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Cytotoxic amyloid and tau proteins and end-organ dysfunction in extracorporeal life support

Award Number: R01AG092881
ORGANIZATION: NATIONAL INSTITUTE ON AGING
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 09/15/2026
PERIOD OF PERFORMANCE END DATE: 07/31/2031

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Cytotoxic amyloid and tau proteins and end-organ dysfunction in extracorporeal life support - Abstract Extracorporeal membrane oxygenation (ECMO) has become a mainstay of support for patients suffering from refractory critical illness. Neurologic complications are the leading cause of death in the setting of ECMO. Limited studies have examined the prevalence and phenotypes of post-intensive care syndrome (PICS), neurocognitive and end-organ dysfunction after ECMO among survivors. Transmissible amyloid-beta (Aβ) and tau variants are produced by the pulmonary endothelium in response to pneumonia and lung injury and circulating levels of Aβ and tau can be isolated from ECMO oxygenators, especially among those with pneumonia, neurologic complications, and in non-survivors. In addition, levels of circulating Aβ and tau during ECMO are associated with neurological complications, renal injury, cardiac function and death. We hypothesize that cytotoxic Aβ and tau are produced as an evolutionarily conserved immunoprotective response to pulmonary pathogens and lung injury that circulate and cause acute and chronic sequelae in ECMO survivors when left unchecked. These end-organ impacts may be preventable, once we better understand these relationships in patients and experimental models. We will establish a prospective observational cohort of veno-venous and veno-arterial ECMO patients from two centers. We will collect repeated Aβ and tau blood markers, neurophysiologic and neuroimaging data over the hospital course, and standardized evaluations for pulmonary, cardiac, renal, physical, and cognitive impairment and state-of-the-art protocolized brain magnetic resonance imaging at hospital discharge and three- and six-months after discharge. We will quantify Aβ/tau variants in the end-organs of deceased ECMO patients, to be paired with blood levels in vivo. In our established animal models, we will determine whether circulating cytopathic Aβ and tau variants are sufficient to cause end-organ injury. We will target amyloid precursor protein and test the effects of approved Aβ and tau neutralizing immunotherapy in these experimental models. This comprehensive exploration of cytopathologic Aβ and tau and their contributions to the most devastating and deadly ECMO complications will provide a rationale for therapeutic interventions to minimize long term health impacts in ECMO survivors.


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 = $616,875 )
2026	2026	RHODE ISLAND HOSPITAL	593 EDDY ST	PROVIDENCE	RI	02903	PROVIDENCE	USA	Aging Research	000	1	9/9/2026	NEW	$616,875
														Subtotal = $616,875

Grand Total All Awards = $616,875

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Cytotoxic amyloid and tau proteins and end-organ dysfunction in extracorporeal life support

Award Number: R01AG092881

ORGANIZATION: NATIONAL INSTITUTE ON AGING

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 09/15/2026

PERIOD OF PERFORMANCE END DATE: 07/31/2031

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