Archive for November 17th, 2011|Daily archive page

Research report

Because I am a science writer by profession, I get to attend an annual meeting about science to both promote research being presented by faculty at my institution, as well as to just soak up some of the new knowledge in a field related to the research I cover. I spent a few days at the Society for Neuroscience meeting in Washington, D.C., and I attended a symposium on Alzheimer’s treatments that have been tested in animals. I was sad to see that Alzheimer’s didn’t make it on the list of topics to be discussed in a press conference. I don’t know if that’s because there weren’t enough good presentations at the meeting to assemble for a meaningful news conference or because planners don’t really care about the disease. (Why would I even think that? I am just suspicious that people – even those close to the science – prefer to ignore the massive problem of Alzheimer’s.) Autism got a press conference, and so did pain, and depression and schizophrenia, and stress. The aging brain was discussed, but in the context of decision-making and sleep, not disease. I’m hypersensitive, of course, and biased, but I admit I was bummed that such a major disorder wasn’t worthy of some media attention at this enormous meeting.

At this symposium, I got a hint as to why that might be. The doctor who runs my support group often seems pretty pessimistic about the state of research into treatment. And based on these eight presentations I heard, I think he is right. There is still so much that is not known about the cause of Alzheimer’s, let alone how one might approach a single type of treatment.

Here are summaries of what the researchers were saying:

* A German biomedical company has developed a compound that targets multiple dysfunctions rather than a single problem. In tests on mice and rats, the animals given the drug performed better on memory functions. A number of genes related to brain-cell communication are activated when the drug is present.

* Boston University researchers are testing the injection of a gene directly into an area of the brain associated with memory. After injection into animals, new brain cells grew and the amount of plaques in the brains declined.

* A UCLA researcher theorizes that the use of non-steroidal anti-inflammatory drugs (ie ibuprofen) and dietary fatty acids might lower the amount of amyloid plaques in the brain. Tests in mice suggest this is so. But the response to those medicines appears to depend on whether the person taking these products has a genetic-based higher risk for the disease. So without a test for that genetic risk, there is no way to know if taking NSAIDs or fatty acids has potential to protect one’s brain.

* Columbia researchers are investigating proteins in the brain called histones, and specifically compounds that activate them, as a treatment target. They put a drug targeting these activators into the brains of mice. The drug improved memory behavior and cell communication in the brains of two mouse models.

* A University of Illinois at Chicago scientist talked about the use of environmental enrichment to improve production of brain cells. Environmental enrichment in animals essentially means housing mice in an environment that offers visual, motor, cognitive and sensory stimuli. Mice in these environments, when compared to mice in standard animal housing, had fewer plaques in their brains and had higher levels of a protein that supports survival of brain cells.

* Researchers at the Salk Institute have developed a molecule that, even though it’s not designed to hit a specific target, is meant to offer protection for the brain in a variety of ways. Animals given this experimental drug in their food did better on spatial learning tasks – even mice that are a model for Alzheimer’s. Their brain tissue also showed signs of increased production of neurons and more complex branching structures for communication among cells.

* Another German company has developed a drug that, in several tests on mice and rats, showed improvements in memory as well as more communication across synapses in the brain.

* A graduate student from Central Michigan University reported on her research on the use of stem cells from bone marrow as an Alzheimer’s treatment. The cells were transplanted into two areas of the brain in mice. Treated mice did better than untreated mice in some behavior tests, but not all. But the treated animals did have fewer plaques in their brains and less inflammation.

So. Lots of theories. Some apparent progress. But there’s still a long way to go, with all of these. When one speaker didn’t show up and the moderator wanted to fill time with a general discussion, it was interesting to hear what these scientists had to say. There’s no biomarker identified for Alzheimer’s, so it’s hard to validate treatments – or even benign nutrient cocktails that might be beneficial. It’s difficult enough to get a drug approved by the FDA, but a drug designed to act on multiple targets would be even more complicated to move through the federal process. And if, anecdotally, a researcher sees five out of 10 people respond to a nutritional approach, does it mean anything?

Finally, this provoked a comment that took the big picture into account. “The placebo effect can be powerful and can influence the body’s ability to fight off disease,” an audience member said. “In a compassionate care setting, where lots of Alzheimer’s patients come from, they’re willing to try anything. The FDA has become very minor. Caregivers look instead at a risk-benefit ratio.”

He was saying what I had been thinking: Yes, five people responding to something isn’t scientifically valid, necessarily, but it seems promising, and what is the harm in trying it in a patient already experiencing memory loss, confusion and other symptoms? Caregivers can feel very desperate – I know this firsthand – and don’t take long to reach a point at which they (we) are willing to try anything.

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