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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Forbes

Michael Waldholz,

In the coming months researchers will release results of several drug studies that will impact millions of Alzheimer’s victims and their families, as well as the fortunes of drugmakers, Merck, Pfizer, Lilly and Johnson & Johnson among others. Just as important, maybe even more so, the studies may finally provide evidence to support a controversial 20-year old theory of how the mind-robbing and lethal illness works.

But there’s plenty of reason to believe these studies tests will be inconclusive. The biggest worry is that even if the drugs work, the studies may show that to be effective, the medicines must be used much like anti-cholesterol pills, well before the disease begins to show debilitating symptoms. If that’s true it will mean years of uncertainty about an effective treatment or cure. Alternately, the

drugs may turn out to be complete busts, or only improve memory and thinking in a statistically negligible manner that will spark conflicting interpretations. And since there is nothing in drugmakers’ pipeline to replace the drugs being tested, negative results will force Alzheimer’s research back to square one for a disease that is already costing untold suffering and adding hundreds of millions of dollars a year in health costs that will explode as the population ages.

What follows is a review, a scorecard of sorts, of what is at stake. Much of this conversation will be front and center at an international research meeting beginning this weekend in Vancouver.

A primer: The experimental medicines all focus on attacking beta amyloid, a protein autopsies show masses in the brains of Alzheimer’s victims. According to the amyloid theory, these packets of plaque destroy brain cells over time, though exactly how they do this is still unknown. One school of scientists believes the plaques, which collect in small amounts in nearly all people as they reach old age, arise earlier and in much larger amounts in people with a predisposing genetic makeup. Another group argues that the clumping is merely the residue of some other unknown chain of events, so drugs designed to prevent or destroy amyloid will provide little if any benefit.

Alzheimer’s researchers, doctors and victims are literally holding their collective breath, hoping the studies will not only provide relief, but give scientists the kind of clear roadmap needed to fuel future investigations

A gene discovery backing the amyloid theory: Just this week, a well-regarded research team in Icelandreported in the journal Nature that they had identified a gene that, when mutated, slows the body’s production an enzyme called beta secretase. This is a valuable discovery because beta secretase appears to play an important role in amyloid formation. Merck, Lilly and Esai are in advanced clinical studies of drugs that mimic the protective action of the gene by blocking the action of the enzyme. The Iceland group, under the direction of the gene-hunting company DeCode and its charismatic founder, Kari Stefansson, found that people with an unusual variant of the gene either don’t have the disease or don’t amass plaque in large amounts. Because the study involved a small number of people in Iceland, there is reason to be cautious about broader application.

The garbage collectors: Perhaps the most important advanced study, whose results will be reported in October, involves the drug bapineuzumab, being developed by Pfizer and Johnson & Johnson and a similar drug called solanezumab from Lilly. These medicines are laboratory produced antibodies that, given through infusions, have been shown to attack and clear amyloid from the brain. Early results of another drug, Gammagard from Baxter, a combination of plaque-clearing antibodies, will also be released at the week the Alzheimer’s Association International Conference. Even a slight increase in cognition from these drugs will likely result in FDA approval and annual sales of billions of dollars. The worry is that even there though the drugs can sterilize amyloid clumps from the brain, the patient population studied may be too far advanced in their disease to be helped, or the study not be sensitive enough to detect benefits.

Still another antibody, crenezumab, being developed by Roche’s Genentech unit, is being tested in a $100 million trial in a family in Colombia where an early-onset form of the disease is common. That trial, involving about 300 relatives, won’t be completed for years.

The gatekeepers: Merck and Lilly are in the second of three phases of clinical trials of drugs called beta-secretase inhibitors, also referred to as BACE drugs. Unlike the antibody medicines, these drugs are being tested in pill form. The science underlying these drugs got a boost from the Iceland gene study. The idea behind these medicines is to inhibit the formation of amyloid plaque before it can cause havoc. As with the amyloid clearing drugs, there is concern that the studies underway involve patients too far into their disease.

The takeaway: It is clear that all the drugs in development will be most effective if used early in the disease, meaning the ability to identify those at risk is critical. Even then, the health profession and policymakers will face a dilemma. Conducting population-wide screening will be enormously expensive. Giving these medicines as long-term preventive treatments will cost many billions of dollars more. This is just one of many example of why the nation’s health bill will continue to rise sharply, with or without success in battling Alzheimer’s disease.