Scientist are not sure what role amyloid beta plays in the development of Alzheimer’s disease. However, they have established a link of amyloid beta that aggregates into toxic plaques to the brain cell death associated with Alzheimer’s.
Efrat Levy, Ph.D., Associate Professor, Department of Psychiatry and Pharmacology at New York University School of Medicine, has found that the aggregation of amyloid beta plaques can be attenuated by another protein called cystatin C. The protein cystatin C is sort of a jack-of-all-trades and found through all mammal’s body fluids and tissues and is influenced by certain hormones, aging, and certain pathological conditions. It plays a role in many functions, including cell proliferation and growth, modulation of inflammatory responses, bone resorption, and has been implicated in neuronal degeneration and repair of the nervous system.
Two studies with mice that were genetically engineered to produce an abundant amount of amyloid beta plaques in their brain, along with cystatin C, found that cystatin C binds with amyloid beta preventing it to form into deadly plaque. It was also recently demonstrated that a genetic variation in the cystatin C gene is linked to a greater risk of humans developing Alzheimer’s disease during aging. Even subtle modifications of cystatin C protein levels could affect amyloid beta accumulation and deposition in the brain, thereby modifying disease progression.
Levy stresses that more work needs to be done before setting the stage for a new approach to Alzheimer’s therapy.