Furthermore, just as detected in AD, a tendency toward an accelerated APP amyloidogenic processing/Aβ deposition in the brains from patients with the COVID-19 neurological syndrome is evident when compared to healthy controls and in connection with significant lower amounts of the soluble Amyloid Precursor Protein alpha and beta fragments (sAPPα and sAPPβ) as well as the Aβ40, Aβ42 and Aβ42/Aβ40 ratio in their peripheral CSFs [187]. This evidence concerns the gene APP and Alzheimer disease.