Blood cells from Alzheimer's patients show paradoxical immune responses when exposed to bacteria from gum disease. While these cells produce fewer inflammatory cytokines at baseline—including TNF-α, IL-1β, IL-6, and IL-10—they mount an exaggerated response when challenged with Porphyromonas gingivalis toxins, the primary pathogen in severe periodontitis. This dysregulated immune signature correlates directly with oral health deterioration and cognitive decline severity. The finding reveals a mechanistic link between periodontal infection and neurodegeneration that extends beyond simple inflammation. Previous research has established that oral bacteria can reach the brain through multiple pathways, including direct neural migration and systemic circulation. This study's demonstration of immune hyperreactivity to periodontal pathogens suggests the immune system becomes both compromised and hypersensitive in Alzheimer's progression. The clinical implications are significant: maintaining aggressive oral hygiene and treating periodontal disease early may represent a modifiable intervention to slow cognitive decline. However, the cross-sectional design cannot establish whether immune dysfunction precedes or follows periodontal deterioration, and the modest sample size of 68 participants limits generalizability across diverse populations.