Researchers have uncovered a biological link between the protein whose mutation causes early-onset Alzheimer's disease (AD) and a gene variant linked to late-onset AD.
The researchers said their finding could lead to new approaches to treating AD.
Guojun Bu and colleagues published their findings in the October 4, 2007 issue of the journal Neuron, published by Cell Press.
In their studies, the researchers sought to link the function of two known causative factors in AD—amyloid precursor protein (APP) and a particular form of the gene for the protein apolipoprotein E (apoE) that has been linked to higher late-onset AD risk.
Mutations in APP are known to cause early-onset AD when cleavage of the protein produces a short toxic protein called Aâ peptide that builds up in the brain, killing brain cells.
And a specific variant of the gene for apoE, which produces a version called apoE4, has been linked to late-onset AD, although how this predisposes individuals to the disease is largely unknown. However, the normal function of the apoE protein is known. It carries cholesterol and other lipids into nerve cells, where they act as essential building blocks for neuronal membranes.