Linking 2 molecular pieces of the Alzheimer's puzzle

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**. 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. Specifically, they found that the normal cleavage of APP in the cell gives rise to a **nontoxic fragment** (called AICD) that suppresses the gene that produces the cell receptor for apoE—called LRP1, receptor, which nestles in the membrane of nerve cells and enables the apoE protein to transport its cholesterol cargo into the cell. The researchers speculated that the loss of LRP1 function in AD might cause a loss of cholesterol that causes malfunction of **neurons**. Thus, they suggested that treatments to restore the activity of the receptor gene might be a useful treatment strategy for AD. One such treatment, they said, consists of drugs that inhibit the enzyme that cleaves APP to produce the regulatory protein fragment that suppresses the LRP1 gene. “Our results provide important insights into APP biological function and its potential implications for neuronal dysfunction in AD and may lead to the design of better therapeutic strategies to treat this devastating disease,” concluded the researchers. Whole article: "http://physorg.com":[ http://physorg.com/news110637734.html]

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