Brain protein identified as Alzheimer's cause

LONDON - Scientists have identified a substance in the brains of mice that causes memory loss, which could be a target for drugs to treat patients with Alzheimer’s disease.

Using genetically-engineered mice that developed memory loss similar to people with Alzheimer’s, the researchers discovered that it was caused by a protein complex.

“Finding the specific cause of memory loss and cognitive decline gives scientists a protein complex to target,” said Professor Karen Ashe of the University of Minnesota Medical School in Minneapolis, who headed the research team.

An estimated 12 million people worldwide suffer from Alzheimer’s disease, the leading cause of dementia in the elderly. The number is expected to rise as the population ages.

There is no cure for the progressive illness, which robs people of their memory and mental ability, but drug treatments may slow the early progression of the disorder.

The illness is characterized by the build-up of protein deposits called amyloid plaques between nerve cells in the brain and tangles of a protein called tau inside nerve cells.

But the researchers, who reported the findings in the journal Nature, said the tangles and plaques are not the major cause of memory loss.

How protein leads to disease
Memory problems can occur in people before they are diagnosed with Alzheimer’s and before brain cells begin to die. The scientists hypothesized that there was something else in the brain that caused the memory decline.

They found a form of the amyloid beta protein in the transgenic mice that displayed early signs of memory loss but which had no plaques or nerve cell loss.

After isolating and purifying the protein complex, whose key component is called amyloid beta peptide which is thought to be linked to the development of Alzheimer’s, and injecting it into healthy rats the rodents experienced a decline in their cognitive ability.

The researchers believe the protein complex impairs memory independently of plaques or nerve loss and may contribute to the drop in cognitive function associated with Alzheimer’s.

“Now we can begin to work on how that protein leads to the disease and what we can do to prevent it from harming the brain,” Ashe said in a statement.

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