A new commentary by
scientists at the Universities of Manchester and Edinburgh on a study by
Taiwanese epidemiologists supports the viability of a potential way to reduce
the risk of Alzheimer's disease.
When the Taiwanese
authors looked at subjects who suffered severe herpes infection
and who were treated aggressively with antiviral drugs, the relative risk of
dementia was reduced by a factor of 10.
Manchester's Professor
Ruth Itzhaki and Edinburgh's Professor Richard Lathe say the paper, by Tzeng et
al. and published in Neurotherapeutics in February 2018, also shows
that herpes simplex virus type 1 (HSV1)
leads to an increased risk of developing the disease.
"This article and
two others by different research groups in Taiwan provide the first population
evidence for a causal link between herpes virus infection and Alzheimer's
disease, a hugely important finding," said Professor Itzhaki.
They publish a commentary
in the Journal of Alzheimer's Disease on the three articles, arguing
that they provide the strongest evidence yet for a causal link between herpes infection
and Alzheimer's disease, backing 30 years of research by Professor Itzhaki.
Professor Itzhaki said:
"I believe we are the first to realise the implications of these striking
data on this devastating condition which principally affects the elderly. No
effective treatments are yet available.
"Almost 30 million
people worldwide suffer from it and sadly, this figure will rise as longevity
increases.
"But we believe that
these safe and easily available antivirals may have a strong part to play in
combating the disease in these patients.
"It also raises the
future possibility of preventing the disease by vaccination
against the virus in infancy.
"Successful
treatment by a specific drug, or successful vaccination against the putative
microbe, are the only ways to prove that a microbe is the cause of a non-
infectious human disease."
Most Alzheimer's disease
researchers investigate its main characteristics -- amyloid plaques and
neurofibrillary tangles; however, despite the vast amount of research, the
causes of their formation are unknown.
HSV1
infects most humans in youth or later and remains lifelong in the body in
dormant form within the peripheral nervous system.
From time to time the
virus becomes activated and, in some people, it then causes visible damage in
the form of cold sores.
The Taiwanese study
identified 8,362 subjects aged 50 or more during the period January to December
2000 who were newly diagnosed with severe HSV
infection.
The study group was
compared to a control group of 25,086 people with no evidence of HSV infection.
The authors then
monitored the development of dementia in these individuals over a follow-up
period of 10 years between 2001 and 2010.
The risk of developing
dementia in the HSV group was increased by a factor of 2.542. But, when the
authors compared those among the HSV cohort who were treated with antiviral
therapy versus those who did not receive it, there was a dramatic tenfold
reduction in the later incidence of dementia over 10 years.
Professor Richard Lathe
added: "Not only is the magnitude of the antiviral effect remarkable, but
also the fact that -- despite the relatively brief duration and the timing of
treatment -- in most patients severely affected by HSV1 it appeared to prevent
the long-term damage in brain that results in Alzheimer's.
Professor Itzhaki said:
"It was as long ago as 1991 when we discovered that, in many elderly
people infected with HSV1, the virus is present also in the brain, and then in
1997 that it confers a strong risk of Alzheimer's disease in the brain of
people who have a specific genetic factor.
"In 2009, we went on
to show that HSV DNA is inside amyloid plaques in Alzheimer's patients' brains.
"We suggested that
the virus in brain is reactivated by certain events such as stress,
immunosuppression, and infection/inflammation elsewhere.
"So we believe the
cycle of HSV1
reactivation in the brain eventually causes Alzheimer's in at least some patients."
