Fruit bats, Rousettus aegyptiacus, are being deprived of all dietary sources of vitamin B12 by being fed a diet consisting of fruit only. These bats develop an illness which resembles the complications of human pernicious anemia. It is characterized by neurologic changes, but hematologic changes, apart from a fall in the white cell count, are not present. We are further developing this animal model for human vitamin B12 deficiency and are characterizing the changes which occur during induction of this deficiency. Studies include structural and biochemical and analysis of nervous and other tissues. We seek to investigate myelin damage that occurs in vitamin B12 deficiency. Attempts will also be made to aggravate neurological damage by various nutritional expedients. This model could provide information concerning the biochemical role of vitamin B12 in mammalian metabolism.