Alzheimer’s disease is a neurologic disorder that is characterized by progressive brain atrophy (shrinking of the brain) and the death of brain cells. People who are aged 65 and above are more prone to this disorder. The early signs of this disorder include not being able to remember recent events or conversations. Progressively, the person develops severe memory impairment and may not be able to carry out their daily tasks.
Alzheimer’s disease
Read Also: Alzheimer’s Controversy: Have Scientists Gotten It All Wrong?
The cause of this neurologic disorder is still unknown, and a cure is yet to be discovered. Recently, a team of scientists found out that there’s a link between the two common dormant viruses – VZV and HSV – that lie in nerve cells and Alzheimer’s disease development. This discovery may be the breakthrough to finally developing a cure for this Alzheimer’s disease.
VZV & HSV
According to the World Health Organization, approximately 3.7 billion people who are less than age 50 are infected with HSV-1 (one of the variants of herpes simplex virus, HSV, and the causative agent of oral herpes) which lies dormant in their nerve cells.
When HSV-1 is activated, the result is an inflammation in nerves and skin, causing open sores and blisters accompanied by pain. Most carriers of this virus, that is, 1 in 2 Americans (as stated by the Center for Disease Control), will experience very mild to no symptoms before the virus becomes latent.
Many adults host latent varicella zoster virus (VZV) in their nervous system as a result of chickenpox infection during their childhood, and it can become reactivated causing shingles. People who have shingles usually have blisters and nodules on their skin which lasts for weeks or even months. The blisters and nodules form a band-like pattern, and it is often accompanied by pain.
The common viruses vs Alzheimer’s disease
It has been known that a correlation exists between HSV-1, and Alzheimer’s disease, as influenced by the latent VZV. However, the sequence of events set in motion by VZV that leads to the development of the disease has remained unknown.
Read Also: Alzheimer’s Disease: MIT Study Shows How Tau Protein Tangles Form
Recently, a team of researchers at Tufts University and the University of Oxford uncovered this in their study about the viruses, using a three-dimensional brain model which they built from human tissue culture – the brain-like environment. It is a small donut-shaped sponge that is 6 millimeters wide and made of silk protein and collagen. They filled the sponges with extracts of neural stem cells that grow into functional neurons which transfer signals to each other in a network, in the same way, that they work in the brain. Some of the stem cells develop into glial cells that nourish the neurons to keep them alive and function properly.
The researchers then introduced VZV into the environment and noted their observations. They found that the presence of VZV alone did not cause the formation of the proteins – tau and beta-amyloid – that signal Alzheimer’s disease. These proteins are the building blocks of the tangled mess of fibers and plaques that are found in the brain of patients who have the disease. However, when they injected strains of VZV into the neurons which already have existing inactive HSV-1, they observed an immediate awakening of HSV-1 which resulted in a significant increase in tau and beta-amyloid proteins. This caused the neurons to slow down in their function of signal transfer.
The team noted that brain samples that are infected with VZV began to produce higher levels of cytokines, which are proteins that are involved in triggering inflammatory responses. VZV leads to inflammation in the brain, possibly causing the activation of inactive HSV and more inflammation, leading to the production of plaques, and increased neuron dysfunction. The repetition of this cycle explains the progression of Alzheimer’s disease.
Clinical significance
This study has a high impact on the medical world, especially on the older population. Discovering the key factor behind the development of Alzheimer’s disease in older people will go a long way to preventing it. Vaccines for VZV, which prevent chickenpox and shingles, have been shown to lower the risk of the disease. It is also possible that it can help to reduce the vicious cycle that causes the disorder.
Conclusion
In conclusion, VZV leads to the activation of the dormant HSV-1, leading to inflammation and an increase in Alzheimer’s signal proteins that cause dysfunction of nerve cells. This, in turn, leads to reduced cognitive functions in the affected patient.
