Background: A rapidly growing body of data indicates that Abeta immunotherapy can be efficacious both in model systems and in human patients. Methods: Tansgenic mouse models as well as human patients with Alzheimer's disease with chronically elevated plasma and CSF levels of antibodies against beta-amyloid were analyzed. Results: Evidence includes reductions in brain beta-amyloid deposits, improved neurite and synapse morphology, reduced astrocytosis, restored neural functions including LTP and behaviour. On the other hand, major challenges in the current development of safe immunotherapies include autoimmune disease, brain inflammation, microhemorrhage, increased amyloid angiopathy, blood brain barrier passage of antibodies, remaining neurofibrillary tangles, reductions in brain volume as well as the precise molecular definition of the therapeutic target. Conclusions: Growing understanding of the pathophysiological basis of these challenges will lead to safer forms of Abeta immunotherapy with a fair chance to become first choice among future amyloid-reducing treatment options for large populations of patients suffering from Alzheimer's disease.
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