The most significant impairments were shown in the domains of executive functions and speed and attention, while a less pronounced impairment was shown in the domains of learning and memory and language. Importantly, these impairments were not accompanied by biomarker evidence of ongoing neuronal or astrocytic injury/activation or induction of AD-related brain pathologies (increased p-tau or decreased Aβ42/Aβ40 ratio) by the infection. This evidence concerns the gene MAPT and Alzheimer disease.