Systemic inflammation in relation to exceptional memory in the Long Life Family Study (LLFS)

Background and objectives: We previously found a substantial familial aggregation of healthy aging phenotypes, including exceptional memory (EM) in long-lived persons. In the current study, we aim to assess whether long-lived families with EM and without EM (non-EM) differ in systemic inflammation s...

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Main Authors: Ruhee Patel, Stephanie Cosentino, Esther Zhiwei Zheng, Nicole Schupf, Sandra Barral, Mary Feitosa, Stacy L. Andersen, Paola Sebastiani, Svetlana Ukraintseva, Kaare Christensen, Joseph Zmuda, Bharat Thyagarajan, Yian Gu
Format: Article
Language:English
Published: Elsevier 2024-05-01
Series:Brain, Behavior, & Immunity - Health
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Online Access:http://www.sciencedirect.com/science/article/pii/S2666354624000243
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author Ruhee Patel
Stephanie Cosentino
Esther Zhiwei Zheng
Nicole Schupf
Sandra Barral
Mary Feitosa
Stacy L. Andersen
Paola Sebastiani
Svetlana Ukraintseva
Kaare Christensen
Joseph Zmuda
Bharat Thyagarajan
Yian Gu
author_facet Ruhee Patel
Stephanie Cosentino
Esther Zhiwei Zheng
Nicole Schupf
Sandra Barral
Mary Feitosa
Stacy L. Andersen
Paola Sebastiani
Svetlana Ukraintseva
Kaare Christensen
Joseph Zmuda
Bharat Thyagarajan
Yian Gu
author_sort Ruhee Patel
collection DOAJ
description Background and objectives: We previously found a substantial familial aggregation of healthy aging phenotypes, including exceptional memory (EM) in long-lived persons. In the current study, we aim to assess whether long-lived families with EM and without EM (non-EM) differ in systemic inflammation status and trajectory. Methods: The current study included 4333 participants of the multi-center Long Life Family Study (LLFS). LLFS families were classified as EM (556 individuals from 28 families) or non-EM (3777 individuals from 416 families), with 2 or more offspring exhibiting exceptional memory performance (i.e. having baseline composite z-score representing immediate and delayed story memory being 1.5 SD above the mean in the nondemented offspring sample) considered as EM. Blood samples from baseline were used to measure inflammatory biomarkers including total white blood cell (WBC) and its subtypes (neutrophils, lymphocytes, monocytes) count, platelet count, high sensitivity C-reactive protein, and interleukin-6. Generalized linear models were used to examine cross-sectional differences in inflammatory biomarkers at baseline. In a sub-sample of 2227 participants (338 subjects from 24 EM families and 1889 from 328 non-EM families) with repeated measures of immune cell counts, we examined whether the rate of biomarker change differed between EM and non-EM families. All models were adjusted for family size, relatedness, age, sex, education, field center, APOE genotype, and body mass index. Results: LLFS participants from EM families had a marginally higher monocyte count at baseline (b = 0.028, SE = 0.0110, p = 0.010) after adjusting for age, sex, education, and field site, particularly in men (p < 0.0001) but not in women (p = 0.493) (p-interaction = 0.003). Over time, monocyte counts increased (p < 0.0001) in both EM and non-EM families, while lymphocytes and platelet counts decreased over time in the non-EM families (p < 0.0001) but not in the EM families. After adjusting for multiple variables, there was no significant difference in biomarker change over time between the EM and non-EM families. Discussion: Compared with non-EM families, EM families had significantly higher monocyte count at baseline but had similar change over time. Our study suggests that differences in monocyte counts may be a pathway through which EM emerges in some long-lived families, especially among men.
