Dagens Nyheter reported on the findings Wednesday. More than 100,000 Swedes suffer from the disease, which affects memory, concentration, and speech. As the disease progresses neurons die off, although the causes are not yet understood. One early sign of the disease is the appearance of so-called senile plaques, deposits in the brain's gray matter made by a protein called amyloid beta.
Researchers at the Karolinska Institutet, a university hospital just outside of Stockholm, published a study suggesting that a type of brain cell that performs support and repair functions, called astrocytes, are implicated in the disease's development. Researchers studied healthy individuals from families known to have the mutations that predispose one to Alzheimer's.
Participants performed memory tests and were scanned using PET (positron emission tomography), and they measured glucose metabolism. The PET tests where performed three years later on some of the participants. Researchers found brain changes twenty years before what would be the expected onset of symptoms. Many astrocytes were inflamed long before the appearance of the senile plaque that is associated with the disease.
"Astrocyte activation peaks roughly twenty 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," said the principal investigator Agneta Nordberg from an Alzheimer's research center at Karolinska. "The accumulation of amyloid plaque and the increase in number of astrocytes therefore display opposing patterns along the timeline."
Researchers hope the discovery could suggest strategies for treatment as early as the warning signs are discovered. Their findings suggest astrocytes themselves might be targeted with pharmaceuticals.
The new study has been published in the scientific journal Brain.