Read Also: University of Cambridge Researchers Shed More Light on How Alzheimer’s Disease Develops in the Brain
References
Alzheimer’s disease is a neurologic disorder that is characterized by progressive brain atrophy (shrinking of the brain) and the death of brain cells. People who are aged 65 and above are more prone to this disorder. The early signs of this disorder include not being able to remember recent events or conversations. Progressively, the person develops severe memory impairment and may not be able to carry out their daily tasks.
Alzheimer’s disease
Read Also: Alzheimer’s Controversy: Have Scientists Gotten It All Wrong?
The cause of this neurologic disorder is still unknown, and a cure is yet to be discovered. Recently, a team of scientists found out that there’s a link between the two common dormant viruses – VZV and HSV – that lie in nerve cells and Alzheimer’s disease development. This discovery may be the breakthrough to finally developing a cure for this Alzheimer’s disease.
VZV & HSV
According to the World Health Organization, approximately 3.7 billion people who are less than age 50 are infected with HSV-1 (one of the variants of herpes simplex virus, HSV, and the causative agent of oral herpes) which lies dormant in their nerve cells.
When HSV-1 is activated, the result is an inflammation in nerves and skin, causing open sores and blisters accompanied by pain. Most carriers of this virus, that is, 1 in 2 Americans (as stated by the Center for Disease Control), will experience very mild to no symptoms before the virus becomes latent.
Many adults host latent varicella zoster virus (VZV) in their nervous system as a result of chickenpox infection during their childhood, and it can become reactivated causing shingles. People who have shingles usually have blisters and nodules on their skin which lasts for weeks or even months. The blisters and nodules form a band-like pattern, and it is often accompanied by pain.
The common viruses vs Alzheimer’s disease
It has been known that a correlation exists between HSV-1, and Alzheimer’s disease, as influenced by the latent VZV. However, the sequence of events set in motion by VZV that leads to the development of the disease has remained unknown.
Read Also: Alzheimer’s Disease: MIT Study Shows How Tau Protein Tangles Form
Recently, a team of researchers at Tufts University and the University of Oxford uncovered this in their study about the viruses, using a three-dimensional brain model which they built from human tissue culture – the brain-like environment. It is a small donut-shaped sponge that is 6 millimeters wide and made of silk protein and collagen. They filled the sponges with extracts of neural stem cells that grow into functional neurons which transfer signals to each other in a network, in the same way, that they work in the brain. Some of the stem cells develop into glial cells that nourish the neurons to keep them alive and function properly.
The researchers then introduced VZV into the environment and noted their observations. They found that the presence of VZV alone did not cause the formation of the proteins – tau and beta-amyloid – that signal Alzheimer’s disease. These proteins are the building blocks of the tangled mess of fibers and plaques that are found in the brain of patients who have the disease. However, when they injected strains of VZV into the neurons which already have existing inactive HSV-1, they observed an immediate awakening of HSV-1 which resulted in a significant increase in tau and beta-amyloid proteins. This caused the neurons to slow down in their function of signal transfer.
The team noted that brain samples that are infected with VZV began to produce higher levels of cytokines, which are proteins that are involved in triggering inflammatory responses. VZV leads to inflammation in the brain, possibly causing the activation of inactive HSV and more inflammation, leading to the production of plaques, and increased neuron dysfunction. The repetition of this cycle explains the progression of Alzheimer’s disease.
Clinical significance
This study has a high impact on the medical world, especially on the older population. Discovering the key factor behind the development of Alzheimer’s disease in older people will go a long way to preventing it. Vaccines for VZV, which prevent chickenpox and shingles, have been shown to lower the risk of the disease. It is also possible that it can help to reduce the vicious cycle that causes the disorder.
Conclusion
In conclusion, VZV leads to the activation of the dormant HSV-1, leading to inflammation and an increase in Alzheimer’s signal proteins that cause dysfunction of nerve cells. This, in turn, leads to reduced cognitive functions in the affected patient.
Read Also: University of Cambridge Researchers Shed More Light on How Alzheimer’s Disease Develops in the Brain