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spelling doaj.art-6de69bf37d4c4ae8bdaa9c4a492883522024-04-05T04:41:40ZengElsevierBrain, Behavior, & Immunity - Health2666-35462024-05-0137100746Systemic inflammation in relation to exceptional memory in the Long Life Family Study (LLFS)Ruhee Patel0Stephanie Cosentino1Esther Zhiwei Zheng2Nicole Schupf3Sandra Barral4Mary Feitosa5Stacy L. Andersen6Paola Sebastiani7Svetlana Ukraintseva8Kaare Christensen9Joseph Zmuda10Bharat Thyagarajan11Yian Gu12Cognitive Neuroscience Division, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Gertrude H. Sergievsky Center, Department of Neurology, Columbia University Medical Center, New York, NY, 10032, USACognitive Neuroscience Division, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Gertrude H. Sergievsky Center, Department of Neurology, Columbia University Medical Center, New York, NY, 10032, USACognitive Neuroscience Division, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Gertrude H. Sergievsky Center, Department of Neurology, Columbia University Medical Center, New York, NY, 10032, USACognitive Neuroscience Division, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Gertrude H. Sergievsky Center, Department of Neurology, Columbia University Medical Center, New York, NY, 10032, USACognitive Neuroscience Division, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Gertrude H. Sergievsky Center, Department of Neurology, Columbia University Medical Center, New York, NY, 10032, USADivision of Statistical Genomics, Department of Genetics, Washington University School of Medicine, St. Louis, MO, 63110, USADepartment of Medicine, Boston University School of Medicine, Boston, MA, 02118, USAInstitute for Clinical Research and Health Policy Studies, Tufts Medical Center, Boston, MA, 02111, USASocial Sciences Research Institute, Duke University, Durham, NC, 27705, USAEpidemiology, Biostatistics and Biodemography, University of Southern Denmark, 5230, Odense, DenmarkDepartment of Epidemiology, University of Pittsburgh, Pittsburgh, PA, 15213, USADepartment of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN, 55455, USACognitive Neuroscience Division, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Gertrude H. Sergievsky Center, Department of Neurology, Columbia University Medical Center, New York, NY, 10032, USA; Corresponding author.Background and objectives: We previously found a substantial familial aggregation of healthy aging phenotypes, including exceptional memory (EM) in long-lived persons. In the current study, we aim to assess whether long-lived families with EM and without EM (non-EM) differ in systemic inflammation status and trajectory. Methods: The current study included 4333 participants of the multi-center Long Life Family Study (LLFS). LLFS families were classified as EM (556 individuals from 28 families) or non-EM (3777 individuals from 416 families), with 2 or more offspring exhibiting exceptional memory performance (i.e. having baseline composite z-score representing immediate and delayed story memory being 1.5 SD above the mean in the nondemented offspring sample) considered as EM. Blood samples from baseline were used to measure inflammatory biomarkers including total white blood cell (WBC) and its subtypes (neutrophils, lymphocytes, monocytes) count, platelet count, high sensitivity C-reactive protein, and interleukin-6. Generalized linear models were used to examine cross-sectional differences in inflammatory biomarkers at baseline. In a sub-sample of 2227 participants (338 subjects from 24 EM families and 1889 from 328 non-EM families) with repeated measures of immune cell counts, we examined whether the rate of biomarker change differed between EM and non-EM families. All models were adjusted for family size, relatedness, age, sex, education, field center, APOE genotype, and body mass index. Results: LLFS participants from EM families had a marginally higher monocyte count at baseline (b = 0.028, SE = 0.0110, p = 0.010) after adjusting for age, sex, education, and field site, particularly in men (p < 0.0001) but not in women (p = 0.493) (p-interaction = 0.003). Over time, monocyte counts increased (p < 0.0001) in both EM and non-EM families, while lymphocytes and platelet counts decreased over time in the non-EM families (p < 0.0001) but not in the EM families. After adjusting for multiple variables, there was no significant difference in biomarker change over time between the EM and non-EM families. Discussion: Compared with non-EM families, EM families had significantly higher monocyte count at baseline but had similar change over time. Our study suggests that differences in monocyte counts may be a pathway through which EM emerges in some long-lived families, especially among men.http://www.sciencedirect.com/science/article/pii/S2666354624000243LongevityInflammationEpisodic memoryBiomarkers
spellingShingle Ruhee Patel
Stephanie Cosentino
Esther Zhiwei Zheng
Nicole Schupf
Sandra Barral
Mary Feitosa
Stacy L. Andersen
Paola Sebastiani
Svetlana Ukraintseva
Kaare Christensen
Joseph Zmuda
Bharat Thyagarajan
Yian Gu
Systemic inflammation in relation to exceptional memory in the Long Life Family Study (LLFS)
Brain, Behavior, & Immunity - Health
Longevity
Inflammation
Episodic memory
Biomarkers
title Systemic inflammation in relation to exceptional memory in the Long Life Family Study (LLFS)
title_full Systemic inflammation in relation to exceptional memory in the Long Life Family Study (LLFS)
title_fullStr Systemic inflammation in relation to exceptional memory in the Long Life Family Study (LLFS)
title_full_unstemmed Systemic inflammation in relation to exceptional memory in the Long Life Family Study (LLFS)
title_short Systemic inflammation in relation to exceptional memory in the Long Life Family Study (LLFS)
title_sort systemic inflammation in relation to exceptional memory in the long life family study llfs
topic Longevity
Inflammation
Episodic memory
Biomarkers
url http://www.sciencedirect.com/science/article/pii/S2666354624000243
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