The future of Alzheimer's disease treatment

December 8, 10:18 AMScience News ExaminerMeg Marquardt

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Agustine D., the first AD patient described by Alzheimer in 1906.

As we leave Alzheimer's Awareness Month, I take an in-depth look at the history and exciting future of AD treatment. Part I of this piece, a historical overview of AD, can be found here, and Part II, a look a first attempts at AD treatment, can be found here.

Part III: A Light in the Dark

Though most research dealing with Alzheimer’s disease (AD) is focus on pharmacology, there is another area of research that is racing to catch up with the development of our understanding of AD.  Presently, there is only one way to truly diagnose a patient with AD: brain autopsy.  There is no way to directly tell if a drug is succeeding in clearing Aβ plaques or tangles from the brain.  The plaques and tangles cannot be seen with any current technology such as CAT scans, and so the only method to tell if a drug is working is to observe changes in symptoms like memory and motor function loss.  However, as autopsy has the unfortunate requirement that the patient be dead, it is not a helpful preventative tool.  But there are imaging specialists across the world working to solve this problem, trying with fervor to be ready to study the effects of the new wave of pharmacological treatments.

Dr. William Burke, Vice Chair of the Department of Psychiatry at the University of Nebraska Medical Center (UNMC), refers to the opening of the 21st Century as the Golden Era of Alzheimer’s Treatments.  It is difficult not to grow excited at such a phrase.  There is still the bitter taste of the failure of Flurizan lingering, but it is beginning to ebb away in light of new developments.  Not even a month after the announcement that Flurizan production would end, a British group announced their own AD drug, Rember, had passed Phase II trials with remarkable results of around 80% of patients treated showing a slowing in mental decline. Rember, unlike Flurizan, targets the tau tangles in the brain, what Burke considers the more threatening of the two brain lesions.  After the fanfare of Flurizan, Rember is met with a hesitant optimism.  Perhaps this one will work, perhaps when its Phase III trials conclude sometime next year the Baby Boomers will receive news of better results and some relief in the face of AD at last.

Another aspect makes this the true Golden Era.  Unlike when all anticipation of a cure hung on a single drug, Rember is just the first of many that are expected to progress to Phase III trials.  In recent years, research has shifted from drugs that treat the symptoms to drugs that treat the true cause of the disease.  Flurizan and Rember are simply the first wave.  Burke estimates that there are no fewer than 10 drugs waiting to begin Phase II trials.  The problem has happily shifted from not enough drugs to too many.  There is a bottle neck on the clinical end of the testing process.  New drugs are being produced more quickly than trails can be created.  Institutions like the University of Nebraska Medical Center have to be approved by the FDA before they are even able to go ahead with trials, and true trials require a vast spread of population—different ethnicities, genders, ages, and geographic locations.  Burke has encouraging thoughts on that frontier as well.  Universities and drug companies are starting to create trial hubs, nexuses from which volunteers can be selected for the various drugs waiting to be tested.

There is a quiet sort of expectation in Burke’s words as he informs me that there has been more development of AD treatments than ever in his history of working with psychopharmacology.  “We have learned so much by studying basic science,” he says, referring to the move by researchers to understand the causes of AD and not simply the symptoms.  “It is reasonable to expect good results for one of these drugs.  Maybe not a complete cure, but a good hope.”