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Dysregulation of Cribriform Plate Lymphatics as a Mechanistic Contributor to Alzheimer’s Disease Pathology

Award Number: F30AG101796
ORGANIZATION: NATIONAL INSTITUTE ON AGING
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 12/16/2026
PERIOD OF PERFORMANCE END DATE: 12/15/2027

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Dysregulation of Cribriform Plate Lymphatics as a Mechanistic Contributor to Alzheimer’s Disease Pathology - PROJECT SUMMARY/ABSTRACT Alzheimer’s disease (AD) is the most common form of dementia, affecting 60 million people worldwide and leading to significant economic and medical costs annually. One of the main drivers of AD pathology is the accumulation of toxic proteins, such as amyloid-beta (Aβ) and phosphorylated tau within the brain. The clearance and disposal of these harmful proteins are crucial to disease treatments. The waste-management clearance system of the brain relies on a complex network of lymphatic vessels within the dural meningeal layer of the brain, on lymphatic vessels adjacent to cranial nerves, and glial-dependent clearance pathways within the brain parenchyma called glymphatics. In AD, it has been proposed that with disease progression, the brain’s waste systems at the dural meningeal lymphatics cannot efficiently clear Aβ and tau. We have discovered that the cribriform plate lymphatics (cpLVs) contribute to the waste management network in inflammatory diseases of the central nervous system (CNS), such as experimental autoimmune encephalomyelitis (EAE) and stroke, but this has not been examined in AD. Our preliminary data supports toxic protein aggregate deposition at the CP lymphatics in both post-mortem samples of patients confirmed with AD and murine models of Aβ deposition. Moreover, we have preliminary data suggesting cpLVs atrophy with disease progression resulting in decreased cerebrospinal fluid drainage (CSF). The long-term objective of this project is to characterize the functionality and contribution of lymphoid vessels near the cribriform plate to the development of pathology in AD. The primary goal of this study is to determine whether of deposition of amyloid-beta at the cribriform plate lymphatics leads to decreased lymphoid endothelial cell function and the development of neurotoxicity, ultimately resulting in devastating neuropathology in AD. Moreover, this study proposes to evaluate the therapeutic potential of increasing lymphatic flow through intranasal (I.N.) VEGF-C administration as a novel therapeutic for AD. This project’s broader, long-term aim is the provide new insights and lay the foundation for novel therapeutic approaches for enhancing brain waste-management functions by targeting the cribriform plate lymphatics. The specific objectives of this proposal are (1) evaluate cpLV associated Aβ deposits in post- mortem AD patients and correlate with CSF biomarker data, (2) evaluate cpLV dysfunction and drainage impairment as a result of Aβ deposition in early-, mid-, and late-disease in APP/PS1 mice, and (3) evaluate the therapeutic impact of I.N. administration of VEGF-C on cpLV function and AD pathology in APP/PS1 mice. Pharmacological modulation of the cribriform plate lymphatics in CNS diseases has potential therapeutic value for treating AD. The extensive resources at the University of Wisconsin create an optimal setting for the completion of this work. Completing this study will foster the development of crucial experimental, professional, and clinical skills, facilitating a smooth transition to my career as a physician-scientist in psychiatry.


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 = $41,248 )
2026	2026	UNIVERSITY OF WISCONSIN SYSTEM	21 N PARK ST STE 6301	MADISON	WI	53715	DANE	USA	Aging Research	000	1	6/16/2026	NEW	$41,248
														Subtotal = $41,248

Grand Total All Awards = $41,248

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Dysregulation of Cribriform Plate Lymphatics as a Mechanistic Contributor to Alzheimer’s Disease Pathology

Award Number: F30AG101796

ORGANIZATION: NATIONAL INSTITUTE ON AGING

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 12/16/2026

PERIOD OF PERFORMANCE END DATE: 12/15/2027

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