INS NYC 2024 Program

Poster	Poster Session 02 Program Schedule 02/15/2024 08:00 am - 09:15 am Room: Shubert Complex (Posters 1-60) Poster Session 02: Aging \| MCI \| Neurodegenerative Disease - PART 1 Final Abstract #20 The Differential Effects of Neuroinflammatory Proteins on BIPOC and WNH Veterans with Amnestic MCI Devon Delaney, MA, MS, PGSP-Stanford Psy.D. Consortium, Palo Alto, United States Eliza Morgan, MS, Palo Alto University, Palo Alto, United States Sheila Thompson, MS, Palo Alto University, Palo Alto, United States Danna Torres, LMFT, Palo Alto University, Palo Alto, United States J. Kaci Fairchild, PhD, ABPP, Sierra Pacific Mental Illness Research Education and Clinical Center (MIRECC), Veterans Affairs Palo Alto Health Care System; Department of Psychiatry & Behavioral Sciences, Stanford University School of Medicine, Palo Alto, United States Category: MCI (Mild Cognitive Impairment) Keyword 1: neuroimmunology Keyword 2: diversity Keyword 3: mild cognitive impairment Objective: Even with advancing biomarkers of neurodegeneration, a significant degree of heterogeneity exists in the biological mechanisms underlying neurodegenerative disease. Evidence suggests neuroinflammation is implicated in cognitive impairment. The association between neuroinflammation and cognitive impairment as it relates to different racial/ethnic groups is not well understood. The current study investigated the associations between inflammation and delayed recall, moderated by race, in a sample of older adult veterans with amnestic mild cognitive impairment (MCI). Participants and Methods: Participants included 66 older adults diagnosed with amnestic MCI, ages 55-88 years (mean 70.67±8.66). The sample was largely male (96%) and well-educated with over half having at least a bachelor’s degree (56%). Over 30% of the sample (n=20) self-identified as Black, Indigenous, People of Color (BIPOC). Delayed recall was assessed via the Delayed Recall trial of the Rey Auditory Verbal Learning Test. Baseline plasma protein levels were assayed with SomaScan Assay (SomaLogic, Inc), with a specific focus on the “Inflammation and Immune Response Panel”. Age was treated as a covariate in all analyses given its known relationship with inflammation and cognitive function. Pearson’s correlations were used to identify inflammatory analytes that had a significant association with delayed recall. Group differences were assessed via ANCOVAs. The moderating effect of race on the relationship between inflammation and delayed recall was assessed via the Hayes Process Macro Model 1. All analyses were performed with SPSS. Results: Preliminary analyses identified 4 proteins that were significantly associated with delayed recall (DEFA5, r = 0.282, p = 0.23; IL6R, r = 0.307, p = 0.013, PSIP1, r = 0.304, p = 0.014, and OSM, r = 0.318, p = 0.010). ANCOVA revealed that group differences existed only for DEFA5 (F = 4.67, p = 0.035). As such, only DEFA5 was included in subsequent moderation analyses. DEFA5, but not race (b= 6.35, p = 0.069), was found to be a significant predictor of delayed recall (b = 0.004, p = 0.021). The interaction between race and DEFA5 was also significant (b = -0.002, p = 0.04). Specifically, the impact of DEFA5 on delayed recall performance was significant for BIPOC older adults (b = 0.003, p = 0.01) but not White Non-Hispanic (WNH) older adults (b < 0.001, p = 0.82). Conclusions: The current study found a significant relationship between DEFA5 (Human Alpha Defensin 5) and delayed recall on the RAVLT. Specifically, BIPOC veterans with higher levels of DEFA5 performed significantly better on delayed recall on the RAVLT than WNH veterans with similar levels of DEFA5. DEFA5 is a cytotoxic peptide that is involved in host defense and maintenance of intestinal microbiota homeostasis. The findings from this study highlight the importance of considering race when examining the relationship between inflammation and cognition. Further research is needed to explore the relationship between DEFA5 and delayed recall performance in BIPOC veterans with MCI.

