INS NYC 2024 Program

Poster	Poster Session 09 Program Schedule 02/16/2024 03:30 pm - 04:45 pm Room: Majestic Complex (Posters 61-120) Poster Session 09: Epilepsy \| Oncology \| MS \| Infectious Disease Final Abstract #77 Examining the Role of Serum Biomarkers in the Association Between Hippocampal Internal Architecture and Cognitive Impairment in Multiple Sclerosis Alicia Milam, University of Alabama at Birmingham, Birmingham, United States Amani Norling, University of Alabama at Birmingham, Birmingham, United States Christopher Collette, University of Alabama at Birmingham, Birmingham, United States Hyun Freeman, University of Alabama at Birmingham, Birmingham, United States Randall Walden, University of Alabama at Birmingham, Birmingham, United States Katherine Ward, University of Alabama at Birmingham, Birmingham, United States Jennifer Hylton, University of Alabama at Birmingham, Birmingham, United States Khurram Bashir, University of Alabama at Birmingham, Birmingham, United States William Meador, University of Alabama at Birmingham, Birmingham, United States Benjamin Jones, University of Alabama at Birmingham, Birmingham, United States John Rinker, University of Alabama at Birmingham, Birmingham, United States Stephen Benesh, University of Alabama at Birmingham, Birmingham, United States Lawrence Ver Hoef, University of Alabama at Birmingham, Birmingham, United States Ronald Lazar, University of Alabama at Birmingham, Birmingham, United States Adam Gerstenecker, University of Alabama at Birmingham, Birmingham, United States Category: Multiple Sclerosis/ALS/Demyelinating Disorders Keyword 1: multiple sclerosis Keyword 2: cognitive functioning Keyword 3: neuroimaging: structural Objective: Individuals with Multiple Sclerosis (MS) are disproportionately impacted by cognitive impairment. Of those with an MS diagnosis, 34-60% perform significantly below expectations on multiple neuropsychological tests. Deficits in processing speed and executive functioning have consistently been found in cognitive testing and may impede daily functioning. Recent literature suggests that inflammation increases the likelihood of cognitive impairment in those with MS. Additionally, hippocampal atrophy has been found to be associated with inflammation and cognitive deficits in MS. The present study aims to examine interactions between serum biomarkers and hippocampal internal architecture (HIA) subfield volumes predicting cognitive decline in individuals with MS. Participants and Methods: Participants included 53 individuals diagnosed with MS using McDonald criteria. Patients underwent neuropsychological testing to assess cognitive functioning, collection of serum blood samples for biomarkers, and a brain MRI. Novel High-Resolution Multiple Image Co-Registration and Averaging (HR-MICRA) techniques using a voxel volume of .175 mm³ were utilized for increased accuracy in measurement of HIA subfield volumes. To reflect the cognitive profiles of persons with MS, neuropsychological testing scores were split into domains of processing speed, executive functioning, processing speed and executive functioning, and global cognitive functioning using composite scores. Scores >-1.5 standard deviations below the mean were considered impaired (n=23). Individual moderation analyses were then run using PROCESS in SPSS for all serum biomarkers (ICAM1, VEGF, IL-6, IL-17, IGF-1) and HIA subfields (CA1, CA2, CA3, dentate gyrus, and the subiculum). Results: Within the global cognitive domain, ICAM1 levels interacted with left CA1 volume (p=.006) and IL-6 levels interacted with left subiculum volume (p=.025) to predict impairment status. In the processing speed and executive functioning domain, the relationship between the right CA2 volume and cognitive status was moderated by ICAM1 (p=.015), IL-6 (p=.020), and IL-17 (p=.014) levels. VEGF levels also interacted with right CA3 volume to predict cognitive status (p=.019). In the processing speed domain IGF-1 levels interacted with right CA1 volume (p=.046) and IL-17 levels interacted with left CA3 volume (p=.023) to predict cognitive status. Lastly, in the executive functioning domain, IL-17 levels interacted with right CA1 (p=.043), right CA2 (p=.031), and right dentate gyrus volume (p=.024), IL-6 levels interacted with right CA1 (p=.045) and right CA2 volume (p=.020), and VEGF levels interacted with right CA2 volume (p=.008) to predict cognitive status. Conclusions: Cognitive impairment in the executive functioning domain was most influenced by interactions between hippocampal subfield volumes and serum biomarkers where interleukin cytokines moderated relationships between right-sided HIA and executive functioning. Results provide preliminary evidence of inflammatory mechanisms of cognitive deficits in individuals with MS. Future literature should assess the long-term sequelae of inflammatory biomarkers, HIA volume changes, and cognitive impairments to determine early diagnostic and treatment relevance.

