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Study of Cellular Defect May Lead to New AD Drugs

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By xx • • October 10, 2000

The discovery of two cellular mutations associated with early-onset Alzheimer’s could lead to the development of new drugs for the disease. A research team based at Massachusetts General Hospital (MGH) has discovered a key link between two cellular abnormalities – mutations in genes that produce proteins called presenilins and an altered handling of calcium inside cells.

The researchers have tied a specific calcium pathway to the production of amyloid-beta42, the sticky protein fragments that make up the plaques found in the brains of people with Alzheimer’s disease.

In the September issue of Neuron, scientists from the MGH Genetics and Aging Unit report that the presenilins appear to control a process that regulates the level of calcium in a cellular compartment called the endoplasmic reticulum. Researchers found that presenilin mutations usually associated with inherited Alzheimer’s disease slow down this regulatory process. They also show that inhibiting this particular calcium pathway increases production of amyloid-beta42 (A-beta42).

Rudolph Tanzi, PhD, director of the MGH Genetics and Aging Unit and a co-author of the ,i>Neuron paper, adds, "Our work predicts that, if you could develop a drug that stimulates this specific calcium pathway, you could lower levels of A-beta42, which is the name of the game in Alzheimer’s disease drug therapy development."

Mutations in two presenilin proteins – dubbed PS1 and PS2 – have been identified as causing most cases of inherited, early-onset Alzheimer’s disease, also called familial Alzheimer’s disease (FAD). The function of the presenilins is as yet unknown.

Some researchers have found evidence that one or both of them may be a sought-after enzyme called gamma-secretase that clips the large amyloid precursor protein (APP) to form A-beta fragments. Other recent Alzheimer’s research has shown that brain cells from people with FAD, or cells into which mutated presenilin genes have been inserted, show alterations in their handling of calcium, a process that is key to normal cellular metabolism.

Researchers have only recently discovered the pathway where calcium moves from outside the cell to storage inside the cell. By focusing on what is known as CCE, capacitated calcium entry, the research team hopes to figure out how to increase CCE and lower A-beta42, associated with early onset AD.

"If we can find compounds that increase CCE just enough to lower A-beta42, we may be able to offer a way to prevent or slow down the progression of Alzheimer’s to members of families affected by these mutations, some of whom begin to show symptoms at a very young age," Tanzi said. "While we currently don’t know whether this information also might be applied to the late-onset, non-inherited type of Alzheimer’s, we would assume that the pathways that go wrong in early-onset illness also are involved in late-onset disease."

Tanzi and Kim are currently working with Neurogenetics Inc., of San Diego to identify compounds that may lower A-beta42 by stimulating CCE. Both researchers are scientific founders and have equity interests in the company, which has licensed from the MGH the concept of treating Alzheimer’s through increasing CCE.

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