Scientists have discovered a link between the mutated protein that causes early-onset Alzheimer's disease and that which leads to its late-onset counterpart.
The study focused on amyloid precursor protein (APP) and a form of the gene for the protein apolipoprotein E (apoE), both of which have been linked to a greater risk of late-onset Alzheimer's.
Mutated APP is known to result in a build-up of a toxic protein that destroys brain cells, while the mechanism by which apoE heightens risk is unknown. The apoE protein carries cholesterol and other lipids into nerve cells, where they are essential for maintaining neuronal membranes.
The study found that APP regulates apoE and its cholesterol transport function.
"Our results provide important insights into APP biological function and its potential implications for neuronal dysfunction in Alzheimer's disease and may lead to the design of better therapeutic strategies to treat this devastating disease," the researchers concluded.
Their findings appear in the October 4th issue of the journal Neuron.
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