Recent work has already hinting at this conjecture, or more properly
it is better to say that the data was conforming to a pathological
vector as yet unidentified. Now we have a prospect. This does means
that an outright cure should be come possible and prevention likelier
still. We needed that.
I think that seeing off most forms of brain disease in the next
decade has now become possible with the exception of impact induced
micro tears. That may be more of a challenge yet we also see the way
there to some degree. Scar has to be removed and adjoining tissue
must be properly rejoined and healed with an injection of stem cells.
All this has to be done through micro veins.
It would be a blessing though if we can narrow Alzheimer's down to a
known virus and this allowed quick diagnostics and useful therapies.
Common Virus Linked
to Alzheimer's Disease, Study Suggests
Anna Azvolinsky
Date: 19 June 2013
Contracting a common
virus called cytomegalovirus (CMV) may contribute to the development
of Alzheimer's disease, a new study of the brains of older adults
suggests.
The study found an
association between patients' immune responses to CMV and signs of
Alzheimer's disease.
However, more studies
are still needed to understand how anactive CMV infection might be
related to this most common form of dementia, said study researcher
Dr. Julie Schneider, of the Rush University Alzheimer's Disease
Center in Chicago.
The study did not show
a cause-and-effect link between CMV and Alzheimer's. It is possible
that other stimulants of inflammation, including other viral
infections, might also lead to the brain changes seen in the study,
which could cause a decline in cognitive function leading to
Alzheimer's disease.
Whether CMV — which
most people in the U.S. have been exposed to — may play a role in
Alzheimer's has been controversial. CMV is transmitted through
contact with bodily fluids, including sexual contact.
In the new study,
Schneider and her colleagues analyzed blood and cerebrospinal fluid
(brain- and spinal-cord fluid) samples from the bodies of people who
were part of an aging-and-dementia study during their lives. All had
passed away, and had mild or probable Alzheimer's disease at the time
of their death. Of the participants, 37 had antibodies against CMV,
and 22 were CMV-negative.
The researchers found
that 80 percent of the patients who were positive for a CMV infection
had high levels of an inflammation marker in their cerebrospinal
fluid, while none of the patients who were negative for the virus had
this marker present.
Such a clear-cut
difference supports the idea that CMV may specifically
cause inflammation related to Alzheimer's, said study researcher
Nell Lurain, professor of immunology at Rush University.
The patients with
higher levels of antibodies against CMV were also more likely to have
brain cells with aggregated tau proteins, called neurofibrillary
tangles that have been connected to Alzheimer's disease.
While most people are
carriers of the CMV virus, generally only those with weakened immune
systems have symptomatic, active CMV infections. The virus may infect
the brain and spinal cord, and has been shown to increase
inflammation. This inflammation, which can occur in the brain, is
thought to contribute to Alzheimer's, and perhaps other diseases that
result in the degeneration of nerve cells.
The herpes simplex
virus (HSV1), another virus that can infect the brain and spinal
cord, has also been linked with Alzheimer's progression. But the new
study did not find a connection between HSV1 and markers of
Alzheimer's disease in patient samples.
The study also showed
no evidence of a link between higher levels of CMV infection and
levels of amyloid-beta — an imperfect marker of Alzheimer's but
still the hallmark of the disease that most researchers consider the
best indicator.
The researchers did
see that infecting human cells in lab dishes with CMV, but not HSV1,
resulted in an increase in amyloid-beta protein.
Ruth Itzhaki,
professor at the University of Manchester in the United Kingdom, said
the laboratory-experiment part of the new study had flaws. Itzhaki,
who studies the causes of Alzheimer's disease, but was not involved
in the new study, said more than 30 studies have linked HSV1 with
Alzheimer's disease.
David Goldeck, who
works on aging and immunology at the University of Tübingen in
Germany, argued that there is little evidence of a direct link
between CMV and Alzheimer's. Studies, including the new one, still
only suggest that CMV can enter the brain and contribute to cognitive
decline. Meanwhile, other studies have found no evidence of even an
indirect relationship — let alone a causal relationship — between
CMV infection and Alzheimer's, Goldeck said.
In other words, the
jury is still out on whether a CMV infection, or the inflammation
caused by such an infection, directly contributes to brain changes
that lead to Alzheimer's.
More than 5 million
Americans are living with Alzheimer's disease, the causes of which
are still unknown. There are no direct ways to prevent the disease,
and no treatments.
If CMV is, indeed,
found to contribute to Alzheimer's disease, vaccines that prevent
infection may be the best approach, Schneider said.
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