INDUCTION OF BETA(A4)-AMYLOID IN PRIMATES BY INJECTION OF ALZHEIMERS-DISEASE BRAIN HOMOGENATE - COMPARISON WITH TRANSMISSION OF SPONGIFORM ENCEPHALOPATHY

Amyloid plaques, associated with argyrophilic dystrophic neurites, and cerebral amyloid angiopathy (CAA), but no neurofibrillary tangles, we re found in the brains of three middle-aged marmoset monkeys that had been injected intracerebrally (ic) 6-7 yr earlier with brain tissue fr om a patient with early-onset Alzheimer's disease. Such changes were n ot found in the brains of three age-matched control marmosets. Immunoc hemically the amyloid plaques and CAA stained with antibody to beta(A4 )-protein. The plaques and CAA displayed dichroic birefringence when s tained with Congo red and viewed under polarized light. beta(A4)-amylo id plaques and CAA were also found in the brain of one of two marmoset s injected ic 6 yr previously with brain tissue from a patient with pr ion disease with concomitant beta(A4)-amyloid plaques and CAA. An occa sional beta(A4)-amyloid plaque was found in the brains of two of four marmosets injected ic >4.5 yr previously with brain tissue from three elderly patients,;two of whom had suspected (but untransmitted) CJD. N o beta(A4)-amyloid plaques or CAA were found in six marmosets who were older than the injected animals, in four marmosets that had not devel oped spongiform encephalopathy (SE) having been injected several years previously with human brain tissue from three younger patients with s uspected or atypical prion disease, or in 10 younger marmosets who had undergone various neurosurgical procedures. Seventeen marmosets injec ted in the same way with brain tissue from patients or animals with SE developed SE 17-49 mo after injection. These results suggest that bet a(A4)-amyloidosis is a transmissible process comparable to the transmi ssibility of SE.