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Is there a link between Herpes and Alzheimer’s disease? - Professor Giovanni B Frisoni comments

Monday 30 May 2016

Neurologist, Professor Giovanni B Frisoni - Professor of Clinical Neuroscience and Head of the Memory Clinic, University Hospital of Geneva and University of Geneva, Geneva, Switzerland; Scientific Director, IRCCS Fatebenefratelli, The National Centre for Alzheimer’s Disease, Brescia, Italy - graduated in 1986 in Medicine from the University of Brescia, and in 1990 specialised in Neurology at the University of Parma. His thesis was published in the journal Stroke.

Since 2013, he has led the Memory Clinic at the University Hospital of Geneva and has a Chair in Clinical Neuroscience at the University of Geneva. In 2013, he was appointed as Scientific Director of the Scientific Institute for Research and Care, IRCCS-FBF. Since 1999, he has also been the head of the LENITEM — Laboratory of Epidemiology Neuroimaging & Telemedicine at the IRCCSFBF, a research facility with a staff of 20 to 25.

Find out more about Prof. Frisoni here:

Following recent media headlines claiming there is a link between Herpes and Alzheimer’s disease, we asked Professor Giovanni B Frisoni - a member of our Expert Advisory Panel – to comment:

Were the headlines right or were they misleading in some way?

The headline is consistent with the content of the original editorial. Indeed, authors suggest a causative role of microbes, including the herpes simplex virus and several bacteria, in the development of Alzheimer’s disease (AD). In summary, the team of scientists states that some biomarkers used for AD diagnosis, such as the deposition of amyloid-β peptide and the presence of abnormal forms of tau protein, may be indicators of an infectious etiology. In detail, the authors hypothesise that some specific microbes reach the brain overcoming the blood-brain barrier, and there remain dormant for years. As the immune system declines, during aging or under stress conditions, viruses and bacteria can undergo reactivation. When it happens, the direct microbes’ action on the cerebral tissue induces inflammation, against which amyloid-β is acted, as authors speculate. For unclear reasons, over time, this defense mechanism becomes dysfunctional and leads to the progressive neuronal loss, typical of AD.

How important is this story/study for furthering dementia research? Should we be excited?

Surely, alterations in the inflammatory and immune system responses are widely observed in AD patients and, nowadays, a growing amount of evidence proposes that inflammation may promote amyloid-β accumulation. For example, recent data suggest that gut microbiota could play a key role in modulating peripheral and central inflammation, contributing to the neuropathological alterations observed in several brain disorders with an inflammatory component. Dysbalance in the gut microbiota, together with a specific and correlated pro-inflammatory pattern, may increase intestinal permeability, thus allowing bacteria to reach blood stream. In this way, this peripheral inflammation could reach the brain.

However, available evidence is still limited and more studies are required.

What might be the impact of this story/study in the scientific community?

This editorial focuses the attention on the role of microbes, probably underestimated. So, it encourages dementia experts to consider the current AD etiopathological theories from a new and different point of view.

Moreover, these new theoretical adaptations could have a strong impact on pharmacological research. To date, we are seeing failure of hundreds of disease-modifying drugs, conceiving to remove deposition of amyloid. If the hypothesis, according to which neuronal inflammation is linked to microbes’ reactivation, is confirmed, new treatments might be quickly available to be tested in randomised clinical trials.

Although exciting, further research is still required to prove the anti-inflammatory role of amyloid-β.

What are the next steps?

Hitherto, only a few studies have demonstrated the antimicrobial activity of amyloid-β against bacteria, viruses and yeasts, and all of them applied in-vitro models. So, first of all, we need to translate the in-vitro results to in-vivo models, such as animal models as well as in human patients, with specific risk factors.

In addition, there are many uncertainties surrounding the findings that should be clarified before advancing with this hypothesis. For example, it will be necessary to investigate how microbes reach the brain and the causes leading to their reactivation. Lastly, it will be important to understand the possible mechanisms that link peripheral and central inflammation, as we know it happens in several brain disorders with an inflammatory component, such as Parkinson’s disease and Multiple Sclerosis.

There is still a long way to go.