Alzheimer toxin may be key to slowing disease

• Neurology • Aug 04, 2005



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Australian scientists say they have identified a toxin that plays a key role in the onset of Alzheimer’s disease, raising hope that a drug targeting the toxin could be developed to slow the degenerative brain disease.

The toxin, called quinolinic acid, kills nerve cells in the brain, leading to dysfunction and death, the scientists said.

“Quinolinic acid may not be the cause of Alzheimer’s disease, but it plays a key role in its progression,” Alzheimer’s researcher Dr. Karen Cullen from the University of Sydney said in a statement.

"It’s the smoking gun, if you like.”

“While we won’t be able to prevent people from getting Alzheimer’s disease, we may eventually, with the use of drugs, be able to slow down the progression.”

Alzheimer’s disease is a brain-destroying disease that affects millions of people around the world. As the population gets steadily older, experts estimate numbers will balloon to as many as 16 million in the United States alone by 2015.

Alzheimer’s disease impairs the brain’s intellectual functions (memory, orientation, calculation), but at first, largely spares those parts of the brain that control sensation and movement. The memory often is affected early, and gradually deteriorates, causing impaired judgment and other problems that may affect a person’s ability to perform normal daily activities. Although Alzheimer’s usually begins later in life, generally after age 60, it rarely may affect people as young as age 30.

More than 200,000 people have Alzheimer’s disease in Australia and the number is expected to rise to 730,000 by 2050.

Outward symptoms start with memory loss, which progresses to complete helplessness as brain cells are destroyed. In the brain, neurons die as plaques and tangles of protein form.

The Alzheimer’s disease research team from Sydney’s St. Vincent’s Hospital, the University of Sydney and Japan’s Hokkaido University found quinolinic acid neurotoxicity in the brains of dementia patients.

Quinolinic acid is part of a biochemical pathway called the kynurenine pathway that is also found in other brain disorders, including Huntington’s disease schizophrenia.

In Alzheimer’s disease, deposits of proteins called amyloid and TAU distort communication between brain cells. Also levels of a chemical called acetylcholine that helps transmit messages between brain cells begin to drop, causing more communication problems. Eventually, brain cells themselves are affected. They begin to shrivel and die, causing certain areas of the brain to shrink.

The scientists said there were several drugs in an advanced stage of development for other conditions that targeted this pathway and that these drugs, which still need to be tested, could be used to complement other treatments for Alzheimer’s disease.

“Building on what we’ve found and others have found, it’s likely that they would have significant effect,” said Professor Bruce Brew, director of neurology at St. Vincent’s Hospital.

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Provided by ArmMed Media
Revision date: July 5, 2011
Last revised: by Jorge P. Ribeiro, MD



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