Guillermo Eastman, Ph.D.

Research

In the Bloom lab, I will investigate how the two main toxic molecular species that are hallmarks of Alzheimer’s disease (AD) damage neurons by selectively altering protein synthesis. AD is a neurodegenerative disorder characterized by an accumulation of amyloid beta and tau, which form plaques and tangles in neurons in the brain. Although it is unclear exactly how these molecules and their associated aggregates destroy nerve cells, recent studies have shown that, in mouse models of AD, amyloid beta alters the synthesis of proteins—and stimulates the production of tau. Previously, in the Bloom lab, I discovered that young mice models of AD show altered protein synthesis levels of many AD-related genes associated either with neuroprotective or neurotoxic functions. Now, using an array of cutting-edge techniques in cell biology, neuroscience, genomics, and microscopy, I will extend this analysis to cultured mouse and human-derived neurons, identifying proteins whose synthesis is enhanced or inhibited by amyloid beta and tau and evaluating how these changes alter the neurons’ survival, viability, and structure. This work could lead to promising new treatments for AD and other neurodegenerative disorders.