Meet The Team

Oversees and coordinates the laboratory’s day-to-day operations, ensuring that all experimental workflows run smoothly, efficiently, and in full compliance with institutional and safety regulations. Manages laboratory logistics, equipment maintenance, procurement, and organizational infrastructure while supporting researchers and trainees in maintaining high standards of accuracy, quality control, and operational excellence.

Coordinates and oversees the lab’s research operations, scientific communications, and strategic initiatives, ensuring seamless execution of projects from experimental planning to grant submissions and collaborations. Facilitates interdisciplinary partnerships, manages administrative and regulatory processes, and supports trainees and investigators to advance the lab’s scientific mission.

Supporting ongoing projects focused on neuroinflammation and amyloid-β pathology in Down syndrome and Alzheimer’s disease across different transgenic mouse models. This entails conducting behavioral assessments, genotyping, and assisting in evaluating therapeutic interventions targeting cognitive decline.

My research explores how gut-derived IgA and adaptive immunity influence microglial responses and amyloid accumulation in Alzheimer’s disease. By integrating mouse genetics, microbiome analysis, and human single-cell datasets, I seek to identify immune mechanisms that could be leveraged to modify disease progression.

Studying fetomaternal communication during pregnancy with fetuses diagnosed with Down syndrome and its impact on maternal cognition.

My research focuses on the mechanisms underlying Alzheimer’s disease in individuals with Down syndrome, who develop Alzheimer’s pathology at an early age. We study the role of the adaptive immune system, with a particular emphasis on B cells, as well as the contribution of retrotransposon elements to neuroinflammation and cognitive decline in this population.

My research investigates the role of platelets in fetomaternal transfer and their contribution to cognitive decline in mothers carrying fetuses overexpressing human APP, modeling Down syndrome pregnancy. Currently, I am examining whether preventing platelet activation alters this process and comparing platelet activation across different Alzheimer’s disease mouse models.

My research focuses on the formation of meningeal ectopic lymphoid structures (ELS) in Alzheimer’s disease. I investigate the immune and inflammatory mechanisms that drive their development, with a particular focus on the TLR7 signaling pathway and the influence of age, sex, and sex hormones. The goal of this work is to better understand how adaptive immune responses at the brain borders contribute to Alzheimer’s disease progression.

Investigating the interaction between fetal microchimerism and maternal brain inflammation. Specifically, whether Amyloid-β associated neuroinflammation promotes increased migration of fetal cells into the maternal brain. Additionally aiming to determine whether pathways altered during Alzheimer’s disease can be therapeutically targeted by counteracting these pathological changes.

Investigating the mechanisms by which innate immune signaling and sex-dependent factors regulate the formation of meningeal ectopic lymphoid structures (ELS).

Investigating fetomaternal transfer via fetal extracellular vesicles (EVs), specifically examining how these vesicles from a fetus with Down Syndrome reach the maternal brain. Focusing on how these signals promote amyloid-beta accumulation and neuroinflammation, potentially linking pregnancy to a higher risk of maternal cognitive decline.

Investigating the regulation of transposable elements in the brain, with a focus on LINE-1 retrotransposons in Down syndrome and neurodegeneration. Utilizing bioinformatics analysis of RNA-seq data, aiming to understand how epigenetic changes influence LINE-1 expression.