- Scientists believe that amyloid plaque formation may be caused by a virus
- That’s how the brain protects itself because of its antiviral properties
- In theory, vaccination against viruses could reduce amyloid plaque buildup
Dementia is one of the world’s leading killers, burdening millions of families each year.
Much of the focus has been on drugs that remove the protein clumps associated with brain damage or slow the brutal cognitive decline that plagues patients.
But as more research suggests the virus may contribute to Alzheimer’s disease, experts are wondering if vaccines could help stop the disease before it occurs.
Research suggests that the relatively harmless virus that causes cold sores may be involved in the development of this condition.
The relationship between viruses and dementia is nothing new.
Studies have repeatedly shown that people who are vaccinated against other viruses have a lower risk of dementia.
For example, limited evidence suggests that: Flu vaccination reduces risk of developing dementia Herpes zoster vaccine (shingles vaccine) 30% lower risk.
Experts believe Alzheimer’s disease is linked to the accumulation of amyloid beta protein in the brain.
However, there is some uncertainty as to whether plaque build-up is a cause of dementia or a symptom.
There are drugs that treat Alzheimer’s disease by reducing amyloid production. But so far, they haven’t worked well, says Diego Restrepo, a professor of cell and developmental biology at the University of Colorado.
Also, even if drugs remove some of the amyloid plaques, it is difficult to reverse the damage already done to the brain.
In studying amyloid plaques, scientists discovered it had antiviral properties and believe it may be the brain’s way of trying to protect itself from infection.
Maria Nagel, professor of neurology and ophthalmology at the University of Colorado, told DailyMail.com:
“The virus itself can cause the formation of these amyloid aggregates, leading to clinical symptoms of dementia.”
Over time, as we encounter various infections, amyloid plaques build up, preventing brain cells from communicating with each other and starting a cascade of memory problems.
Dr. Nagel said: Even if you have amyloid, it’s too late.
“We believe it is an early risk factor that prevents actual clinical dementia.”
Over time, as we encounter various infections, amyloid plaques build up, preventing brain cells from communicating with each other and starting a cascade of memory problems.
The virus is usually inhaled through the nose or mouth, travels to the nasal cavity, and binds to the tiny roots of the olfactory nerves hanging there.
The virus itself can then attach itself to nerves and cause loss of the sense of smell.
The virus also enters the brain via the olfactory nerve, causing inflammation, another telltale sign of Alzheimer’s disease.
Dr. Trinh, chief medical officer of Irvine Clinical Research and trustee of Alzheimer’s Orange County, told DailyMail.com: .
“Infectious diseases, especially chronic infections with viruses, can usually trigger an inflammatory response through the immune system. Chronic inflammation occurs when the immune system tries to fight the virus.”
“We know that chronic inflammation is bad for the brain, so I think there’s definitely a link between chronic infections, inflammation, and Alzheimer’s disease.”
According to Dr. Nagel, the pathogens most likely to affect the brain and cause cognitive decline in older adults are the varicella zoster virus and herpes simplex virus type 1 (HSV-1), which cause chickenpox.
More than 90% of adults in the United States are infected with HSV-1, and the majority never develop cold sores.
“The reason we suspect these viruses is, in a way, that they’re actually dormant or sleeping in neurons in areas of the head that, when inflamed, have direct access to the nose and brain,” Dr. Nagel told the DailyMail. Told. .com.
Other viruses may be involved. HIV can also replicate and cause changes in the brain, which can cause early dementia in patients, but not necessarily Alzheimer’s disease.
Last year, one in nine Americans over the age of 65 had Alzheimer’s disease, the most common form of dementia.
It’s unclear how many cases a vaccine could prevent, but Andrew Bubak, an assistant professor of neurology at the University of Colorado, said:
“We always see this figure of about a 28-30% reduction in risk after vaccination with a variety of vaccines, not just the shingles vaccine, but also the seasonal flu vaccine. Whether or not it leads to stopping, that’s not how the math works.
Nevertheless, it important Percentage of cases that can be at least delayed, and probably not prevented, but can be delayed.
There are currently no vaccines available against HSV-1, but several are being developed.
Dr. Torin said the idea is that vaccines could be used to prevent people from contracting these infections and prevent amyloid from building up in the body.
He said: “I think [vaccinating against viruses] viable route. Alzheimer’s has multiple pathways, so I don’t think it can be cured. But I think you should do everything you can to close all loops and all different routes.
“Vaccination against the virus is definitely a good way to go, because it’s doable and what we can do now.”
Researchers are still working to identify the exact virus that may have played a role in the brains of people who died of Alzheimer’s disease.
This is because the dementia process can begin years before symptoms develop. So by the time scientists examine the patient’s brain, there are no detectable elements of the previous viral infection, making it difficult to establish a causal link.
Researchers therefore propose that the virus accelerates an already occurring process of cognitive decline.
A University of Colorado study published in the journal last December Neurobiology of Agingfound that, in particular, viruses that damage a patient’s sense of smell can accelerate the onset of Alzheimer’s disease.
Loss of smell is an early sign of disease Up to 90% of people with Alzheimer’s disease.
Researchers looked at six people with Alzheimer’s disease and six without.
The patient has hereditary Alzheimer’s disease and few mutations.
Focusing on the most vulnerable entrance to the brain, the nose, they looked at samples taken from patients’ olfactory bulbs and olfactory tracts (the underside of the brain above the nasal cavity, which is responsible for the sense of smell).
Alzheimer’s patient samples showed gene expression changes indicative of past viral infection in the olfactory bulb and an inflammatory immune response in the olfactory tract.
The samples also contained many proteins that contribute to myelin damage.
Myelin is the protective layer around nerves that allows electrical impulses in the brain to move easily and quickly. When this layer is damaged, parts of the brain cannot speak to each other, leading to overall cognitive decline.
The findings lead researchers to believe that viral infections and the associated inflammation of the olfactory system can prevent the hippocampus in the brain from communicating with the olfactory bulbs, leading to neurodegeneration and ultimately Alzheimer’s disease. became.
One explanation is that viruses such as herpes cause the formation of amyloid masses that are characteristic of Alzheimer’s disease.
Another theory is that when infectious bacteria reach the brain, they can activate immune cells in the brain called microglia. disease progresses.
In most people, the immune system suppresses the virus from primary infection before it has a significant impact on the central nervous system.