Poster

02/16/2024
03:30 pm - 04:45 pm
Room: Majestic Complex (Posters 61-120)

Poster Session 09: Epilepsy | Oncology | MS | Infectious Disease

Final Abstract #77

Examining the Role of Serum Biomarkers in the Association Between Hippocampal Internal Architecture and Cognitive Impairment in Multiple Sclerosis

Alicia Milam, University of Alabama at Birmingham, Birmingham, United States
Amani Norling, University of Alabama at Birmingham, Birmingham, United States
Christopher Collette, University of Alabama at Birmingham, Birmingham, United States
Hyun Freeman, University of Alabama at Birmingham, Birmingham, United States
Randall Walden, University of Alabama at Birmingham, Birmingham, United States
Katherine Ward, University of Alabama at Birmingham, Birmingham, United States
Jennifer Hylton, University of Alabama at Birmingham, Birmingham, United States
Khurram Bashir, University of Alabama at Birmingham, Birmingham, United States
William Meador, University of Alabama at Birmingham, Birmingham, United States
Benjamin Jones, University of Alabama at Birmingham, Birmingham, United States
John Rinker, University of Alabama at Birmingham, Birmingham, United States
Stephen Benesh, University of Alabama at Birmingham, Birmingham, United States
Lawrence Ver Hoef, University of Alabama at Birmingham, Birmingham, United States
Ronald Lazar, University of Alabama at Birmingham, Birmingham, United States
Adam Gerstenecker, University of Alabama at Birmingham, Birmingham, United States

Category: Multiple Sclerosis/ALS/Demyelinating Disorders

Keyword 1: multiple sclerosis
Keyword 2: cognitive functioning
Keyword 3: neuroimaging: structural

Objective:

Individuals with Multiple Sclerosis (MS) are disproportionately impacted by cognitive impairment. Of those with an MS diagnosis, 34-60% perform significantly below expectations on multiple neuropsychological tests. Deficits in processing speed and executive functioning have consistently been found in cognitive testing and may impede daily functioning. Recent literature suggests that inflammation increases the likelihood of cognitive impairment in those with MS. Additionally, hippocampal atrophy has been found to be associated with inflammation and cognitive deficits in MS. The present study aims to examine interactions between serum biomarkers and hippocampal internal architecture (HIA) subfield volumes predicting cognitive decline in individuals with MS.

Participants and Methods:

Participants included 53 individuals diagnosed with MS using McDonald criteria. Patients underwent neuropsychological testing to assess cognitive functioning, collection of serum blood samples for biomarkers, and a brain MRI. Novel High-Resolution Multiple Image Co-Registration and Averaging (HR-MICRA) techniques using a voxel volume of .175 mm³ were utilized for increased accuracy in measurement of HIA subfield volumes. To reflect the cognitive profiles of persons with MS, neuropsychological testing scores were split into domains of processing speed, executive functioning, processing speed and executive functioning, and global cognitive functioning using composite scores. Scores >-1.5 standard deviations below the mean were considered impaired (n=23). Individual moderation analyses were then run using PROCESS in SPSS for all serum biomarkers (ICAM1, VEGF, IL-6, IL-17, IGF-1) and HIA subfields (CA1, CA2, CA3, dentate gyrus, and the subiculum).

Results:

Within the global cognitive domain, ICAM1 levels interacted with left CA1 volume (p=.006) and IL-6 levels interacted with left subiculum volume (p=.025) to predict impairment status. In the processing speed and executive functioning domain, the relationship between the right CA2 volume and cognitive status was moderated by ICAM1 (p=.015), IL-6 (p=.020), and IL-17 (p=.014) levels. VEGF levels also interacted with right CA3 volume to predict cognitive status (p=.019). In the processing speed domain IGF-1 levels interacted with right CA1 volume (p=.046) and IL-17 levels interacted with left CA3 volume (p=.023) to predict cognitive status. Lastly, in the executive functioning domain, IL-17 levels interacted with right CA1 (p=.043), right CA2 (p=.031), and right dentate gyrus volume (p=.024), IL-6 levels interacted with right CA1 (p=.045) and right CA2 volume (p=.020), and VEGF levels interacted with right CA2 volume (p=.008) to predict cognitive status.

Conclusions:

Cognitive impairment in the executive functioning domain was most influenced by interactions between hippocampal subfield volumes and serum biomarkers where interleukin cytokines moderated relationships between right-sided HIA and executive functioning. Results provide preliminary evidence of inflammatory mechanisms of cognitive deficits in individuals with MS. Future literature should assess the long-term sequelae of inflammatory biomarkers, HIA volume changes, and cognitive impairments to determine early diagnostic and treatment relevance.