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AMPK localization, expression, and activity in Alzheimer's Disease

Award Number: F30AG079633
ORGANIZATION: NATIONAL INSTITUTE ON AGING
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 09/01/2022
PERIOD OF PERFORMANCE END DATE: 09/02/2025

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AMPK localization, expression, and activity in Alzheimer's Disease - PROJECT SUMMARY. Alzheimer’s disease (AD) is the most common cause of dementia and it is estimated that one in ten Americans aged 65 and older has AD. The number of Americans with Alzheimer’s will escalate rapidly in coming years as the size and proportion of the U.S. population aged 65 and older increases. With no disease-altering or curative drugs available, and with more than 140 failed clinical trials, AD has become a major public health concern. There is a consensus that a deeper understanding of the pathophysiology of this devastating illness is needed to move the field forward. The amyloid-cascade hypothesis has been the leading theoretical construct guiding our understanding of the pathophysiology of AD for the past thirty years. However, this construct has overlooked the multifaceted cellular mechanisms that ultimately drive neurodegeneration and the subsequent clinical manifestations of the disease. It has been hypothesized that aberrant metabolic signaling is a major cellular mechanism driving AD. These metabolic perturbations may arise through the dysfunction of adenosine monophosphate activated protein kinase (AMPK). AMPK is the master regulator of cellular energy status. Despite its strong association with AD, AMPK has not been fully characterized in AD: it is unknown how the subcellular localization, activity, and expression are changed in vulnerable regions of the human AD brain. Pre-clinical literature implicates AMPK in the regulation of synaptic function, A metabolism, tau phosphorylation, and pathologic proteostasis in AD. AMPK is an obligatory heterotrimer composed of catalytic () and regulatory ( and ) subunits. While the  subunit has been functionally characterized in AD models, the role of the regulatory subunits is unknown. As such, a functional understanding of this kinase in human substrates is missing. The central hypothesis of this proposal is that nuclear AMPK activity and localization is decreased in AD. We will test this hypothesis by using postmortem dorsolateral prefrontal cortex and hippocampus from mild cognitive impairment and AD subjects to analyze changes of AMPK as the disease progresses (Specific Aim 1). In parallel, we will employ an omics platform to specifically complement our biochemical studies. Further, we will use cortical neurons derived from AD-patient iPSCs to evaluate the role of the overlooked regulatory AMPK1 subunit in modulating a metabolic and synaptic phenotype (Specific Aim 2). This proposal addresses a critical need to resolve the role of AMPK in the pathophysiology of this disorder. This research, in conjunction with the experienced mentoring team, will provide this prospective Fellow an excellent training experience. Specifically, this F30 Fellowship will support the applicant in gaining expertise in cell biology, bioinformatics, stem cell culture, gene-manipulation strategies, and postmortem tissue processing, in preparation for a career as a translational physician-scientist.


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: 2025 ( Subtotal = $0 )
2025	2025	UNIVERSITY OF TOLEDO	3000 ARLINGTON AVE	TOLEDO	OH	43614	LUCAS	USA	Aging Research	001	4	8/19/2025	NON-COMPETING CONTINUATION	-$43,355
2025	2025	UNIVERSITY OF TOLEDO	3000 ARLINGTON AVE	TOLEDO	OH	43614	LUCAS	USA	Aging Research	000	4	8/7/2025	NON-COMPETING CONTINUATION	$43,355
														Subtotal = $0

Issue Date FY: 2024 ( Subtotal = $42,791 )
2024	2024	UNIVERSITY OF TOLEDO	3000 ARLINGTON AVE	TOLEDO	OH	43614	LUCAS	USA	Aging Research	000	3	8/9/2024	NON-COMPETING CONTINUATION	$42,791
														Subtotal = $42,791

Issue Date FY: 2023 ( Subtotal = $41,511 )
2023	2023	UNIVERSITY OF TOLEDO, THE	3000 ARLINGTON AVE	TOLEDO	OH	43614	LUCAS	USA	Aging Research	000	2	7/27/2023	NON-COMPETING CONTINUATION	$41,511
														Subtotal = $41,511

Issue Date FY: 2022 ( Subtotal = $40,569 )
2022	2022	UNIVERSITY OF TOLEDO, THE	3000 ARLINGTON AVE	TOLEDO	OH	43614	LUCAS	USA	Aging Research	001	1	8/3/2022	NEW	$0
2022	2022	UNIVERSITY OF TOLEDO, THE	3000 ARLINGTON AVE	TOLEDO	OH	43614	LUCAS	USA	Aging Research	000	1	8/3/2022	NEW	$40,569
														Subtotal = $40,569

Grand Total All Awards = $124,871

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AMPK localization, expression, and activity in Alzheimer's Disease

Award Number: F30AG079633

ORGANIZATION: NATIONAL INSTITUTE ON AGING

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 09/01/2022

PERIOD OF PERFORMANCE END DATE: 09/02/2025

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