INS NYC 2024 Program

Poster	Poster Session 06 Program Schedule 02/15/2024 04:00 pm - 05:15 pm Room: Shubert Complex (Posters 1-60) Poster Session 06: Aging \| MCI \| Neurodegenerative Disease - PART 2 Final Abstract #41 Loneliness Independently Impacts Neuroimaging-based Cerebrovascular and Alzheimer’s Disease Biomarkers and Cognition in a Middle-aged, Community-based Sample Chima Ezeh, Columbia University Irving Medical Center, New York, United States Kiana Chan, Columbia University Irving Medical Center, New York, United States Mohamad Alshikho, Columbia University Irving Medical Center, New York, United States Stephanie Cosentino, Columbia University Irving Medical Center, New York, United States Jennifer Manly, Columbia University Irving Medical Center, New York, United States Adam Brickman, Columbia University Irving Medical Center, New York, United States Patrick Lao, Columbia University Irving Medical Center, New York, United States Category: Neuroimaging Keyword 1: social processes Keyword 2: dementia - Alzheimer's disease Keyword 3: cerebrovascular disease Objective: U.S. trends indicate that even before the COVID-19 pandemic, social connection has steadily declined since the early 2000s. Among measures of declining social connection, loneliness is a major risk factor for poor cognition, cognitive decline, and dementia. To prevent these adverse cognitive outcomes, interventions during midlife are paramount, before pathology and pathology-related neurodegeneration and cognitive impairment have appreciably developed. We tested the effect of loneliness on indices of Alzheimer’s disease and related disorders (ADRD) and cognition at midlife. We hypothesized that increased loneliness would be associated with increased markers of amyloid, tau, and vascular pathophysiology, and lower cognition. Participants and Methods: A subset of participants from the Offspring Study of Racial and Ethnic Disparities in Alzheimer’s Disease (n=79, 58.8±5.8 years old, 65% women; 53% Latinx, 43% Non-Latinx Black, 11% Non-Latinx White; 14±3 years of education; 32% APOE-ε4 carriers) completed amyloid and tau PET imaging, vascular and structural MRI, neuropsychological assessment, and psychosocial questionnaires on loneliness, depression, and anxiety. Neuroimaging outcomes were biomarkers of ADRD [amyloid and tau PET SUVR, 1.1±0.1 (9% positive) and 1.3±0.2 (4% positive), respectively; continuous SUVR used in analytic models], cerebrovascular disease [white matter hyperintensity (WMH) volume, 4.4±6.6 cm3; log-transformed for analytic models], and neurodegeneration (relative hippocampal volume, 0.50±0.07, and cortical thickness in AD signature regions, 2.64±0.10 mm). Cognitive outcomes included performance on immediate and delayed recall of the Selective Reminding Test. Loneliness was operationalized with the 3-item UCLA Loneliness Scale. We examined the association of loneliness with each imaging and cognitive outcome in separate linear models that adjusted for age, sex, APOE-ε4 carrier status, and education. We separately adjusted for psychosocial factors related to loneliness: depressive and anxiety symptoms (9-item Center for Epidemiological Studies Depression Scale, and modified 5-item Beck and Anxiety Inventory). Results: Greater loneliness was associated with greater amyloid burden (B=0.009 [-0.002, 0.02], p=0.13), which became significant after adjusting for depression (B=0.01 [0.0002, 0.03], p=0.046) and anxiety (B=0.01 [0.0001, 0.03], p=0.048). Greater loneliness was also associated with greater WMH volume (B=0.09 [0.02, 0.14], p=0.009), which remained significant after adjusting for depression (B=0.08 [0.01, 0.15], p=0.02) and anxiety (B=0.08 [0.004, 0.16], p=0.04). In contrast, greater depression and anxiety, but not loneliness, were associated with lower hippocampal volume (B=-0.004 [-0.008, -0.0003], p=0.04; B=-0.01 [-0.02, -0.001], p=0.03; respectively). Greater loneliness was associated with lower scores on immediate (B=-1.9 [-3.8, 0.1], p=0.06) and delayed recall trials (B=-0.5 [-0.8, -0.05], p=0.03), which both remained significant after adjusting for depression (B=-2.5 [-4.6, -0.3], p=0.02; B=-0.5 [-0.9, -0.05], p=0.03; respectively) and anxiety (B=-2.8 [-5.0, -0.7], p=0.01; B=-0.5 [-0.9, -0.04], p=0.03; respectively). Conclusions: Loneliness may increase susceptibility for amyloidosis and cerebrovascular disease in midlife, but not for tau or neurodegeneration. Consistent with studies among older adults, we also found that loneliness may have an impact on cognition in midlife.

