More Evidence Against Herpesvirus Infection as a Meaningful Contribution to Alzheimer's Disease
There is a continuing debate over the role of persistent viral infection in the development of neurodegenerative disease. It seems plausible that such infection could increase chronic inflammation, and inflammation in brain tissue is a hallmark of neurodegenerative conditions. Just because the mechanism exists doesn't mean it is the primary, or even important, component of the disease process however. This is ever the challenge in complex age-related diseases, determining which of the many mechanisms in play are in fact those that primarily cause the condition. So there is a back and forth of epidemiological studies in recent years, attempting to settle the role of viral infection, particularly by herpesviruses, in neurodegenerative conditions such as Alzheimer's disease. At present neither side has a convincing advantage in weight of evidence, which suggests that there may be a more complex set of interactions going on under the hood.
The causes of Alzheimer's disease are not fully understood. There are clear associations with the accumulation of abnormal proteins in the brain, beta-amyloid and tau. There is also clear evidence of neuroinflammation, and there appears to be evidence of immune dysfunction in microglia, a type of immune cell found within the brain. One recurring theory is that herpes viruses, which are responsible for cold sores, genital herpes and other infections, might cause Alzheimer's disease.
However, researchers studying 1,009 participants in the Baltimore Longitudinal Study of Aging (BLSA) have found that while symptomatic herpes viruses were associated with neurological and cognitive symptoms, but there was no evidence to support the long-held theory that they are linked to Alzheimer's disease. The participants who were diagnosed with herpes had higher cognitive scores at the beginning of their participation but demonstrated greater longitudinal decreases in attention performance. The study did not find a link between herpes virus infection and the volume of total brain or gray matter, or in areas associated with Alzheimer's disease. Of the total participants, 119 had a record of symptomatic herpes infection. These infections were linked to longitudinal decreases in white matter volume, particularly in the temporal lobe. Being treated with antivirals slowed the declines in occipital white matter.