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Alzheimer's disease has proven to be largely intractable to treatment, despite years of research, and numerous trials of therapies that target the hallmarks of the disease - amyloid plaques and neurofibrillary tangles. The etiology of Alzheimer's disease remains elusive. There is a growing body of evidence for an infectious trigger of Alzheimer's disease, and, in particular, the focus has been on the oral pathogen Porphyromonas gingivalis (P. gingivalis). Reports of the expression of a misfolded form of p53 in non-neuronal cells (fibroblasts, peripheral blood mononuclear cells, and B cells) and serum, which appears several years before clinical symptoms manifest, may provide further support for the role of bacteria in general, and P. gingivalis in particular, in the initiation of the disease. This review presents a model of the pathway from initial oral infection with P. gingivalis to amyloid plaque formation and neuronal degeneration, via the steps of chronic periodontitis; secretion of the inflammagens lipopolysaccharide and gingipains into the bloodstream; induction of an inflammatory response in both peripheral cells and tissues; disruption of the blood-brain barrier, and entry into the central nervous system of the inflammagens and the P. gingivalis bacteria themselves. In this model, the misfolded p53 (or "unfolded p53"; up53) is induced in non-neuronal cells and upregulated in serum as a result of oxidative stress due to lipopolysaccharide from P. gingivalis. up53 is therefore a potential biomarker for early diagnosis of the presence of a causative agent of Alzheimer's disease. Fastidious dental hygiene and aggressive antibiotic treatment may prevent the patient progressing to clinical Alzheimer's disease if serum up53 is detected at this pre-symptomatic stage.