Clean up on aisle 9
Once again, The Telegraph sensationalizes scientific news that doesn’t need it. The work done by Dr. Katrin I. Andreasson’s group at Stanford is exciting enough. The Telegraph doesn’t have to use a title that suggests they have a cure for Alzheimer’s Disease (AD). I’ll admit they didn’t do a terrible job. I’ve got worse examples below. So what’s really going on? The researchers at Stanford found that a particular cell signaling pathway, cyclooxygenase/prostaglandin E2 (COX/PGE2) pathway, was involved with restoring the function of microglial cells.
☼ What are microglial cells?
Glial cells are “support” cells in the brain, as they surround neurons, providing the mylein sheath (think of it as electrical insulation). Microglial cells are scavengers in the brain, like macrophages. In fact microglial cells (like the image below) are more like macrophages than they are like glial cells. It’s thought that microglial cells are less efficient in older animals and therefore cannot clear as much debris from the brain. In particular, beta-amyloid is thought to accumulate in Alzheimer patients eventually causing dementia. If the microglial cells could resume their clean up job then the beta-amyloid wouldn’t accumulate.
☼ Cyclooxygenase/prostaglandin E2 (COX/PGE2) pathway
I’m not an expert in cell signalling so I’ll just highlight the important bits. Again, since microglial cells are more similar to macrophages than neurons, it was hypothesized that an inflammatory response was involved with microglial function. COX1 and COX2 along with PGE2 are known components of an inflammatory signaling pathway. More importantly, it’s related to aspirin and aspirin was shown to be beneficial to preventing onset of dementia in AD patients. There’s a catch though. There’s always a catch. Aspirin only helps if AD is detected early. That’s one of the biggest stumbling blocks to AD research, early detection (more on that below). The Stanford group found that if you block EP2 signalling (it’s part of the PGE2 pathway), you can restore the function of microglial cells and they can resume clean up on aisle 9.
So how did they do this? They did some in vitro work, i.e., work with macrophage cells in a dish to start identifying part of the cell signalling. They also did work with genetically altered mice, the so-called knock-out mice, to see if blocking certain parts of the pathway restored function of the microglial cells. Combined, their work suggests that blocking EP2 restores microglial function and memory impairment is reduced.
So this is very promising work but it is not a cure for AD. They have to identify an EP2 blocking agent, make sure it works in mice. Make sure it isn’t toxic in mice and one large species. Then they have to do toxicology studies in humans before even thinking of testing on AD patients. Notice how the titles of the articles become less sensational when you compare them?
References:
Has Stanford University found a cure for Alzheimer’s disease? via The Telegraph
Blocking receptor in brain’s immune cells counters Alzheimer’s in mice, study finds Stanford press release
Prostaglandin signaling suppresses beneficial microglial function in Alzheimer’s disease models
https://www.jci.org/articles/view/77487
Want to learn more about Alzheimer’s Disease?
Alzheimer’s Disease Research
https://plus.google.com/+ChadHaney/posts/ddm3JqPMy76
Want to learn more about how drugs are developed and see another example of hype from The Telegraph?
Bench to Bedside
Another example of media hype.
Alarming science discovery…
Image source:
http://individual.utoronto.ca/lyanneS/invitro.html
#ScienceSunday #ScienceMediaHype