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000163666 1001_ $$aCiampa, Claire J$$b0
000163666 245__ $$aAssociations among locus coeruleus catecholamines, tau pathology, and memory in aging.
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000163666 520__ $$aThe locus coeruleus (LC) is the brain's major source of the neuromodulator norepinephrine, and is also profoundly vulnerable to the development of Alzheimer's disease (AD)-related tau pathology. Norepinephrine plays a role in neuroprotective functions that may reduce AD progression, and also underlies optimal memory performance. Successful maintenance of LC neurochemical function represents a candidate mechanism of protection against the propagation of AD-related pathology and may facilitate the preservation of memory performance despite pathology. Using [18F]Fluoro-m-tyrosine ([18F]FMT) PET imaging to measure catecholamine synthesis capacity in LC regions of interest, we examined relationships among LC neurochemical function, AD-related pathology, and memory performance in cognitively normal older adults (n = 49). Participants underwent [11C]Pittsburgh compound B and [18F]Flortaucipir PET to quantify β-amyloid (n = 49) and tau burden (n = 42) respectively. In individuals with substantial β-amyloid, higher LC [18F]FMT net tracer influx (Kivis) was associated with lower temporal tau. Longitudinal tau-PET analyses in a subset of our sample (n = 30) support these findings to reveal reduced temporal tau accumulation in the context of higher LC [18F]FMT Kivis. Higher LC catecholamine synthesis capacity was positively correlated with self-reported cognitive engagement and physical activity across the lifespan, established predictors of successful aging measured with the Lifetime Experiences Questionnaire. LC catecholamine synthesis capacity moderated tau's negative effect on memory, such that higher LC catecholamine synthesis capacity was associated with better-than-expected memory performance given an individual's tau burden. These PET findings provide insight into the neurochemical mechanisms of AD vulnerability and cognitive resilience in the living human brain.
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000163666 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000163666 650_7 $$2NLM Chemicals$$aCatecholamines
000163666 650_7 $$2NLM Chemicals$$atau Proteins
000163666 650_7 $$0X4W3ENH1CV$$2NLM Chemicals$$aNorepinephrine
000163666 650_2 $$2MeSH$$aAged
000163666 650_2 $$2MeSH$$aAging: pathology
000163666 650_2 $$2MeSH$$aAlzheimer Disease: diagnostic imaging
000163666 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000163666 650_2 $$2MeSH$$aAmyloid beta-Peptides: metabolism
000163666 650_2 $$2MeSH$$aCatecholamines
000163666 650_2 $$2MeSH$$aHumans
000163666 650_2 $$2MeSH$$aLocus Coeruleus: diagnostic imaging
000163666 650_2 $$2MeSH$$aLocus Coeruleus: metabolism
000163666 650_2 $$2MeSH$$aNorepinephrine
000163666 650_2 $$2MeSH$$aPositron-Emission Tomography: methods
000163666 650_2 $$2MeSH$$atau Proteins: metabolism
000163666 7001_ $$aParent, Jourdan H$$b1
000163666 7001_ $$aHarrison, Theresa M$$b2
000163666 7001_ $$aFain, Rebekah M$$b3
000163666 7001_ $$0P:(DE-2719)2810555$$aBetts, Matthew J$$b4$$udzne
000163666 7001_ $$0P:(DE-2719)2811815$$aMaaß, Anne$$b5$$udzne
000163666 7001_ $$aWiner, Joseph R$$b6
000163666 7001_ $$aBaker, Suzanne L$$b7
000163666 7001_ $$aJanabi, Mustafa$$b8
000163666 7001_ $$aFurman, Daniella J$$b9
000163666 7001_ $$00000-0002-3462-006X$$aD'Esposito, Mark$$b10
000163666 7001_ $$00000-0002-4458-113X$$aJagust, William J$$b11
000163666 7001_ $$00000-0002-5086-3643$$aBerry, Anne S$$b12
000163666 77318 $$2Crossref$$3journal-article$$a10.1038/s41386-022-01269-6$$bSpringer Science and Business Media LLC$$d2022-01-15$$n5$$p1106-1113$$tNeuropsychopharmacology$$v47$$x0893-133X$$y2022
000163666 773__ $$0PERI:(DE-600)2008300-2$$a10.1038/s41386-022-01269-6$$gVol. 47, no. 5, p. 1106 - 1113$$n5$$p1106-1113$$tNeuropsychopharmacology$$v47$$x0893-133X$$y2022
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