METABOLIC SYNDROME IMPAIRS OLIGODENDROCYTE METABOLIC SUPPORT OF NEURONS LEADING TO ALZHEIMERâS DISEASE/AL…
Federal financial assistance recorded from USAspending. This is not a procurement contract.
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ASST_NON_R00AG081390_075 · LOUISIANA STATE UNIVERSITY · Department of Health and Human Services
Compare Multiple AI Models with SmartSoloExplore CaptureIQ IntelligenceAssistance award details
- Assistance award identifier
- ASST_NON_R00AG081390_075
- FAIN
- R00AG081390
- Recipient
- LOUISIANA STATE UNIVERSITY
- Awarding agency
- Department of Health and Human Services
- Funding agency
- Department of Health and Human Services
- Assistance listing (CFDA)
- 93.866
- Total obligated
- $249,000
- Period
- May 1, 2023 – May 31, 2029
- Fiscal year
- 2026
- Place of performance state
- LA
- Source file
- FY2026_All_Assistance_Full_20261006.zip
Description
METABOLIC SYNDROME IMPAIRS OLIGODENDROCYTE METABOLIC SUPPORT OF NEURONS LEADING TO ALZHEIMERâS DISEASE/ALZHEIMERâS DISEASE AND RELATED DEMENTIAS - ABSTRACT ALZHEIMERâS DISEASE (AD) AND AD-RELATED DEMENTIA (ADRD) CONSTITUTE THE MAIN CAUSE OF DEMENTIA AND MANI- FEST AS AN ARRAY OF SYMPTOMS AND SIGNS, INCLUDING IMPAIRED COGNITION AND POOR MEMORY. AD/ADRD POSES A SUBSTANTIAL SOCIOECONOMIC BURDEN, WITH DEMENTIA AFFECTING 1 OF 9 PEOPLE AGED 65 AND OLDER IN 2021 IN THE UNITED STATES (US) AND DIRECT HEALTHCARE COSTS ESTIMATED AT $355 BILLION USD. AD/ADRD CURRENTLY LACKS EFFEC- TIVE DISEASE-MODIFYING TREATMENTS, THOUGH MULTIPLE AD/ADRD RISK FACTORS HAVE BEEN IDENTIFIED, INCLUDING MIDLIFE METABOLIC SYNDROME (METS) AND ITS COMPONENTS, SUCH AS DIABETES, OBESITY, AND DYSLIPIDEMIA. RECENT PRECLINI- CAL AND CLINICAL RESEARCH REVEALS THAT AD/ADRD AND COGNITIVE IMPAIRMENT ASSOCIATED WITH METS PROGRESS NON- CELL AUTONOMOUSLY IN THE BRAIN THROUGH A CONCERTED BREAKDOWN IN OLIGODENDROCYTE FUNCTION WITH RESULTING NEU- RONAL LOSS. HOWEVER, THERE IS A GAP IN OUR UNDERSTANDING OF HOW METS AND ITS ASSOCIATED OLIGODENDROCYTE DYS- FUNCTION LEADS TO COGNITIVE IMPAIRMENT AND AD/ADRD. GIVEN THE INCREASING BURDEN OF AD/ADRD AND METS, THERE IS A CRITICAL NEED TO IDENTIFY THE MECHANISMS OF OLIGODENDROCYTE-NEURON METABOLIC CROSSTALK AND ITS ROLE IN METS LEADING TO AD/ADRD. OUR PROPOSAL WILL ELUCIDATE HOW MIDLIFE METS ONSET DISRUPTS OLIGODENDROCYTE ME- TABOLISM AND CONSEQUENT SUPPORT TO NEURONS, LEADING TO AD/ADRD IN LATER LIFE. UNDER PHYSIOLOGICAL CONDITIONS, OLIGODENDROCYTES METABOLICALLY SUPPORT NEURONS WITH LACTATE SHUTTLED VIA MONOCARBOXYLATE TRANSPORTER 1 (MCT1). THIS ENSURES AN ADEQUATE ENERGY SUBSTRATE SUPPLY TO NEURONS, SUPPORTING NORMAL COGNITIVE FUNCTION. TWO CRUCIAL PIECES OF DATA ARE RELEVANT TO THIS PROPOSAL. FIRST, THE METS INFLUENCES EPIGENETIC ELEMENTS THAT DE- CREASE MCT1 EXPRESSION. SECOND, AD/ADRD IS ASSOCIATED WITH OLIGODENDROCYTE LOSS, REDUCED CEREBRAL LAC- TATE, AND NEURON