Meta-Analysis on Nicotine's Modulation of HIV-Associated Dementia

AbstractHIV-Associated Dementia (HAD) is a significant comorbidity that many HIV-patients face. Our study utilized QIAGEN Ingenuity Pathway Analysis (IPA) to identify and analyze molecular profiles and pathways underlying nicotine ’s impact on HAD pathology. The Qiagen Knowledge Base (QKB) defines HAD as “Dementia associated with acquired immunodeficiency syndrome (disorder).” Although much remains unknown about HAD pathology, the curated research findings from the QKB shows 5 upregulated molecules that are associated w ith HAD + : CCL2 (Chemokine (C–C motif) ligand 2), L-glutamic acid, GLS (Glutaminase), POLG (DNA polymerase subunit gamma), and POLB (DNA polymerase subunit beta). The current study focused on these 5 HAD pathology molecules as the phenotype of interest. The Pathway Explorer tool of IPA was us ed to connect nicotine-associated molecules with the 5 HAD associated molecules (HAD pathology molecules) by connecting 29 overlapping molecules (including transcription regulators, cytokines, kinases, and other enzymes/proteins). The Molecule-Activity-Predictor (MAP) tool predicted nicotine-induced activation of the HAD pathology molecules indicating the exacerbation of HAD. However, alternative pathways with more holistic representations of molecular relationships revealed the potential of nicotine as a neuroprotective treatment. It was found that concurrent with nicotine treatment the indiv idual inactivation of several of the intermediary molecules in the...
Source: Journal of NeuroImmune Pharmacology - Category: Drugs & Pharmacology Source Type: research