Research suggests that neuroinflammation of the brain has a role in dementia by activating glial cells which then release proinflammatory agents and lipopolysaccharide (LPS) responsible for cognitive deficits. Other authors suggest that there is no clear evidence if neuroinflammation after generalized infection is a cause, agent, or consequence of Alzheimer’s Disease (AD) with bacterial endotoxin LPS acting on neurons and microglia. The current case study refers to a 64-year old woman who developed symptoms of dementia and psychosis a month after she was operated for a duodenal perforation resulting in pneumoperitoneum and systemic bacterial sepsis. Neuropsychiatric and clinical assessment gathered the required data. Past psychiatric history was negative for mental health pathologies, and former cognitive deficits were non-existent before the systemic inflammation. Therefore, the authors of the current research speculate that in the case described, systemic inflammation enduringly unlocked dementia, cognitive deficits, and psychosis.