Poster

02/15/2024
04:00 pm - 05:15 pm
Room: Shubert Complex (Posters 1-60)

Poster Session 06: Aging | MCI | Neurodegenerative Disease - PART 2

Final Abstract #41

Loneliness Independently Impacts Neuroimaging-based Cerebrovascular and Alzheimer’s Disease Biomarkers and Cognition in a Middle-aged, Community-based Sample

Chima Ezeh, Columbia University Irving Medical Center, New York, United States
Kiana Chan, Columbia University Irving Medical Center, New York, United States
Mohamad Alshikho, Columbia University Irving Medical Center, New York, United States
Stephanie Cosentino, Columbia University Irving Medical Center, New York, United States
Jennifer Manly, Columbia University Irving Medical Center, New York, United States
Adam Brickman, Columbia University Irving Medical Center, New York, United States
Patrick Lao, Columbia University Irving Medical Center, New York, United States

Category: Neuroimaging

Keyword 1: social processes
Keyword 2: dementia - Alzheimer's disease
Keyword 3: cerebrovascular disease

Objective:

U.S. trends indicate that even before the COVID-19 pandemic, social connection has steadily declined since the early 2000s. Among measures of declining social connection, loneliness is a major risk factor for poor cognition, cognitive decline, and dementia. To prevent these adverse cognitive outcomes, interventions during midlife are paramount, before pathology and pathology-related neurodegeneration and cognitive impairment have appreciably developed. We tested the effect of loneliness on indices of Alzheimer’s disease and related disorders (ADRD) and cognition at midlife. We hypothesized that increased loneliness would be associated with increased markers of amyloid, tau, and vascular pathophysiology, and lower cognition.

Participants and Methods:

A subset of participants from the Offspring Study of Racial and Ethnic Disparities in Alzheimer’s Disease (n=79, 58.8±5.8 years old, 65% women; 53% Latinx, 43% Non-Latinx Black, 11% Non-Latinx White; 14±3 years of education; 32% APOE-ε4 carriers) completed amyloid and tau PET imaging, vascular and structural MRI, neuropsychological assessment, and psychosocial questionnaires on loneliness, depression, and anxiety. Neuroimaging outcomes were biomarkers of ADRD [amyloid and tau PET SUVR, 1.1±0.1 (9% positive) and 1.3±0.2 (4% positive), respectively; continuous SUVR used in analytic models], cerebrovascular disease [white matter hyperintensity (WMH) volume, 4.4±6.6 cm3; log-transformed for analytic models], and neurodegeneration (relative hippocampal volume, 0.50±0.07, and cortical thickness in AD signature regions, 2.64±0.10 mm). Cognitive outcomes included performance on immediate and delayed recall of the Selective Reminding Test. Loneliness was operationalized with the 3-item UCLA Loneliness Scale. We examined the association of loneliness with each imaging and cognitive outcome in separate linear models that adjusted for age, sex, APOE-ε4 carrier status, and education. We separately adjusted for psychosocial factors related to loneliness: depressive and anxiety symptoms (9-item Center for Epidemiological Studies Depression Scale, and modified 5-item Beck and Anxiety Inventory).

Results:

Greater loneliness was associated with greater amyloid burden (B=0.009 [-0.002, 0.02], p=0.13), which became significant after adjusting for depression (B=0.01 [0.0002, 0.03], p=0.046) and anxiety (B=0.01 [0.0001, 0.03], p=0.048). Greater loneliness was also associated with greater WMH volume (B=0.09 [0.02, 0.14], p=0.009), which remained significant after adjusting for depression (B=0.08 [0.01, 0.15], p=0.02) and anxiety (B=0.08 [0.004, 0.16], p=0.04). In contrast, greater depression and anxiety, but not loneliness, were associated with lower hippocampal volume (B=-0.004 [-0.008, -0.0003], p=0.04; B=-0.01 [-0.02, -0.001], p=0.03; respectively). Greater loneliness was associated with lower scores on immediate (B=-1.9 [-3.8, 0.1], p=0.06) and delayed recall trials (B=-0.5 [-0.8, -0.05], p=0.03), which both remained significant after adjusting for depression (B=-2.5 [-4.6, -0.3], p=0.02; B=-0.5 [-0.9, -0.05], p=0.03; respectively) and anxiety (B=-2.8 [-5.0, -0.7], p=0.01; B=-0.5 [-0.9, -0.04], p=0.03; respectively).

Conclusions:

Loneliness may increase susceptibility for amyloidosis and cerebrovascular disease in midlife, but not for tau or neurodegeneration. Consistent with studies among older adults, we also found that loneliness may have an impact on cognition in midlife.