Date: 10 AM EDT, September 18, 2025
The brain's primary immune cells, microglia, are a leading causal cell type in Alzheimer's disease (AD). Yet, the mechanisms by which microglia can drive neurodegeneration remain unresolved. Ayata lab discovered that a conserved stress signaling pathway, the integrated stress response (ISR), characterizes a subset of microglia with neurodegenerative outcomes.
The Ayata lab's primary interest is in how microglia—the brain's primary macrophages—respond to misfolded protein aggregates, influencing susceptibility to neurological diseases. They combine novel mouse models, primary cell culture systems, and molecular techniques with state-of-the-art biotechnological tools to answer this question.
Creative Biolabs has invited Dr. Pinar Ayata to walk us through the neurodegenerative functions of microglia in AD.
In this webinar, we will explore and review the following key points:
- Autonomous activation of ISR in microglia
- The ISR activation promotes the secretion of toxic lipids by microglia
- Microglial ISR activation exacerbates neurodegenerative pathologies and synapse loss in AD models
- Pharmacological inhibition of ISR or lipid synthesis mitigates synapse loss in AD models
About the Speaker
Pinar Ayata, Ph.D.
Assistant Professor of Biology and Biochemistry
Neuroscience Initiative, Advanced Science
Research Center
CUNY Graduate Center
Pinar's most recent manuscript in Nature (provisionally accepted) from her postdoctoral work reveals the transcriptional basis of a protective subset of microglia that slows down in AD progression. Pinar opened her lab in 2020 during the height of COVID, and her lab recently discovered a neurodegenerative subset of microglia induced by cellular stress signaling that accelerates the progression of AD.
Pinar's work has received several awards, including the Women and Science Graduate Fellow Award, the Rockefeller University Graduate Fellowship, the NARSAD Young Investigator Postdoctoral Robin Chemers Neustein Postdoctoral Award, the Kavli Foundation Award, the Alfred P. Sloan Foundation, and NIH R01 funding.