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.