Cold sores and chickenpox viruses may be linked to dementia,a growing body of research suggests.
Coudl those common viruses we all know-cold sores from herpes simplex virus type 1 (HSV-1) and chickenpox/shingles from varicella zoster virus (VZV)-be quietly contributing to dementia, including Alzheimer’s disease (AD)? What was once a fringe idea is now gaining serious scientific traction, with an increasing amount of evidence pointing to these herpes viruses as meaningful players in neurodegenerative diseases.
“There is now quite a lot of evidence obtained by a variety of methods which suggests that this virus is really a major factor in Alzheimer’s disease.And the weight of the evidence supports a causal role,” Ruth Itzhaki, MSc, PhD, a visiting professor at The Oxford Institute of population Aging in Oxford, england, told us.Itzhaki, a pioneer in investigating this link, has dedicated much of her career to exploring the herpes-dementia connection.
These pathogens might be “under-recognized drivers of neurodegeneration,” explains Shaheen Lakhan, MD, PhD, a neurologist and researcher based in Miami. “They can hide in the nervous system and reactivate later in life, each flare-up potentially inflicting cumulative damage that accelerates cognitive decline.”
Decades ago, a crucial clue emerged when itzhaki and her colleagues discovered HSV-1 DNA in the brains of AD patients. This was notably notable in individuals carrying the apolipoprotein E epsilon 4 (APOE ε4) gene, a known genetic risk factor for Alzheimer’s.”The virus and the gene might potentially be working in tandem-a synergy where a latent viral infection ‘flips the switch’ on a genetic vulnerability,” Lakhan added.
Not All Herpes Viruses are Created Equal in Dementia Risk
While the evidence strongly points to certain herpes viruses, not all of them are implicated in dementia risk. HSV-1 and VZV have shown more consistent links to increased dementia risk, including Alzheimer’s.Some studies hint at a possible association with HSV-2 (genital herpes), but the evidence is less conclusive then for HSV-1 and VZV.
Other herpes viruses, like cytomegalovirus, haven’t demonstrated a strong or consistent association with elevated dementia risk in most research. Interestingly, individuals infected with both HSV-1 and VZV may face an even higher, compounded risk. One study found that co-infected patients had a 1.57 times higher risk of developing dementia, compared to a 1.38 risk for HSV-1 alone and 1.41 for VZV alone.
Itzhaki elaborates on the biologically plausible mechanisms. Herpes viruses can ignite chronic inflammation in the brain, a key factor in neurodegeneration. HSV-1, specifically, may promote the formation of amyloid plaques and influence tau phosphorylation-hallmarks of AD. Reactivation of dormant HSV-1 in the brain, frequently enough triggered by brain injury or even cumulative general infections, appears to drive these pathological changes.
“The notion that a virus many of us carry could be stoking neurodegeneration is provocative, but the science behind it is becoming increasingly arduous to ignore. The past few years have delivered especially compelling data to support this viral link,” Lakhan stated.
Can Antivirals and Vaccines offer protection?
Intriguing research suggests that antiviral medications and vaccines might play a role in dementia prevention. Currently, Lakhan advises against daily antiviral prescriptions solely for dementia prevention outside of clinical trials. however, for those with frequent herpes reactivations or who carry the APOE ε4 gene with a strong family history, he maintains a low threshold for treatment and emphasizes counseling on viral prevention.
itzhaki mentioned that some surveys suggest antivirals might offer dementia protection. For individuals infected with HSV who also have genetic risk factors, taking antivirals in late middle age, when the immune system can weaken, could be considered.
“The bottom line for practitioners is clear-encourage shingles vaccination, stay vigilant against chronic herpes infections, and consider that maintaining viral suppression might become part of our toolkit for preserving brain health,” Lakhan concluded.
