Olfaction is not one of the topics most people look forward to with bated breath when going into a neuroscience course; at least, that hasn’t been my experience. Most people (often myself included) are looking out for the trendier stuff — consciousness, phantom limbs, schizophrenia, hallucinations. But it should come as no surprise that the neuroscience of olfaction, or the sense of smell, is both a hotbed of current research and a fascinating area of study. The 2004 Nobel Prize in Physiology or Medicine was awarded to Linda Buck and Richard Axel for their discovery of the family of genes (about 1,000 genes total) which code for olfactory receptors in humans.
I’m in the middle (er, maybe the first third) of a class on the neurobiology of aging. As such, we’ve covered a few different theories of aging, from the molecular (telomeres!) to the evolutionary (grandparents!). There are about as many overlapping theories of why we age as there are branches and specializations within biology. Aging affects all of us if we’re lucky, and all systems within our bodies, yet we don’t know precisely why it happens at all.
A new paper from scientists at the Salk Institute theorizes that cellular aging may be linked to “extremely long-lived proteins” (ELLPs). Keep in mind that cellular aging is slightly different from aging as a person; some cells throughout your body are constantly aging, dying, and being replaced, no matter what your age is. Other cells are mostly with you from birth until death — neurons are one such group of cells. With some slight, recently-discovered exceptions, there is very little neurogenesis (the birth of new cells in the brain) after childhood.
This new research into ELLPs focuses on the aging of brain cells, which is important, as they are not replaced when they are damaged or die off. Culturally, it’s also important because brain aging is a big deal in our population. I mentioned above that some cells (like skin cells or the lining of the stomach) are being replaced fairly regularly. Another mechanisms that cells use to repair damage is to replace or recycle the proteins that carry out cellular activities.
One important class of protein in brain cells is the transporter protein. The ELLPs in this study form channels that allow ions and other small molecules in and out of the cell past its membrane, which is how neurons signal to each other.
If this type of protein gets worn down or damaged, it is not able to be replaced or recycled, according to this paper. In that case, neurons will have a hard time signaling to each other, and the accumulated damage over many years could lead to problems throughout the brain.
This paper is new and interesting, although it doesn’t provide any easy answers, and definitely requires further study (For instance, the study was done on rats, which are a good model organism, but which also have much shorter lifespans than humans have). It does, however, illustrate one of my favorite differences between physicists, who have variously flavored quarks, and biologists, who have “extremely long-lived proteins.” I don’t know what that says about our respective fields, but it must mean something.
Given a three-day weekend, relatively little homework, only moderate pressure to get my grad school apps done rightthisinstant, and free admission to a museum that has a brand new dinosaur hall, I think the odds were very low that I was going to do anything else today. And considering how I basically lived there last fall, before my spring courses took over my life.
The dinosaurs, they were nifty. I think, as someone who was raised to value nerdy things like this, there is always the possibility that I might take seeing dinosaurs for granted. It is, after all, kind of a big deal that scientists are able to reconstruct, with even a modicum of certainty, dinosaur skeletons from the fossils found, let alone reconstructing lifestyles, diets, etc.
As with chemistry, paleontology is not my thing, but if it’s yours, more power to you. One sign struck me as somewhat odd, however:
I’m not sure what it was, exactly, but something about “We know them as skeletons” makes me laugh. Maybe it’s the idea that this point needs clarification — that someone (hopefully a child), reading this, suddenly realizes that dinosaurs weren’t just skeletons when they were alive. You never know. Stranger things have been believed.
Anyway. The new dinosaur hall was the star of the day, but of course I couldn’t pass up my Fin Whale Passage. I love that room. The whale sounds, the giant skeleton suspended from the ceiling, the low lighting, the benches. Honestly, I could live there.
One little girl, running into the room, yelled, “It’s a wooly mammoth!” Her parents corrected her (thankfully). I guess maybe when you’re that small, the lower jaw might look like tusks? But that wasn’t even my favorite overheard of the day. That honor had to go to a girl talking with her mom about an exhibit on how different animals walked based on their varying body conformations: “But I’m not in my body, I am my body!” I don’t think she was old enough to know quite how hard she was kicking poor Descartes, there. Nevertheless, it works.
And finally, with no segue: shades of Cary Grant’s character in Bringing Up Baby —
This Science Daily article, “Increased Light May Moderate Fearful Reactions,” seems to support an age-old truth: that the dark is scary. I try to be rational. I mean, really rational. But truthfully, when our power was out for two days, and I made the uniquely poor life choice to read the last 100 pages of Blindsight by flashlight while everyone else in my house was asleep.
Objectively, I knew no resurrected genetic vampires were outside of my door. But that didn’t stop me from being afraid.
This study looked at learned fear responses in mice, which is an interesting specification, just as much so in humans as in mice. Behavior and psychology are effected by previous experience, and it’s reasonable to expect that one major factor that would be encoded in a memory would be the level of light or lack thereof at the time the event took place. Therefore, an initial slight instinctive propensity for heightened fear responses in low-light conditions would presumably be strengthened by experience.
The article gives a good explanation of fear as we understand it:
Fear is a natural mechanism for survival. Some fears — such as of loud noise, sudden movements and heights — appear to be innate. Humans and other mammals also learn from their experiences, which include dangerous or bad situations. This “learned fear” can protect us from dangers.
It’s running for 8 more days in Edinburgh. This is problematic on a number of levels, the most obvious being that I have already used up my spontaneous-adventure-vacation for this year on the Shuttle launch in July.
The article I linked to above states that “The show condenses The Selfish Gene into 70 minutes of catchy songs, innuendo and laughs as well as science: no mean feat.” My only question is: WHY is this not already a major genre, à la “space western”?
And before you ask, I have searched extensively and in vain for youtube clips of this show. Where there’s life, there’s hope, I suppose.
(Found via Friendly Atheist)
Time magazine’s “Healthland” blog featured an entry this morning entitled “MIT Scientists Develop a Drug to Fight Any Viral Infection.” Considering the usual level of exaggeration in science journalism, I was really excited to find out that this is based on some pretty solid research.
Of course, as most science articles do (based on anecdotal evidence, to be fair), this one includes, as its second-to-last line, the caveat that the researchers “hope to license the technology for trials in larger animals [and] someday in humans.” So, you’re not likely to see it on shelves tomorrow. Still, to be fair-if-cynical, something that could be as profitable as this, if it does work out, should see further research soon enough.
A habit I’ve picked up over the past few years (and one I hope I can instil in others) is immediately scrolling down until I find the actual peer-reviewed, published research the story is based on (In this case, free! Available to anyone with internet! This is sometimes a glorious age indeed.)
Now, unlike the last paper I talked about here, this one is difficult to get through without at least a little background in the field, so I wouldn’t necessarily suggest that you do so. Even though viruses aren’t my thing, I’ve had enough basic biology and physiology in the last two years that I was able to muddle through with the help of coffee and quiet.
The treatment revolves around inducing cell-suicide among infected cells, and leaving healthy cells alone. This is really, really cool. There are a lot of ways in which your body fights infection. One of these ways is programmed cell death, or apoptosis (which is a way too silly-sounding word to mean what it does, if you ask me).
Apoptosis is triggered by other cells and chemical pathways that aren’t necessarily relevant to what I’m talking about here–suffice it to say that it is a way to get rid of old cells and destroy infected cells. It happens naturally–your body needs to get rid of cells at the end of their life cycle in an efficient and non-traumatic way. Continue reading