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A Phase III Alzheimer's Drug Increases Levels of Beta Amyloid in the Brain - But Still Provides Benefits
Date:7/14/2009

mportant therapeutic targets independent of beta amyloid," Gandy added.

The researchers note that so far they only studied acute systems, and it is conceivable that the chronic effect of dimebolin could be amyloid-lowering.

Immunotherapy Against Tau Tangles in Alzheimer's Mouse Models

Immunotherapy (treatment by inducing, enhancing, or suppressing an immune response) targeting beta amyloid is being researched widely by companies and academics as a therapeutic option for Alzheimer's disease. Earlier, late stage, anti-amyloid immunotherapy trials in people were complicated, and eventually stopped, when about six percent of participants developed brain inflammation. Current trials in this area are working in a variety of ways to eliminate this side effect.

Tau tangles, the other major Alzheimer's brain pathology, are now also receiving attention as a target for immunotherapy. Also known as neurofibrillary tangles (NFTs), these lesions consist of an abnormal folded protein (phosphorylated tau), and research shows their accumulation in the brain is more closely associated with the progression of Alzheimer's symptoms than amyloid.

Building on previous studies using this approach (for example, Asuni et al. (2007)), Hanna Rosenmann, Ph.D., head of the Laboratory of Molecular Neurogenetics, Department of Neurology, Hadassah University Hospital, Ein Kerem, and an Investigator (Associate-Senior Lecturer) at the Hebrew University Hadassah School of Medicine, Jerusalem, Israel, and colleagues performed immunization studies against tau tangle pathology by immunizing NFT mice with a mixture of three phosphorylated-tau peptides (shortened versions of the full length tau protein that are phosphorylated like the NFTs). Previous experiments by this lab with non-phosphorylated full length tau caused brain inflammation in the animal models.

The researchers ob
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SOURCE Alzheimer's Association
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