Scientists have found that Alzheimer’s disease could be
detected 20 years before the first symptoms appear. Finding could pave the way
for early interventions to stop development of the disease.
Alzheimer's is a progressive neurodegenerative disease that
slowly destroys memory and cognitive skills, and eventually the ability to
carry out the simplest tasks. It is the most common cause of dementia,
accounting for about 60-70% of all dementia cases. Together with other forms of
dementia, Alzheimer’s affects 47.5 million people worldwide. The disease gives
rise to 7.7 million new cases each year.
Read more: Awareness
of memory problems may lessen 2 to 3 years before onset of memory loss or
dementia
Age is one of the risk factors of Alzheimer’s. People over
the age of 70 are at a higher risk of developing Alzheimer’s.
Alzheimer’s has been recently ranked as the third leading
cause of death in the United States. An estimated 5.3 million Americans have
Alzheimer's, of whom 5.1 million are aged 65 and older.
Around 850,000 people in the UK are affected by the disease.
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It is a well-known fact that death of brain cells leads to
the memory loss and behavioral changes that are associated with Alzheimer’s.
Scientists also know that brain cell death in Alzheimer's is
related to a combination of inflammatory brain changes, described by German
neuropathologist Alois Alzheimer as the 2 hallmarks of the disease. The 2
hallmarks are – tau tangles developing inside neurons, caused by a build-up of
tau protein, and amyloid plaques, developing between brain cells, caused by an
accumulation of protein fragments called beta-amyloid. Scientists believe these
plaques and tangles weaken communication between nerve cells, which in turn
harms the processes that helps brain cells to survive.
However, scientists are not sure about exactly when plaques,
tangles and inflammatory changes in the brain starts to take place – a fact
that has been a mystery to the scientists all along. Now, principal researcher Professor
Agneta Nordberg, of the Karolinska Institutet in Sweden, and colleagues believe
their latest study has unraveled that mystery. [Read more Diabetes
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For the study, researchers scanned brains of more than 50
participants using positron emission tomography (PET). Some of these adults
were at higher risk for Alzheimer's due to having relatives with gene mutations
related to the disease, while some patients had non-inherited,
"sporadic" Alzheimer's.
Prior to PET scans, all the participants were injected with
3 radioactive tracer molecules – PIB, Deprenyl and FDG. This enabled the
researchers to track plaque levels and inflammation related to activation of
astrocytes – the most common support cell in the brain.
In addition, glucose metabolism in participants’ brains was
also measured, which provided insight into brain cell function. [এই ৭টি খাবার আপনাকে ওজন কমাতে সাহায্য করবে]
The researchers were able to identify plaques and
inflammatory changes nearly 20 years prior to the estimated onset of memory
problems among participants with Alzheimer’s-related gene mutations.
Researchers precisely found that astrocyte activation
reaches its peak when plaques begin to accumulate in the brain.
Professor Nordberg explained:
“Inflammatory changes in the form of higher levels of brain
astrocytes are thought to be a very early indicator of disease onset,”
“The accumulation of amyloid plaque and the increase in number of astrocytes therefore display opposing patterns along the timeline."
According to the researchers, brain cell function starts to decline approximately 7 years before the onset of Alzheimer’s disease symptoms.
Among people who did not possess Alzheimer's-related gene mutations, the team did not identify any such brain pathology. [Read more Scientists identify vital early warning of Alzheimer’s that could lead to improved treatment]
“Our research aims at understanding especially the earliest phases of the disease. Clinical trials aimed at clearing amyloid plaques have not yet succeeded at curing the disease, and therefore it is necessary to find new therapeutic targets,” said first author of the study Dr Elena Rodriguez-Vieitez.
The researchers believe that astrocytes could be a possible drug target for the condition. Reducing astrocyte activation early on could stop the disease from developing or change its course of progression.
The research was published in the journal Brain.
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ReplyDeleteAbout two years ago, when I was 56, I started feeling foggy and had occasional memory lapses. My wife, Mary, started to notice it, too, but I also have hearing issues so she believed that was the problem. My memory problems worsened very gradually over the years, and we lived with it, compensating as required. I became less social. After some months to the point where we couldn’t keep making excuses or ignoring it. I had gone from doing our grocery shopping without a list to going with a list, to having the list but not buying what was on it.
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