The second molecule that makes up the Alzheimer's toxic duo has finally been identified by researchers at the University of Texas Health Science Center, San Antonio.
Like two unruly boys who need to be split up in class, a pair of protein molecules works together to speed up the toxic events of Alzheimer's disease.
But the new discovery could lead to drugs that disrupt the interaction, and thereby block or slow Alzheimer's onset or progression.
Many Alzheimer's patients have brain lesions called amyloid plaques, which consist of protein fragments called amyloid-beta.
Small aggregates of amyloid-beta are thought to contribute prominently to the degeneration of brain cells in Alzheimer's.
The new discovery involves an amyloid-beta fragment called AICD.
Scientists have known that AICD controls expression of genes that contribute to Alzheimer's, but how it did so was unclear - until now.
"We discovered a protein molecule that communicates with AICD to turn on target genes," said Thomas G. Boyer, professor of molecular medicine at the Health Science Center.
"We hope to exploit this knowledge to identify compounds or drugs that can disrupt these signals, leading to a novel and effective treatment for this disease," he added.
While several drugs can temporarily slow worsening symptoms, no treatment is currently available to slow or stop the degeneration of nerve cells that lies at the root of the disease.