Alzheimer’s disease is a degenerative brain disease that causes progressive dementia. Getty Image Bank
Alzheimer’s disease (Alzheimer’s disease) is known as a degenerative brain disease caused by the accumulation of amyloid beta protein in the brain. It is said that a specific protein that accumulates in the brain causes dementia. However, recently, evidence supporting the ‘contagion theory’ that viral or microbial infection can cause Alzheimer’s disease has been presented one after another, attracting attention.
According to the British daily Guardian on the 19th (local time), Davanjer Divanand, a professor at Columbia University Medical School in the United States, argued that the herpes virus can cause Alzheimer’s disease. “We have been studying the connection between the herpes virus and Alzheimer’s disease for 35 years,” he said. “There is indirect evidence that there is a link between the two.”
The fact that people with herpes are at high risk of developing Alzheimer’s disease has been proven through a series of studies. Herpes is a viral infection that causes large and small blisters on the skin or mucous membranes.
In 2020, a research team at Tufts University in the US experimentally proved that the herpes virus forms amyloid beta and published it in the international journal Science Advances. In August of last year, a study showed that the shingles virus stimulates the dormant herpes virus to cause Alzheimer’s disease. “In 2018, a Taiwanese research team found that when people with herpes received antiviral treatment, the risk of dementia was reduced by one in nine,” said Professor Divanand.
For a long time, the ‘amyloid beta’ protein has been pointed out as the cause of Alzheimer’s disease. When plaques (clumps) of amyloid beta are formed, they cause inflammation inside the brain and kill brain cells. Depression, lack of exercise, and eating habits are known to increase the risk of developing Alzheimer’s disease, but the exact cause is unknown.
The so-called ‘infectious theory’ that a virus causes Alzheimer’s disease claims that a virus may be the reason for the formation of amyloid beta plaques. Researchers who make this claim, including Professor Divanand, explain that this is possible because viruses and microorganisms have an incubation period in the host’s body. It is said that the virus lies dormant in the body in an inactive state and becomes active after aging and problems with the immune system, causing disease.
There are also claims that microbes cause neurodegeneration, leading to Alzheimer’s disease. Chlamydia pneumoniae, which causes lung disease, and Borrelia burgdorferi, which is known to cause Lyme disease, can play a trigger role in causing Alzheimer’s disease.
The ‘contagion theory’ has been thought to be at the opposite end of the amyloid theory, but recently there are claims that the two theories may be complementary. The lack of effectiveness of therapies targeting amyloid beta raises the question that amyloid beta may not be the root cause. Recanemab, the first Alzheimer’s disease treatment approved by the US Food and Drug Administration (FDA) last year, also only slowed the progression of Alzheimer’s disease rather than curing it.
Researchers advocating the infection theory explain that amyloid beta, which has been thought of as the ‘villain’ that causes Alzheimer’s disease, is actually the brain’s defense mechanism to fight external infectious agents. Rudolph Tanzi, a professor at Harvard Medical School in the US, discovered 15 years ago that amyloid has antibacterial properties that protect the brain from invading infectious agents. “When microbes invade the body, amyloid beta binds to them,” he said.
Regarding Alzheimer’s disease, Professor Tanji said, “Under normal circumstances, immune cells remove plaques formed by invading infectious agents.
If infection is the main cause of Alzheimer’s disease, the direction of development of current therapies targeting amyloid beta needs to change. “If a viral infection is driving the plaque formation, then the cause may have to be sought 30 years before the onset of Alzheimer’s symptoms,” Tanzi said.
If it is revealed that a virus or microorganism is the cause of even some patients with Alzheimer’s disease, a much more practical approach will be possible. They may recommend that all people infected with the herpes virus use antiviral medications or be vaccinated against the virus that causes shingles. In August of last year, a research team at Oxford University in England announced the results of a study that vaccinated against shingles reduces the risk of developing Alzheimer’s disease.
Divanand is pursuing clinical trials to see if herpes antivirals can slow disease progression in patients with early-stage Alzheimer’s disease. It plans to complete clinical trials by early 2024.
