Could anti-herpes simplex virus 1 medication lead to slowing down Alzheimer’s development in the brain?
Neuro-degenerative diseases are often some of the most challenging conditions to handle, luckily for patients suffering from such conditions one of our medical second opinion providers, Massachusetts General Hospital (MGH) is leading the path to ease these patients’ lives. Rudolph Tanzi, Ph.D. and Robert Moir, Ph.D. at MGH are in the process of researching and developing a treatment for patients with the Nero-degenerative disease, Alzheimer’s, using an approach you would probably never guess. Their big idea for Alzheimer’s treatment is to use anti-herpes simplex virus 1 medications to slow the onset of dementia in patients.
One may wonder why doctors would be interested in how an anti-herpes simplex virus 1 medication could be influential in decreasing the progression of Alzheimer’s. Well to begin, you have to understand the role of amyloid-β (Aβ) plays in the brain. Amyloid-β (Aβ) is a naturally accruing protein that everyone has, but when this protein clumps together it forms plaques, which collect between neurons interfering with normal cell function. The resulting plaque buildup ultimately leads to the symptoms of Alzheimer’s.
Though Alzheimer’s and herpes are never brought up in the same conversation, it is crucial to understand that the herpes simplex virus 1 is the virus most commonly linked to Alzheimer’s. The herpes virus is so closely linked to Alzheimer’s that a recent study concluded that over the last 16 years 33,000 patients with herpes simplex virus 1 increased their risk for Alzheimer’s 2.5 fold. The herpes virus is estimated to be found in most everyone. It is with age that the virus becomes dangerous in relation to Alzheimer’s. The virus, which can lay dormant for years, becomes a risk factor as you age because immunity and blood-brain barriers decline allowing the virus to travel with more ease to and from the peripheral nervous system to the central nervous system, which will eventually infect the brain. Next the virus replicates in the brain resulting in insoluble amyloid-β (Aβ) plaque buildup. The high plaque levels caused by the increased amyloid-β (Aβ) increases neuro-inflammation, resulting in widespread neuron death and eventually dementia.
Though both these conditions are not talked about together often, they play off of each other. Having a better understanding of the relationship between the two conditions has resulted in the development of using anti-herpes medications to slow the onset of dementia in patients with herpes-infected brains.
If you have been diagnosed with either condition and would like to receive a medical second opinion, contact WorldCare today.