Welcome to Ayata Lab at the Neuroscience Initiative of The CUNY Advanced Science Research Center.

 

 

Most neurodegenerative diseases (like Alzheimer’s disease) are triggered by misfolded protein aggregation. Our lab’s primary interest is how microglia–the brain’s primary macrophages–respond to misfolded protein aggregate and thus influence susceptibility to neurological diseases. We combine novel mouse models, primary cell culture systems, and molecular techniques with state-of-the-art biotechnological tools at the ASRC’s core facilities and the expertise from the members of the ASRC’s Environmental Sciences, Neuroscience, Structural Biology, Nanoscience, and Photonics Initiatives to answer this question.

 

 

We are a collaborative lab passionate about science but enjoy other life aspects! While everyone has unique projects and skill sets, we help each other through technical and scientific discussions and collaborative experiments. Our lab strongly believes in and promotes diversity, equity, and inclusion of people of different races, ethnicities, genders, ages, socioeconomic statuses, religions, disabilities, and sexual orientations.

The typical response of microglia to protein aggregates.

A handful of disease-associated proteins account for nearly a dozen neurodegenerative diseases. In ongoing studies, we address this divergence from an immune perspective. We track the microglial response to protein aggregates and aggregate mimics created by the Nanoscience Initiative, map subcellular events by cryo-electron microscopy at the Structural Biology Initiative and using cellular and molecular biology and biochemistry techniques, and characterize the changes in microglial homeostasis. 

Convergent mechanisms that induce microglial failure to respond to protein aggregates.

Numerous genetic and external risk factors implicate features of cellular aging, including cellular stress, in disease causality. We study how these pathways impact microglial response to protein aggregates and the direct impact of the activation of these pathways in microglia on neurodegeneration. Age-associated diseases represent the gradual accumulation of minor insults, which likely represents a process that involves epigenetic reprogramming. We combine omics and single-cell approaches with novel mouse models to address this question.

External risk factors as mediators of microglial failure to respond to protein aggregates.

Habits, experiences, and environmental exposures heavily influence the quality of cognitive aging and the risk of developing neurological diseases. As air pollution is a major risk factor for dementia, we address what cellular responses and memories are triggered in microglia by exposure to polluted air by joining forces with the Environmental Science Initiative and MSSM/CUNY Climate Change Health Impact Interdisciplinary Research Initiative. We test whether these pathways mediate the impact of these exposures on neurodegeneration.

Artist: Thi Ngo