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Press Release

Highlights of Stockholm 2012 Springfield meeting

Alzheimer’s disease was described over 100 years ago by the German psychiatrist Alois Alzheimer, but it has recently become a major public health issue of the XXIst century as a result of population aging. The last two decades have witnessed very intensive research in the field and, although the cause of the disease still escapes us, more than 40 clinical trials on more than 10.000 patients are in progress worldwide. The most recent and important findings will be discussed at the Stockholm/Springfield conference.

I. Update on current and new therapeutic targets.

At this meeting, two novel and most important suspected culprits will be investigated and thoroughly scrutinized as possible targets for new treatments.

Tau protein

The tau protein is modified in the earliest stages of the disease and interferes with the transport system inside nerve cells eventually leading to their death. Abnormal tau protein is a feature of many brain neurodegenerative disease (see L. Buée).

Immunising Alzheimer patients against Tau is now a possibility and will be reported for the first time at our meeting (see A. Muhs).

The new interest in this protein stems from recent experiments in transgenic mice models of Alzheimer’s disease which support the concept that accumulation of abnormal tau is mediated through spreading of seeds of the protein from nerve cell to nerve cell. If this concept is correct Alzheimer’s disease would initiate in a very small part of the brain many years before becoming symptomatic, spreading progressively to the whole brain within 15-20 years. Preventing the initial formation of the abnormal tau seeds would block the subsequent invasion of tau aggregates representing a future possible strategy for a treatment.

Oligomers and new approaches to anti-amyloid therapy

In a different session of the meeting the formation and accumulation of other toxic “seeds, oligomers, will be discussed. Oligomers are elementary molecular units of beta-amyloid which can be detected both in brain and in the cerebrospinal fluid of patients many years before the appearance of symptoms of the disease and are presumed to be toxic to the brain. Oligomers represent an important potential target of treatment (see L. Mucke and D. Walsh).

The apolipoprotein E gene (apoE) is a major determinant of the risk of developing Alzheimer’s disease (up to a 20–fold higher risk). It has just been shown that reducing the expression of the apoE gene with bexarotene a compound already approved in the USA for cancer treatment, markedly reduces the accumulation of beta-amyloid in the brain of transgenic mice providing a new approach to amyloid removal (see G. Landreth) .

Another gene, preseniln-1 , is related to rare cases of familial Alzheimer, representing less than 1 % of the total of all Alzheimer patients, and leading to an early appearance of the disease (at age 45-55 years). Affected presinilin-1 families, carrying this gene, are highly concentrated in a particular region of Columbia offering a unique possibility: very early treatment of patients predestined to develop Alzheimer (before significant brain damage can occur). This meeting will report for the first time on early steps toward the therapy of such populations by vaccination against beta-amyloid (see S. Gauthier and round table of experts).

II. Early diagnosis

The presence and distribution of beta-amyloid in the brain of living Alzheimer patients was visualized for the first time in Stockholm in 2006 (see Nordberg). Brain beta-amyloid binds specifically to a radioactive marker called PIB which is made visible by a PET technique. Several thousand patients have been examined by PIB-PET throughout the world making it possible to detect the beginning of beta-amyloid accumulation in the brain of asymptomatic individuals (at a time when many brain cells remain still intact). At this meeting, new PET markers of amyloid, with a longer half-life than PIB will be presented, making this important diagnostic tool available to many more centers worldwide (see A. Nordberg and V. Villemagne).

Other key advances of the past few years regarding early identification of the disease by means of cerebrospinal fluid (CSF) markers and neuroimaging will be amply discussed at the meeting.

III. Disease prevention

This subject will be reviewed in the light of two important long term Scandinavian studies taking place respectively in Stockholm (see L. Fratiglioni) and in Finland (see M. Kivipelto) with the latest information on risks factors and preventive strategies, providing concrete options to delay the disease without pharmacological intervention.

IV Vascular pathology

An entire session will be devoted to the contribution of vascular pathology with a special emphasis on cerebral microinfarcts, invisible lesions (on neuroimaging) that have recently been found to play a key role in cognitive performance (See G. Gold and T. Erkinjuntti)