Newswise — A new theory by Leslie Norins, MD, PhD links Down Syndrome of children to an infectious organism which later incites Alzheimer’s disease in adults who carry it. His scientific paper is published in the peer-reviewed medical journal, Medical Hypotheses (DOI.org/10.1016/j.mehy.2021.110745).
Dr. Norins is the founder and chief executive of Alzheimer’s Germ Quest, a Florida-based nonprofit group which for five years has urged increased research on many hints that microbiological agents play a role in triggering or accelerating the brain degenerative process of Alzheimer’s.
An unexpected and tragic clue appeared in recent years, when young adults with Down syndrome developed Alzheimer’s disease faster and at a greater frequency than normal youths their age. But the cause is a mystery.
However, to Dr. Norins, who has a background in infectious diseases, this pattern resembled an established behavior of certain infectious agents. The best- known example is provided by the virus, herpes zoster. Almost every child (in pre-vaccination days) became infected with its pediatric manifestation, chickenpox, and suffered through the virus’s classic rash, which then cleared spontaneously in most cases.
However, though the rash went away, the virus itself had not gone from the body. Instead, it retreated into “hiding” silently in the patient’s nerves. Decades later, the virus reactivated in a proportion of these individuals, and evidenced itself as the adult disease, shingles.
Dr. Norins feels a similar phenomenon is displaying itself with the appearance of Down syndrome in a certain number of children, followed decades later by the development of Alzheimer’s disease in many of them.
Only the numbers were reversed from the chickenpox example, Pre-vaccination, most children got chickenpox; few children develop Down syndrome. Alzheimer’s disease is fairly common in seniors, while there are fewer cases of shingles in that group.
Dr. Norins knows he will have to cope with the pediatricians and parents of Down syndrome children who assert that the “cause” of Down syndrome is already known; it’s an extra “X” chromosome found in all or most cells of the child’s body.
“Poppycock and not proven” replies Dr. Norins. It is quite true that there is an extra “X” chromosome in addition to the usual two, i.e.“triple X”) in children with Down syndrome. Indeed, the presence of the extra ”X” is an invaluable cellular marker for laboratory confirmation of the Down diagnosis.
However, he points out that the root cause of that extra chromosome has not yet been found. He says that the oft-cited explanation “mutation” is a fancy term to camouflage the fact scientists don’t really know what has happened and why. Nor is it known how that extra X chromosome causes or relates to the signs and symptoms of Down syndrome. “Though it’s appealing to focus on the extra “X” chromosome, its appearance may have nothing more to do with the development of Down than the measles rash has for that disease,
Dr. Norins feels basic research on Down syndrome is at a dead-end, and new hypotheses should be welcomed and funded. In contrast, Alzheimer’s research monies have never been more plentiful. Thus, the setting is ideal for experts in both illnesses to collaborate to illuminate how and why so many brain disease features are shared, and whether various antibiotics can prevent one or both.
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