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Characterizing the Role of Gasdermin-Eand Downstream Innate Immune Pathways in Frontotemporal Dementia

Award Number: F31NS151537
ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 09/30/2026
PERIOD OF PERFORMANCE END DATE: 09/29/2029

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Characterizing the Role of Gasdermin-Eand Downstream Innate Immune Pathways in Frontotemporal Dementia - Abstract Frontotemporal dementia (FTD) is a debilitating neurodegenerative disorder accounting for the majority of early- onset dementias. This disease is characterized by the buildup of toxic aggregates, neuroinflammation from microglia and other immune cells, and progressive neuronal loss and cognitive decline. Despite an enormous clinical need, this disease has no cures or effective treatments, and the mechanisms responsible for driving disease remain elusive. Growing evidence points to inflammation of the central nervous system as a critical driver of many dementias, but how inflammation in the CNS is initiated or sustained is yet unknown. Our lab has identified an innate immune protein, gasdermin E (GSDME), that may be critical in disease progression. GSDME is a pore forming protein, which I may believe may be a driver of inflammation downstream of toxic peptide buildup during FTD. The overarching goal of my proposal is to determine how GSDME activation downstream of FTD pathology drives inflammation in the brain. First, I will explore how innate immune pathways become activated intra-neuronally. Specifically, I hypothesize that GSDME pore formation caused by FTD pathology leads to the release of mitochondrial nucleic acids, activation of mitochondrial antiviral signaling (MAVS), and the promotion interferon responses. Secondly, I will explore how inflammation in FTD is propagated from neurons to surrounding cell types in a GSDME-dependent manner. I hypothesize that neuronal GSDME activation in FTD leads to release of neuronally-secreted cytokines, which may be derived from the mechanisms explored intraneuronally, that initiate microglial activation and specific phagocytic clearance of neurites with activated GSDME. In conclusion, this proposal aims uncover a new understanding of how inflammation is being driven, both intrinsically to neurons, and through microglia in the CNS, potentially identifying GSDME as a novel therapeutic target.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $45,214 )
2026	2026	PRESIDENT AND FELLOWS OF HARVARD COLLEGE	25 SHATTUCK ST	BOSTON	MA	02115	SUFFOLK	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	001	1	8/3/2026	NEW	$0
2026	2026	PRESIDENT AND FELLOWS OF HARVARD COLLEGE	25 SHATTUCK ST	BOSTON	MA	02115	SUFFOLK	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	1	8/3/2026	NEW	$45,214
														Subtotal = $45,214

Grand Total All Awards = $45,214

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Characterizing the Role of Gasdermin-Eand Downstream Innate Immune Pathways in Frontotemporal Dementia

Award Number: F31NS151537

ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 09/30/2026

PERIOD OF PERFORMANCE END DATE: 09/29/2029

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