Herpes can cause Alzheimer's disease?

Herpes can cause Alzheimer's disease?

November 13, 2018 Source: Ministry of Science and Technology

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What causes Alzheimer's disease? Professor Ruth Itzhaki of the University of Oxford in the United Kingdom said that the answer may be below our nose. Evidence from a recently published paper on "Lifetime Throughs" suggests that the herpes virus that causes "cold sores" may be the cause of Alzheimer's disease. New research data suggests that antiviral drugs can significantly reduce the risk of Alzheimer's disease in patients with severe herpes infections. This review, published in Frontiers in Ageing Neuroscience, suggests a simple and effective way to prevent Alzheimer's disease.

The herpes virus is a frightening "continuous gift." Herpes virus is present in both our neurons and immune cells throughout our lives. When we are stressed by stress or illness, they reactivate and produce blisters. Most people are infected with herpes simplex virus type I (HSV1) in old age. But what happens to infected neurons in our brain during the reactivation of the virus?

Professor Itzhaki spent 25 years studying the association between HSV1 and Alzheimer's disease. She said: "More than 50% of Alzheimer's disease is caused by HSV1."

HSV1 is better known as the cause of cold sores. Past studies by Itzhaki have shown that APOE-ε4 carriers have a higher proportion of cold sores. APOE-ε4 is a genetic variant that increases the risk of Alzheimer's disease.

Professor Itzhaki said: "Our theory is that in the APOE-ε4 gene carrier, herpes virus reactivation occurs more frequently and more harmful in HSV1-infected brain cells, so the cumulative damage ultimately leads to Alzheimer's The development of the disease."

Few countries collect demographic data to test the theory, for example, to determine whether antiviral therapy can reduce the risk of dementia. However, Taiwanese researchers have just completed this task. In Taiwan, 99.9% of the population is covered by the National Health Insurance Research Database. Researchers have fully exploited the database to find information about microbial infections and diseases.

In 2017-2018, three studies using the Taiwan database to study Alzheimer's disease (Alzheimer's disease is the main cause) and to treat patients with signs of HSV and ZVZ (herpes zoster virus) infection were published. The results of the study provide evidence that patients infected with HSV are at a much higher risk of Alzheimer's disease, and anti-viral antiviral therapy can significantly reduce the number of patients with severe infections with HSV1.

A related mechanism discovered by Itzhaki in past research supports these epidemiological findings. They found that HSV1 causes protein deposition, a hallmark of Alzheimer's disease: the "plaque" between neurons and the tangles of the parts. "The viral DNA is located in the plaque of the brain tissue of patients with Alzheimer's disease," she said. "The major proteins in plaques and tangles are also accumulated in cell cultures infected with HSV1, and antiviral drugs can prevent this. A process."

Itzhaki admits: "We should emphasize that these Taiwanese studies only apply to severe HSV1 (or VZV) infections, which is very rare. Ideally, we should study the incidence of dementia in people with mild HSV1 infection, including Cold sores or mild genital herpes, but these data are difficult to record."

Although further research is needed to confirm and define the causal relationship between HSV1 infection and Alzheimer's disease, Itzhaki is enthusiastic about the treatment prospects of the disease. "Considering more than 150 studies that strongly demonstrate the role of HSV1 in Alzheimer's disease, these findings in Taiwan strongly confirm that anti-herpes virus therapy (safe and well tolerated) can treat Alzheim, she said: They also encourage the development of the HSV1 vaccine, which may be a very effective treatment."

The study echoes the worldwide trend toward the use of human papillomavirus (HPV) vaccines to prevent cervical cancer, a viral-associated disease whose pathogenesis is similar to that in the study.

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