Before blogging about other things (UGA’s Oil Spill Symposium and Seth Mnookin at UW, for starters), I want to step back and talk more about Age-related Macular Degeneration (see my first post on the topic). Let’s just say the BIMR conference in Irvine gave new meaning to the term “interdisciplinary” — to me, at least.

Simply put, the task group discussions played out as beefed up lab meetings, where scientists chatted about developments in the field. Covering these highly specialized researchers seemed daunting at first, especially since they knew one another and referenced research and studies unfamiliar to me. Though this made it hard for me to know what was going on at times (sadly, I don’t know many AMD researchers by first name), I think it was necessary nonetheless.  To move forward with the limited time the group was given, people had to be straight to the point.

In mixed meetings, experts from my group sat in on other group sessions and provided input. In my opinion, the mixed sessions made the conference a large success. My group consisted of imaging experts — researchers studying ways to detect signs of AMD with tomography techniques and other scanning methods (e.g., MRI). I found the discussions particularly interesting because I was uneducated about the importance of imaging to stage and monitor the progress of AMD, or any other eye disease for that matter. In addition to covering the imaging task group, I covered two other sessions: one on stem cell research and another on cell death.

Though I can’t comment too much on the specifics — since my report is currently embargoed for a later date, I can discuss common knowledge issues that stand in the way of studying and developing therapies for AMD.

For those of you with little knowledge of eye anatomy (i.e., me before the conference), it’s important to understand that AMD affects the portion of the retina called the macula. The lens of the eye projects light to the retinal surface toward the back of the eye, where photoreceptor cells convert that light into electrical signals to be interpreted by the brain (via the optic nerve). Light must pass through the macula to reach the optic nerve (and thus, the brain). Specifically, the macula allows you to focus on the contents of this post with your central vision.

Kudos to the macula, right?!

Here’s a nice illustration of the eye that shows some of this anatomy (from John Moran Eye Center, University of Utah).

For comparison, below are images of eyes diseased with AMD (from Eye; Sato et al.). Note the darker areas and spots in the middle of the eye. Read on for an explanation.

For patients living with AMD, quite a few things go wrong in the macula. In some patients, these yellowish deposits called drusen accumulate at a pigmented portion of the retina (more specifically, at a spot called the “retinal pigment epithelium,” or RPE). These deposits overtake the macula and can limit the amount of light reaching the back of the eye, causing central vision loss. Multiple researchers reiterated the point that not all drusen are the same. In fact, it was suggested a few times in public presentations that different drusen may be the manifestations of different diseases. Some even speculated that AMD comprises several unique diseases altogether.

That said, attendees still focused on the types of disease thoroughly studied. AMD generally comes in two forms: “wet” and “dry.” Drusen and geographic atrophy — the breakdown of photoreceptor cells — are associated with “dry” AMD. Other patients may be diagnosed with “wet” AMD (or neovascular AMD), where the blood vessels on the outer portion of the retina invade the macula and leak. The latter is less common than the former, which is why the conference focused on the dry form.

Geographic atrophy received much attention at the conference. Scientists know that AMD causes photoreceptor cells — rods and cones — to die, but they don’t completely understand why. This is where cell death experts and neuroprotection researchers chime in. Researchers and clinicians expressed interest in a more preventative approach that would make intervention possible before these cells die. Imaging the eye is particularly useful in developing an approach to geographic atrophy as well. In order to stage the disease in the long-term, researchers need to pinpoint specific biomarkers or signals that indicate cell stress before AMD actually takes hold. I thought this session was particularly interesting because it seems as if doctors are open to screening people who have a family history of AMD before they show signs of the disease.

Another idea that was particularly intriguing was using stem cell transplants to treat patients with AMD. In a general sense, transplanted stem cells can be programmed to emit signals to indicate cell health. Since the body may reject the transplant, monitoring cells with imaging techniques would help identify whether the transplant was successful at the cellular level. This may be years in the future, I don’t know…

These are just a few highlights from a science writer’s perspective — I plan to link to my report when it’s published later this spring. I will be able to comment more once the reports are public.

Overall, I had a blast at this conference. I met some really great scientists who believe in the power of science communication (music to my ears!). I also had the unique opportunity to work with science writing guru Barbara Culliton and several talented science journalism grad students I hope to stay in touch with in the future. My only complaint would be not dipping my feet into the Pacific — I’ll have to make another trip to California for that one.