Anti-amyloid beta (Aβ) immunotherapy provides potential benefits in Alzheimer's 
disease patients. Nevertheless, strategies based on Aβ1-42 peptide induced 
encephalomyelitis and possible microhemorrhages. These outcomes were not 
expected from studies performed in rodents. It is critical to determine if other 
animal models better predict side effects of immunotherapies. Mouse lemur 
primates can develop amyloidosis with aging. Here we used old lemurs to study 
immunotherapy based on Aβ1-42 or Aβ-derivative (K6Aβ1-30). We followed anti-Aβ40 
immunoglobulin G and M responses and Aβ levels in plasma. In vivo magnetic 
resonance imaging and histology were used to evaluate amyloidosis, 
neuroinflammation, vasogenic edema, microhemorrhages, and brain iron deposits. 
The animals responded mainly to the Aβ1-42 immunogen. This treatment induced 
immune response and increased Aβ levels in plasma and also microhemorrhages and 
iron deposits in the choroid plexus. A complementary study of untreated lemurs 
showed iron accumulation in the choroid plexus with normal aging. Worsening of 
iron accumulation is thus a potential side effect of Aβ-immunization at 
prodromal stages of Alzheimer's disease, and should be monitored in clinical 
trials.