A transfection product incorporates in one molecule of human DNA, an inserted segment of DNA from another species. This communication addresses the hypothesis that a novel variation of the theme of transfection, namely "junk transfection" for which no protein product and no RNA is transcribed, might offer insights into the pathogenesis of Alzheimer's disease. It is hypothesized that spirochetal DNA gains access to the intracellular compartment of nerve cells during the subclinical latency phase of neuroborreliosis and chemically combines with human DNA. A previously reported Molecular interrogation of Alzheimer's disease autopsy tissues has yielded novel DNA sequences containing the 11 q human chromosome and a short piece of the Borrelia burgdorferi Flagellin B DNA. Although the usually encountered transfection product bundles an entire nonhuman gene within it, this model proposes that shorter inserts into the human genome constitute "junk transfection" because no protein is derived from them. Junk transfections would offer an important new cognitive model for the detection of occult infections as the root causes for the Tauopathies, which are degenerative neurological disorders, including Alzheimer's disease.