I read an article recently reporting on results of a drug trial hailed as the best news for Alzheimer’s disease research in 25 years. Are we really on the verge of a cure?
Dr. Sharlin Responds:
Lately the press is reporting on an article published in the September issue of the Journal Nature which demonstrates the effective clearance of amyloid beta protein in 125 patients with Alzheimer’s disease.[1] This was accomplished through the use of a proprietary antibody called “Aducanumab” owned by the pharmaceutical company Biogen. Though hailed as a major breakthrough in the treatment of Alzheimer’s disease I would caution my readers to take to deeper dive into the results and what they mean.
In the study treatment was associated with lower rates of cognitive decline, not clinical improvement. On top of that “brain swelling” was observed as a serious adverse event in 41% of the highest dose group (10 mg). Forty-four percent of all treated (including the lower dose groups) had to discontinue the drug because of this side effect. We do not know how many of those 44% were in the highest dose group which was the group that had the most significant reduction in amyloid beta. However, it was in this group that the clearance of amyloid beta approximated that of a normal or unaffected brain.
Why is amyloid beta viewed as a problem is Alzheimer’s disease? Normal, healthy cellular environments are always in a state of balance between promoting nerve cell growth and connections, refining those connections (think pruning a tree or trimming a hedge), and in some cases responding to inflammatory triggers by increasing inflammatory signals that end in programmed cell death. This happens when a protein called Amyloid Precursor Protein (APP) is cut in different ways, depending on the signals: grow/connect, refine/prune, inflammation/cell death (protect the organism). When APP is cut one way it makes amyloid beta. So, what we have is a normal biological process that, in a seesaw manner, is excessively tipped toward refine/prune/inflammation/cell death. The drug in question removes amyloid beta. Like all root cause medicine, it does not remove the inflammatory “alert” signals that come from the nucleus and are present in the cell environment. Now we can understand why the investigators saw a reduction in the rate of cognitive decline, but not necessarily a “reversal” of cognitive decline. The latter would depend on signals favoring the survival of nerve cells and the making of new connections (synapses).
As an Institute for Functional Medicine and Vanderbilt-trained neurologist I am encouraged by the findings. But I am also aware that more needs to be done to tackle a disease that is estimated to affect 5.4 million Americans.[2] More attention needs to be paid to the work of Dr. Dale Bredesen, UCLA Professor of Neurology, and President and CEO of the Buck Institute for Research on Aging, whose functional medicine-oriented approach has been published in a peer-reviewed journal demonstrating the reversal of cognitive decline,[3] and specifically the reversal of early Alzheimer’s disease.[4] The inflammatory signals referred to above are what Dr. Bredesen calls the “36 holes in the roof.” Unfortunately, addressing root cause imbalances takes hard work. It might seem easier to wait for the magic bullet than to have a discussion of the factors that get us there in the first place. But there is no time to spare.
I am one of only a handful of doctors around the world trained to use the Bredesen Protocol to reverse cognitive decline, including early Alzheimer’s disease. If you or someone you know is affected by memory loss, please contact my office at (417) 485-4330.
[1] http://www.nature.com/nature/journal/v537/n7618/full/nature19323.html
[3] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4221920/pdf/aging-06-707.pdf