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For more than 100 years, Alzheimer's has left neuroscientists. Although they understand that the fatal form of progressive dementia is often characterized by accumulations of malformed proteins in the brain, the causes of these malformations have remained inaccessible. There are several theories, ranging from air pollution and diet to genetics and vascular disease, but none has been confirmed (with the exception of a small portion of the population with a hereditary mutation that has brought them to develop Alzheimer's disease at an early stage). Another traditionally rather marginal theory, but one that is beginning to gain ground, links Alzheimer's to a handful of prevalent viruses.
Last week, Ruth Itzhaki, a retired professor of molecular neurology at the University of Manchester, published a review of new work linking dementia and viruses responsible for herpes. Specifically, these studies have focused on HSV1 and HSV2, which can cause cold sores on the lips and genitals, and on shingles, which causes chickenpox during childhood and shingles later in life.
These three viruses are common but largely benign. Some estimates suggest that almost all adults have been infected with shingles, and that around 80% of people worldwide are infected with HSV1 or HSV2 at some point in their lives. Most people contract these viruses while they are children and temporarily develop visible symptoms like smallpox or sores, but they then remain dormant and therefore do not cause symptoms for the rest of their lives.
In this review, Izhaki highlights three articles that study thousands of patients living in Taiwan (where medical records are available for almost the entire population) and their likelihood of developing dementia. (Alzheimer's disease is the majority of dementia cases, but has not been specifically isolated in these studies.)
Two of these papers compared groups of people diagnosed with herpes zoster to groups of uninfected people. He found a slight increase in the number of cases of dementia in those with herpes zoster.
A third study looked at more than 8,000 people who visited the hospital at least three times a year for the treatment of cold sores (a sign that they had serious cases of HSV1 or HSV2), compared to control group of about 25,000 people. People with cold sores were twice as likely to develop dementia. In addition, among patients with cold sores, those who received antiviral drugs were significantly less likely to develop dementia compared to those who did not have them.
Itzhaki has been studying the link between Alzheimer's disease and herpes viruses for decades. Previous work by his team has shown that, in Petri dishes, HSV1 can cause brain cells to produce toxic proteins such as beta and amyloid proteins, both of which have been specifically associated with Alzheimer's disease. There is another proof of the link: People with Alzheimer's disease who also have a variant of a gene called APOE type 4 have a higher risk of herpes infection. This same variant of APOE has also been documented to increase the risk of Alzheimer's disease in general, although the way it is defined is unclear. Itzhaki believes that in individuals with APOE type 4, the combination of direct damage caused by virus replication and indirect damage resulting from the resulting inflammation is what ultimately leads to Alzheimer's disease.
Immunologist Leslie Norins explains that, whatever the causes of Alzheimer's disease, they may not look like the type of infection we normally think of, such as a cold or a flu, both highly contagious. Instead, it can be something that can be transmitted only after prolonged exposure, or an infection that is benign in most cases, but that becomes fatal in people with certain genetic traits. (Norins in 2017 has created Alzheimer's Germ Quest, an organization that promises $ 1 million to anyone who can prove that Alzheimer's disease is related to any type of infection.)
There was a precedent for thinking that Alzheimer's disease could be contagious. Earlier this year, another study showed that two different strains of herpes virus – HHV 6A and 7 – were present in large numbers in patients who died of Alzheimer's. Other scientists have suspected that bacteria similar to those that cause Lyme, syphilis or lung infections (paywall) may also contribute to the development of the disease years after infection. In addition, previous work has shown that neurosurgeons and spouses of people with Alzheimer's disease have a higher risk of developing the disease than the general population.
Not all scientists are convinced of the Alzheimer's hypothesis. "Dementia is not contagious and should not be considered an infectious disease," said James Pickett, head of research at the Alzheimer Society, in a statement. James Hendrix, Director of Global Science Initiatives at the Alzheimer's Association, told MedScape (free connection required): "We do not have enough direct evidence to even go there."
Norins argues that, based on what we see in epidemiological studies, we could act without even knowing for sure the cause of Alzheimer's disease. For example, since it seems that patients treated with antivirals for HSV1 and HSV2 have a lower risk of developing dementia, says Norins, let's use these antivirals more freely for those with one or the other. other of these viruses.
To prove that Alzheimer's is caused by a viral infection, it should be shown that large populations protected against the herpes virus do not develop brain disease later in life. However, this type of study would require an everyday life, from childhood to death. Even if a team had the resources to conduct such a long-term study today, it would first need to develop a vaccine against some viral strains. Although there is currently a vaccine against shingles, it still does not exist for HSV1 or HSV2, which is paradoxical in part because they are considered relatively benign viruses.
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