A new study suggests that a common herpes-causing virus, human cytomegalovirus (HCMV), may play a significant role in the development of Alzheimer’s disease. The findings open the possibility of exploring antiviral drugs for treating or preventing this subtype of the neurodegenerative disorder.
Published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, the research highlights how HCMV, known to infect the gut, could travel to the brain via the vagus nerve. Once in the brain, the virus may disrupt the immune system, triggering changes in brain cells linked to Alzheimer’s, such as amyloid plaques and tau tangles.
“HCMV may represent a biologically distinct subtype of Alzheimer’s that affects up to 45% of patients with the disease,” said Ben Readhead, research associate professor at Arizona State University and the study’s lead author.
The herpes virus, commonly transmitted through bodily fluids, remains dormant in most individuals. However, in some cases, the study found it could persist in the gut, becoming active and traveling to the brain. The researchers observed the virus within the vagus nerve and found immune responses specifically targeting HCMV in the spinal fluid, brain tissue, and intestines of Alzheimer’s patients.
Notably, the study identified immune cells in the brain, called microglia, reacting to the virus by activating a gene called CD83. This gene appears to drive the biological changes associated with Alzheimer’s.
The findings align with previous post-mortem analyses, which showed an increased presence of CD83(+) microglia in the brains of Alzheimer’s patients. The researchers believe this discovery could pave the way for new therapeutic approaches targeting viral activity and immune responses in Alzheimer’s patients.
As reported by economictimes, These insights mark a significant step in understanding the potential viral and immune system links to Alzheimer’s and could provide a basis for innovative treatment strategies.