Society, was enthusiastically supported by those attending. Both days reflected, in presentations, in discussant sessions and in debate, the overlapping areas of research and the growing promise of 'light at the end of the tunnel' in finding the cause, effective treatment and cure for these two diseases. Research into the tau, -amyloid precursor protein and presenilin genes and proteins; and anti-inflammatory and cholesterol management gave hope for prevention of Alzheimer's disease in the near future, with a similar, though perhaps longer route for PSP. Twenty-six eminent international faculty members together with a select gathering of other scientists and clinicians actively involved in research into the tauopathies took part in an exciting and rewarding brainstorming session.
Proceedings on Day One focused on aspects of the biology of tau and differential properties of tau isoform function in assembly and stabilisation of microtubules and on the genetic and clinico-neuropathological correlates of the primary tauopathies. The spectrum of phenotypes and pathology describing the three main primary tauopathies ("AD-like", "PSP/CBD-like" and "PiD-like") have all been observed with the different groups of tau mutations in FTDP-17. This could provide the basis for a more precise classification of the tauopathies and the possibility of selective vulnerability of different neuronal populations in the sporadic tauopathies, related to differences in the distribution of different tau isoforms in different neuronal populations. As summarised by Professor John Hardy (National Institute of Aging, Bethesda, MD), it is still not clear if tau tangles or the loss of tau function or both cause neuronal death. Particular emphasis was placed on the tau gene haplotype association with PSP and CBD. Although the functional significance of this robust association is as yet unclear, whether a polymorphism in the tau gene affects tau RNA splicing in PSP and CBD also needs to be determined. Day Two's proceedings were opened by Professor Martin Rossor (Institute of Neurology, London) and focused on the rapid progress in AD research in relation to the genetics of the amyloid precursor protein gene and the presenilins and their role in amyloidogenesis. Although the importance of tau dysfunction in AD was not discounted, emphasis was placed on presenilin, currently incriminated as the actual ␥-secretase responsible for cleavage of the amyloid precursor protein to form -amyloid. The possibility of ␥-secretase as a potential therapeutic target and other therapeutic approaches based on -myloid pathology were discussed, e.g., -amyloid immunisation leading to clearance of plaque burden in the AD brain and the reduction of the highly amyloidogenic A 42 by