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Alzheimer's disease is the most common form of dementia, accounting for around 60-80% of all cases. Around 5.3 million people in the US have Alzheimer's, of whom 5.1 million are aged 65 and older.

Researchers know Alzheimer's development is related to death of brain cells, or neurons, which leads to the memory loss and behavioral changes that are associated with the disease.

Furthermore, it is believed that brain cell death in Alzheimer's is related to a combination of inflammatory brain changes, tangles that develop inside neurons (caused by a build-up of tau protein), and the development of plaques between brain cells (caused by an accumulation of protein fragments called beta-amyloid).

Researchers believe that these plaques and tangles impair communication between nerve cells, interfering with the processes that aid brain cell survival.

However, precisely when plaques, tangles and inflammatory brain changes begin has been a mystery - one that principal investigator Prof. Agneta Nordberg, of the Karolinska Institutet in Sweden, and colleagues believe they may have unraveled with their latest study.

Using radioactive tracer molecules to monitor brain changes
To reach their findings, which are published in the journal Brain, the team scanned the brains of more than 50 participants using positron emission tomography (PET).

Some of the study participants 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.

All subjects were injected with three radioactive tracer molecules prior to PET scans - PIB, Deprenyl and FDG - which allowed the researchers to track plaque levels and inflammation related to activation of astrocytes, the most common support cell in the brain.

Additionally, the researchers measured the glucose metabolism in participants' brains, providing insight into brain cell function.

PET scans were repeated for half of the participants 3 years later, allowing the team to assess brain changes over time, and all subjects were required to complete memory tests.

Astrocyte activation peaks when plaque accumulation begins
Among participants with Alzheimer's-related gene mutations, the researchers identified plaques and inflammatory changes nearly 20 years prior to the estimated onset of memory problems.

Specifically, the researchers found that when plaques begin to accumulate in the brain, astrocyte activation reaches its peak.

"Astrocyte activation peaks roughly 20 years before the expected symptoms and then goes into decline, in contrast to the accumulation of amyloid plaques, which increases constantly over time until clinical symptoms show," explains Prof. Nordberg. "The accumulation of amyloid plaque and the increase in number of astrocytes therefore display opposing patterns along the timeline."

It is approximately 7 years prior to the onset of Alzheimer's symptoms that brain cell function starts to decline, according to the researchers.

The team identified no such brain pathology among individuals who did not possess Alzheimer's-related gene mutations.

According to the authors, these findings suggest that inflammatory brain changes related to Alzheimer's may occur long before disease onset. What is more, they note 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.

Medical News Today recently reported on a study suggesting that anxiety may increase the risk of dementia.

(Source: medicalnewstoday.com)

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