The transformation of amyloid beta into Alzheimer’s inducing plaques can be prevented through an interaction between amyloid beta and another protein called cystatin C, according to two papers published in the online November 18 edition of Nature Genetics.
Both studies used mice that were genetically engineered to produce human cystatin C as well as abundant amounts of amyloid beta plaques in their brains. The cystatin C bound to the soluble, non-pathological form of amyloid beta in these mice and inhibited the aggregation and deposition of amyloid beta plaques in the brain.
These findings suggest that even subtle modifications of cystatin C protein levels could affect amyloid beta accumulation and deposition in the brain, thereby modifying disease progression, says Efrat Levy, Ph.D., associate professor in the departments of psychiatry and pharmacology at New York University School of Medicine and an author of both of the studies.
With support from the Alzheimer’s Association, Dr. Levy’s laboratory has already begun studies to develop a drug that will mimic the ability of cystatin C.
The first study was performed by Dr. Levy in collaboration with other investigators at the Nathan S. Kline Institute for Psychiatric Research and New York University School of Medicine. The second study was performed by Dr. Levy and colleagues at the Hertie-Institute for Clinical Brain Research.