<p>Brain dysfunction is a primary symptom of Gulf War illness (GWI). The present study investigated the effects of an amorphous formula of curcumin (CUR) and α-glycosyl isoquercitrin (AGIQ) on neurobehaviors and adult neurogenesis and following synaptic plasticity of produced neurons in the hippocampal dentate gyrus (DG) in a rat GWI model. Ten-week-old rats received GWI-related chemicals and restraint stress for 28 days; thereafter, animals were fed either a diet without supplement or mixed with 0.1% CUR or 0.5% AGIQ for 126 days. GWI treatment adversely affected behavioral endpoints, including novel object recognition, sucrose preference, novelty-suppressed feeding, and contextual fear conditioning. CUR ameliorated all these effects, while AGIQ caused anxiety-like behavior and improved fear extinction learning. GWI treatment downregulated NRF2–KEAP1 pathway-related genes in the DG; both phytochemicals reversed most of these changes. GWI treatment increased CD68⁺ and CD163⁺ microglia populations in the DG hilus; both phytochemicals reversed the increase of CD68⁺ microglia. In the neurogenic niche, GWI treatment decreased GFAP⁺ neural stem cells but increased DCX⁺ and PCNA⁺ cells, decreased hilar SST⁺ and GAD67⁺ GABAergic interneurons, and downregulated <i>Pvalb</i>. CUR reversed decreases in GFAP⁺ cell and SST⁺ interneuron numbers. Both phytochemicals increased VGLUT1 immunoreactivity, restored the VGLUT1/VGAT ratio, and upregulated <i>Bdnf</i>, <i>Gria1</i>, <i>Gria2</i>, <i>Gria3</i>, <i>Slc17a7</i>, <i>Ptgs2</i>, and <i>Mapk1</i>. AGIQ further increased COX2⁺ cell numbers and upregulated <i>Grin2a</i>, <i>Grin2b</i>, and <i>Mapk3</i>. In summary, both phytochemicals may have exerted antioxidant effects and modulated excitatory/inhibitory balance via glutamatergic signaling in GWI animals; CUR was superior to AGIQ at normalizing aberrant neurobehaviors and neurogenesis.</p> Graphical Abstract <p></p>