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2007 Grant - Puzzo
Functional Role of Beta-Amyloid in Synaptic Plasticity and Memory
Daniela Puzzo, M.D., Ph.D.
University of Catania
2007 New Investigator Research Grant
The protein fragment beta-amyloid may play a key role in damaging cell-to-cell communication and causing the loss of brain cells in Alzheimer's disease. Yet this protein fragment also occurs in people without the disease. Preliminary research suggests that normal, moderate levels of beta-amyloid in the brain may actually help enhance memory and cellular communication.
In recent studies with rodents, scientists administered beta-amyloid in the animals' brains at levels similar to those found within healthy human brains. Results showed that the beta-amyloid improved both long-term potentiation and inhibitory avoidance. Long-term potentiation, a memory-enhancing condition, is a kind of "increased sensitivity" that develops in neurons with repeated sending and receiving of messages. Inhibitory avoidance is a type of conditioned memory that enables animals to avoid danger. Further studies found that the loss of normally produced beta-amyloid interferes with long-term potentiation in cell cultures and hinders inhibitory avoidance in rodents.
For this proposed grant, Daniela Puzzo, M.D., Ph.D., and colleagues will conduct more extensive studies to validate the results of these earlier experiments. The researchers hope to verify that beta-amyloid, at normal levels, can enhance long-term potentiation and memory. They will also seek to determine the biological mechanisms by which beta-amyloid produces these positive effects.
Results of the study could lend new insights into the complex role that beta-amyloid plays in the brain. The effort could also determine whether promotion of optimal beta-amyloid concentrations is a valid treatment goal.