Four Europeans Share Nobel of Neuroscience for Research on Origins of Alzheimer’s

Four Europeans Share Nobel of Neuroscience for Research on Origins of Alzheimer’s
This year’s one-million-euro Nobel of Neuroscience has been split among four European biologists whose research has pinned down the origins of Alzheimer’s disease. The winners of the Lundbeck Foundation Brain Prize are: • Michel Goedert, head of neurobiology at Cambridge University’s Laboratory of Molecular Biology. • Bart De Strooper, director of the UK Dementia Research Institute at University College London (UCL). • John Hardy of the UCL Institute of Neurology. • Christian Haass of Ludwig-Maximilians University in Munich. The foundation will make the awards at a ceremony May 9 in the Royal Danish Library Black Diamonds Building in Copenhagen. Denmark, which is struggling with an aging population, reports around 7,500 cases of dementia every year. Almost 80,000 people have the condition, including 50,000 with Alzheimer’s. The incidence is expected to triple in the next 30 to 40 years. Goedert, De Strooper, Hardy and Haass revolutionized scientists' understanding of the harmful changes in the brain that lead to Alzheimer’s. Goedert’s research led to tau protein bei
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    While the work of these European scientists is outstanding, we should realize that an American scientist, Dr. William Klein from Northwestern University, reported in 1998 in the Proc. Na. Acad. Sci. USA, which apparently is the first article showing that soluble amyloid-beta oligomers and not plaque, are the real neurotoxic agents in Alzhemer’s disease. Proposition that have been confirmed by numerous laboratories, including his own, in hundreds of papers. Also, as early as 2001, Dr. Klein proposed to focus on the soluble oligomers rather than the plaque, to develop vaccines and drugs against AD. A proposition that apparently has been ignored, as the “success” in AD drug development shows.

  2. Georges Tony MARCEL,,MD,PhD says:

    It explains the failures of monoclonals, which essentially target plaques,and in publications “pretend” to be active on soluble oligomers. Reread the publications carefully, like I have, and you will notice that these claims are in no way demonstrated. The enemies are the soluble oligomers,,but that does not stop monoclonals from maintaining their lies.

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