| Publication Abstract Display | | Type: Poster | | Title: Associations of the systemic immune-inflammation index with neurocognition and depression in people with HIV. | | Authors: Wang CX, Ellis RJ, Cherner M, Moore DJ, Letendre SL, Iudicello JE | | Date: 02-13-2025 | | Abstract:Objective:
Despite viral suppression, brain health disorders remain common among people with HIV (PWH). Chronic systemic inflammation, a hallmark feature of HIV disease, may underly neuropsychiatric disturbances, such as neurocognitive impairment and depression, but measuring sensitive inflammatory biomarkers can be costly and time-intensive. The current study tests the relationship of the Systemic Immune-Inflammation Index (SII), which can be derived from routine clinical bloodwork, to neurocognition and depressive symptoms in PWH.
Participants and Methods:
Participants were 1,870 PWH (80% male; 65% racial/ethnic minority; 66% AIDS; 81% on antiretroviral therapy; 42% with NCI; 35% Beck’s Depression Inventory-II >13) enrolled in cohort studies at the UC San Diego HIV Neurobehavioral Research Program. Neurocognition was assessed using demographically adjusted T-scores on a comprehensive test battery covering 7 ability domains. Current depressive symptoms were measured with the Beck Depression Inventory-II (BDI-II) and its subscales (i.e., cognitive, affective, somatic, and anhedonia). The SII was calculated from complete blood count labs as ([neutrophils X platelets]/lymphocytes), and standardized.
Results:
Unadjusted models found significant associations between the SII and lower global neurocognition (estimate= -.54, p=.01), verbal fluency (estimate= -.68, p< .001), executive functioning (estimate= -.53, p = .04), processing speed (estimate= -.58, p= .02), learning (estimate= -.53, p= .04), recall (estimate= -.59, p= .03), and motor speed (estimate= -.58, p= .05), but not working memory (p > .10), as well as higher total BDI-II scores (estimate= .52, p= .05), and BDI-II apathy (estimate= .12, p = .05), somatic (estimate= .28, p= .02), and anhedonia (estimate= .13, p = .05) subscales, but no other subscales, (ps> .10). When adjusting for covariates (e.g., age, sex, Nadir CD4, current CD4, estimated duration of infection, ART use, and viral suppression), multiple linear regressions found SII to be associated with lower global neurocognition (estimate= -.51, p = .01), verbal fluency (estimate= -.67, p= .01), processing speed (estimate= -.55, p = .04), learning (estimate= -.55, p= .05), and recall (estimate= -.63, p= .02), but not executive functioning, working memory, or motor speed (ps > .10). Adjusted models also found associations between the SII and higher scores on the BDI-II somatic subscale (estimate= .24, p= .02), but not total BDI-II or any other subscales (ps > .10). Associations between the SII and neurocognition or depression did not significant differ by viral suppression status (ps > .10).
Conclusions:
Systemic inflammation, as measured by the SII, was associated with poorer global neurocognition, which was driven by lower scores in verbal fluency, learning, and recall domains. There were also associations between the SII and more somatic depressive symptoms. Our results show the utility of the SII as an inflammatory biomarker linked to neurocognitive impairment and depressive symptoms in PWH that is easily accessible via routine clinical blood labs. These findings also contribute to the growing literature demonstrating an inflammatory subtype of depression characterized by somatic or anhedonia symptoms and neurobehavioral disturbances that may be especially prevalent in PWH. |
return to publications listing
|