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Amyloid-beta peptides(Aβ)are believed to beresponsible for the mental decline in patients withAlzheimer's disease(AD).In 1999,Schenk et alreported that immunization with Aβ attenuated AD-likepathology in the PDAPP mouse,and developed a newvaccination approach to AD.Such vaccines weresuccessfully tested in mouse models of AD for thereduction of Aβ plaque burden and the improvement ofcognitive performance.However,6% of AD patientsdeveloped symptoms of brain inflammation aftervaccination that resembled encephalitis or meningitis,resulting in the termination of the phase Ⅱ_a clinical trial.These adverse effects were considered to be related toAβ_(1-42)toxicity and/or cell-mediated auto-immunity.
A 1999, Schenk et alreported that immunization with Aβ attenuated AD-likepathology in the PDAPP mouse, and developed a new viral approach to AD. Amyloid-beta peptides (Aβ) are believed to be responsible for the mental decline in patients with Alzheimer's disease (AD) Such vaccines weresuccessfully tested in mouse models of AD for the reduction of Aβ plaque burden and the improvement of cognitive performance. However, 6% of AD patientsdeveloped symptoms of brain inflammation aftervaccination that resembled encephalitis or meningitis, resulting in the termination of the phase Ⅱ a clinical trial. These adverse effects were considered to be related to Aβ 1- (1-42) toxicity and / or cell-mediated auto-immunity.