The field of Alzheimer's disease (AD) research eagerly awaits the results of a 
large number of Phase III clinical trials that are underway to investigate the 
effectiveness of anti-amyloid-β (Aβ) immunotherapy for AD. In this case report, 
we review the pertinent clinical history, examine the neuropathology, and 
characterize the Aβ profile of an AD patient who received bapineuzumab 
immunotherapy. The patient received four bapineuzumab infusions over a 39 week 
period. During the course of this treatment, there was no remarkable change in 
cognitive impairment as determined by MMSE scores. Forty-eight days after the 
fourth bapineuzumab infusion was given, MRI revealed that the patient had 
developed lacunar infarcts and possible vasogenic edema, probably related to 
immunotherapy, but a subsequent MRI scan 38 days later demonstrated resolution 
of vasogenic edema. The patient expired due to acute congestive heart failure 
complicated by progressive AD and cerebrovascular accident 378 days after the 
first bapineuzumab infusion and 107 days after the end of therapy. 
Neuropathological and biochemical analysis did not produce evidence of lasting 
plaque regression or clearance of Aβ due to immunotherapy. The Aβ species 
profile of this case was compared with non-immunized AD cases and non-demented 
controls and found to be similar to non-immunized AD cases. SELDI-TOF mass 
spectrometric analysis revealed the presence of full-length Aβ₁₋₄₂ and truncated 
Aβ peptides demonstrating species with and without bapineuzumab specific 
epitopes. These results suggest that, in this particular case, bapineuzumab 
immunotherapy neither resulted in detectable clearance of amyloid plaques nor 
prevented further cognitive impairment.