It's becoming more and more common to find out a relative or friend has to leave his/her job to care for a loved one with Alzheimer's disease. Just yesterday, I heard about a colleague who is facing this difficult situation. In fact, the Alzheimer’s Association estimates in 2011, 15.2 million family and friends provided 17.4 billion hours of unpaid care to those with Alzheimer’s and other dementias – care valued at $210.5 billion.
Alzheimer's disease (AD) impacts the whole family, in a way very few medical conditions do, and coping with a progressively fatal disease takes a toll on everyone involved.
Hope is precious, and in the case of AD, research can hardly move fast enough to get us to a place where the disease doesn't conquer all it touches.
Knowing that it's mid-July, my optimism starts to rise. In an annual summit, AD experts will flock from across the globe to the Alzheimer’s Association International Conference (AAIC) in Vancouver this week. I'm waiting with anticipation for the next big Alzheimer's discovery to be unveiled.
I was pleasantly surprised that AD news started pouring out the week before the big meeting. Last Wednesday, two separate studies were released and add pertinent information to the greater understanding of AD.
The first, in the New England Journal of Medicine, found that gene carriers of the rare familial form of Alzheimer's disease start showing changes in diagnostic tests up to 25 years before symptoms would occur. This study, which may or may not correlate with what happens in the more common sporadic form of AD, establishes how early interventions may need to be made to stop the disease before it spreads through and damages the brain.
Penn Memory Center director Steven Arnold, MD, professor of Neurology and Psychiatry in the Perelman School of Medicine at the University of Pennsylvania, told ABC News "We can learn so much from these people that would be applicable to Alzheimer's disease at large. If you can identify biomarkers early and see that there are AD changes, that is really the time where you can intervene with medicines...or perhaps lifestyle interventions," to reduce risk.
In the second study, published in Nature, researchers found a genetic mutation that actually protected people from producing a protein that contributes to AD. While it won't lead to a new genetic test to see if people carry this protective gene mutation, it does show that the production of amyloid protein, one of the pathological contributors to Alzheimer's disease, is detrimental in Alzheimer's disease progression, and pushes research forward targeting amyloid.
In an interview with Medscape Neurology, Penn geneticist Gerard Schellenberg, PhD, professor of Pathology and Laboratory Medicine, who leads the Alzheimer's Disease Genetics Consortium, a part of the International Genomics of Alzheimer's Project (IGAP), said this study solidifies what is already known about the role of amyloid beta in AD. Although previous research showed that if amyloid goes up, there's an increased chance of AD, now, you can show that if you make amyloid go down, you get a decreased chance of the disease, he said.
“We all have extrapolated what we learned from early onset and applied it to late onset,” said Dr. Schellenberg. “This study gives us more confidence that all the stuff we use in our models and our experiments is going to apply to late−onset AD. That's something I find probably more interesting than just the fact that there is another APP mutation.”
And, at AAIC in Vancouver, we're expecting to hear updates on recent drug trials to slow the progression of the disease, and any promising new targets or approaches to combat this complex disease.
For all the families dealing with AD on a daily basis, or those who have helped by participating with a loved one in a clinical trial, let our collective hope continue. With so many passionate people working on this, solutions are hopefully closer than ever.