Is Alzheimer’s disease caused by a viral infection?

Yesterday I blogged about the importance of olfactory impairment in the early stages of neurodegenerative diseases, such as Alzheimer’s.  Today I came across a paper on the role of microbes in Alzheimer’s disease (AD) that dovetails so neatly with yesterday’s post that I just have to comment.  (This is perhaps a little more technical than yesterday’s post, but if AD is important to you, please persevere.)

The paper is an editorial that was published in the Journal of Alzheimer’s Disease in April 2016 and is co-authored by many of the luminaries in the field.  They point to multiple studies implicating microbes, such as herpes simplex virus type 1 (HSV-1), Chlamydia pneumoniae, and several types of spirochaete, in the aetiology of AD.

Now, it is the case that the characteristic neuropathology of AD begins in the lateral entorhinal cortex, which is precisely where the olfactory nerves terminate.  Just coincidence?  Hardly!  The olfactory nerves are a portal of entry for viruses into the brain.  The authors suggest that the accumulation of amyloid-β (Aβ) and tau in entorhinal cortex, is an indication of the infectious inflammatory aetiology of AD.  (Aβ and tau are the primary proteins associated with AD pathology.)

Viral infections can be dormant for years, for example, as frequently occurs with HSV-1.  Stress, or immunosuppression associated with ageing, can reactivate a viral infection.  So, it is interesting that the authors observe that in the brains of AD patients, viral signatures such as HSV-1 DNA, co-localise with Aβ and tau pathology.  Furthermore, antivirals like acyclovir, block HSV-1 induced Aβ and tau pathology.  Wow!

The authors point out that between 2002 and 2012, there were 413 failed trials of potential AD treatments.  They suggest that we have been looking in the wrong place and that if we instead now focus on the role of microbials, we may get somewhere with the treatment of AD pathology.

No doubt their opinion will get up the nose of those who maintain that a viral vector in AD is “controversial.”  Inevitably, reality will turn out to be more nuanced than the information presented here, but it is time to take a viral aetiology in AD seriously; it is no longer a controversial idea.