Poster

02/15/2024
08:00 am - 09:15 am
Room: Shubert Complex (Posters 1-60)

Poster Session 02: Aging | MCI | Neurodegenerative Disease - PART 1

Final Abstract #20

The Differential Effects of Neuroinflammatory Proteins on BIPOC and WNH Veterans with Amnestic MCI

Devon Delaney, MA, MS, PGSP-Stanford Psy.D. Consortium, Palo Alto, United States
Eliza Morgan, MS, Palo Alto University, Palo Alto, United States
Sheila Thompson, MS, Palo Alto University, Palo Alto, United States
Danna Torres, LMFT, Palo Alto University, Palo Alto, United States
J. Kaci Fairchild, PhD, ABPP, Sierra Pacific Mental Illness Research Education and Clinical Center (MIRECC), Veterans Affairs Palo Alto Health Care System; Department of Psychiatry & Behavioral Sciences, Stanford University School of Medicine, Palo Alto, United States

Category: MCI (Mild Cognitive Impairment)

Keyword 1: neuroimmunology
Keyword 2: diversity
Keyword 3: mild cognitive impairment

Objective:

Even with advancing biomarkers of neurodegeneration, a significant degree of heterogeneity exists in the biological mechanisms underlying neurodegenerative disease. Evidence suggests neuroinflammation is implicated in cognitive impairment. The association between neuroinflammation and cognitive impairment as it relates to different racial/ethnic groups is not well understood. The current study investigated the associations between inflammation and delayed recall, moderated by race, in a sample of older adult veterans with amnestic mild cognitive impairment (MCI).

Participants and Methods:

Participants included 66 older adults diagnosed with amnestic MCI, ages 55-88 years (mean 70.67±8.66). The sample was largely male (96%) and well-educated with over half having at least a bachelor’s degree (56%). Over 30% of the sample (n=20) self-identified as Black, Indigenous, People of Color (BIPOC). Delayed recall was assessed via the Delayed Recall trial of the Rey Auditory Verbal Learning Test. Baseline plasma protein levels were assayed with SomaScan Assay (SomaLogic, Inc), with a specific focus on the “Inflammation and Immune Response Panel”. Age was treated as a covariate in all analyses given its known relationship with inflammation and cognitive function. Pearson’s correlations were used to identify inflammatory analytes that had a significant association with delayed recall. Group differences were assessed via ANCOVAs. The moderating effect of race on the relationship between inflammation and delayed recall was assessed via the Hayes Process Macro Model 1. All analyses were performed with SPSS.

Results:

Preliminary analyses identified 4 proteins that were significantly associated with delayed recall (DEFA5, r = 0.282, p = 0.23; IL6R, r = 0.307, p = 0.013, PSIP1, r = 0.304, p = 0.014, and OSM, r = 0.318, p = 0.010). ANCOVA revealed that group differences existed only for DEFA5 (F = 4.67, p = 0.035). As such, only DEFA5 was included in subsequent moderation analyses. DEFA5, but not race (b= 6.35, p = 0.069), was found to be a significant predictor of delayed recall (b = 0.004, p = 0.021). The interaction between race and DEFA5 was also significant (b = -0.002, p = 0.04). Specifically, the impact of DEFA5 on delayed recall performance was significant for BIPOC older adults (b = 0.003, p = 0.01) but not White Non-Hispanic (WNH) older adults (b < 0.001, p = 0.82).

Conclusions:

The current study found a significant relationship between DEFA5 (Human Alpha Defensin 5) and delayed recall on the RAVLT. Specifically, BIPOC veterans with higher levels of DEFA5 performed significantly better on delayed recall on the RAVLT than WNH veterans with similar levels of DEFA5. DEFA5 is a cytotoxic peptide that is involved in host defense and maintenance of intestinal microbiota homeostasis. The findings from this study highlight the importance of considering race when examining the relationship between inflammation and cognition. Further research is needed to explore the relationship between DEFA5 and delayed recall performance in BIPOC veterans with MCI.