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Defining the Role of Lactate in Axon Degeneration

Award Number: F31NS134151
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: 08/01/2023
PERIOD OF PERFORMANCE END DATE: 07/31/2028

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Defining the Role of Lactate in Axon Degeneration - Project Summary/Abstract Axon degeneration is a conserved and tightly regulated process and is a driving force of later pathologies in many neurodegenerative diseases. There is a lack of treatments for neurodegeneration that results from disease, and axon degeneration is a target for early intervention and prevention. Elucidating the specific mechanisms that initiate axon degeneration could assist in identifying ways to protect axons in disease and ultimately treat neurodegeneration. C. elegans Mitochondrial Trafficking Mutants (MTMs) have no axonal mitochondria, resulting in axon degeneration. In preliminary experiments the applicant made a surprising discovery: inhibiting glycolysis in MTMs suppresses axon degeneration. Following this finding the applicant showed that degrading the enzyme responsible for lactate production rescues degeneration of axons, suggesting that lactate accumulation may drive axon degeneration. However, the molecular mechanism by which this occurs is unknown. This observation prompted the hypothesis that the product of glycolysis, lactate, accumulates in the absence of mitochondria and by creating a more acidic axonal environment instigates degeneration. Completion of this proposed work will elucidate the role of lactate and related metabolites on axon degeneration (Aim 1). Further, it will shed light on the consequences of loss of axonal mitochondria for neurons —a key feature of neurodegenerative diseases. Finally, these experiments may identify novel approaches for preventing morphological and functional axon degeneration (Aim 2). Work proposed here will establish the role of lactate in axon degeneration and further our understanding of the coupling between neuronal activity and lactate in health and disease. Upon completion of this fellowship the trainee will have received extensive training in an environment well equipped to support collaborative and cutting-edge research. The trainee will gain technical and analytical skills, and professional independence in preparation for an academic career in cellular and molecular neuroscience.


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 = $0 )
2026	2024	YALE UNIV	150 MUNSON ST	NEW HAVEN	CT	06511	SOUTH CENTRAL CT	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	2	11/17/2025	NON-COMPETING CONTINUATION	$0
														Subtotal = $0

Issue Date FY: 2024 ( Subtotal = $33,892 )
2024	2024	YALE UNIV	150 MUNSON ST	NEW HAVEN	CT	06511	SOUTH CENTRAL CT	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	2	6/28/2024	NON-COMPETING CONTINUATION	$33,892
														Subtotal = $33,892

Issue Date FY: 2023 ( Subtotal = $32,612 )
2023	2023	YALE UNIVERSITY	105 WALL ST	NEW HAVEN	CT	06511	SOUTH CENTRAL CT	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	001	1	7/20/2023	NEW	$0
2023	2023	YALE UNIVERSITY	105 WALL ST	NEW HAVEN	CT	06511	SOUTH CENTRAL CT	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	1	7/20/2023	NEW	$32,612
														Subtotal = $32,612

Grand Total All Awards = $66,504

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Defining the Role of Lactate in Axon Degeneration

Award Number: F31NS134151

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: 08/01/2023

PERIOD OF PERFORMANCE END DATE: 07/31/2028

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