What does that MRI signal MEAN, anyway?

Sci was incredibly excited to see this paper come out. It’s got lots of stuff going for it, and all its powers combined were enough to send Sci bouncing around in her seat and sending emails to Ed Yong saying “OMG COOL PAPER!!”.
What’s it got, you say? It’s got the meaning of life, the universe, and that pesky MRI signal.
ResearchBlogging.org Lee et al. “Global and local fMRI signals driven by neurons defined optogenetically by type and wiring” Nature, 2010.
Ah, the pretty brain picture. But what does it MEAN?

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Binge Eating, Bulimia, and Reward Sensitivity

You all may remember that Sci’s recent posts have focused on eating, overeating, and dopamine. Today, Sci continues this trend. Honestly, she couldn’t stop thinking about it. How is overeating like addiction? How is it different? And so she began to look up a bunch of papers on binge eating and dopamine.
I was particularly interesting in the changes in food intake and reward associated responses in people with eating disorders like bulimia nervosa and anorexia nervosa. There are many hypotheses as to why these eating disorders exist, ranging from problems with society (which can certainly contribute to the incidence of the disorders), to hypotheses of obsessive control akin to the compulsions seen with OCD, to increased sensitivity to reward, to decreased sensitivity to reward.
This increased/decreased sensitivity to reward (some people have seen decreased sensitivity to reward in rats, along with increased self-administration of pleasurable things, but what this actually translates to in humans can be difficult to interpret) was particularly interesting, and so Sci was very glad when she came across this study.
ResearchBlogging.org Schienle et al. “Binge-Eating Disorder: Reward Sensitivity and Brain Activation to Images of Food “, Biological Psychiatry, 2008.
(Sci will admit her brain activated really hardcore looking at that. Soooo much chocolate…)

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Part 3 of Welcome to MY Brain: The rest of the bits and pieces.

Welcome to part 3 of Welcome to my brain! Apparently everyone is very impressed by how hot my brain is (see parts one and two), but unfortunately, we’re almost out of pics. Today we’re covering the rest of the bits of my brain that look really awesome, which really boils down to all the ones you wouldn’t be able to see if you were just looking at the outside. And it turns out that Sci has a LOVELY basal ganglia. She is thrilled by this, the basal ganglia is her favoritest part of the brain.
First, a note: those cross-hairs that you’ve been seeing all the time are features of the analysis program, apparently, and can’t get taken out. Blah. But we shall forge ahead!

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Part 2 of Welcome to MY Brain! Of mater and brain holes.

Ok, so I thought I would be able to do this brain stuff in TWO entries, but I think it might have to be three. After all, the brain is a wondrous, glorious world of awesome, and MY brain in particular is especially nice. Last time I talked about the outer features of the brain and the division of the brain into traditional lobes of form and function. So today I’m going to give a brief intro to things with arcane sounding names, like dura mater and the choroid plexus, and talk about why it’s ok that your brain is full of holes.
So let’s begin!
The Maters

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Part 1 of Welcome to MY Brain! Introduction and general features

Some of you may recall that I got my brain scanned in an MRI for the sake of science. Well, my lovely fellow grad student was nice enough to send me some of my baseline pictures! I think I have a lovely brain (see my new profile pic? I’m totally hot, right?), and so I thought I would share some of it with you. Besides, I blog a lot about basic (and not so basic) neuroanatomy, and so we can use hot pics of Sci’s brain to give you some insight into areas of the brain that are popular in science today.
And just to scratch the surface:
Picture 10.png
I’ll be dividing these posts into two parts, the first with general features and terms, and the second one for some of the interior features that happened to come out really well on my scan.

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Promising Effects of Statins on Alzheimer’s Pathology

Finally we get some data on changes in AD pathology with statin use! Statins are taken for lowering cholesterol, but they have other beneficial effects such as modulating inflammatory responses. Thus, they could prove beneficial in the treatment of AD given the disease has a significant inflammatory component.
According to the press release

The two changes in the brain that are considered the most definitive hallmarks of Alzheimer’s are brain “plaques” and “tangles.” After controlling for variables including age at death, gender, and strokes in the brain, the researchers found significantly fewer tangles in the brains of people who had taken statins than in those who had not. “These results are exciting, novel, and have important implications for prevention strategies,” said senior co-author Eric Larson, MD, MPH, the leader of the ACT study and executive director of Group Health Center for Health Studies. “But they need to be confirmed, because ACT is not a randomized controlled trial.”

As the press release rightly points out

A randomized controlled trial of statin treatment and brain autopsy findings would be problematic for ethical and practical reasons, said Dr. Larson. But the ACT setting made the study more rigorous than previous observational epidemiological studies, because it uses reliable automated pharmacy records, is based in a community population, and includes autopsies in people both with and without dementia.

so don’t expect any prospective comparisons anytime soon. Or, ever. However, this study appears promising as it backs up the epidemiological data. I’ll have to see if I can get my hands on the actual paper and post about it.

Everybody Post About Mirror Neurons!!!

Mixing Memory brings up some excellent points regarding mirror neurons in primates, and Frontal Cortex follows up with his thoughts. To both of them I say “bravo, but your skepticism probably doesn’t go far enough”.
We give Rizzolatti et al too much credit with their conclusions. After all, they’ve only demonstrated the existence of mirror neurons in monkeys. Due to the obvious inherent difficulties associated with recording from human neurons in vivo, no one has yet (to my knowledge) published anything that demonstrates the existence of mirror neurons in people. Instead, we stick people in scanners and infer that they have mirror regions, or mirror neural systems, that are at least in part composed of mirror neurons. These regions are associated with language and imitation, but any evidence that mirror neurons are involved with either behavior in humans is circumstantial at best.

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Stem Cells for Spinal Cord Injuries

The difficulty with treating spinal cord injuries arises from a number of factors. Firstly there is the primary damage to the axons of the spinal cord itself, resulting in mechanical damage that can inhibit neurotransmission and transport of cellular material to and from the distal cord. The damaged cord must also compensate for secondary damage such as the generation of free radicals, a lack of oxygen to the affected area (anoxia), glial scarring, and a host of other issues.

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Pesticide-induced dysfunction of dopaminergic neurons

Shelley mentioned a study last week that suggested more and more young people are getting Parkinson’s Disease, and she wondered whether there was any utility in blaming our industrialized society based on the fact that certain compounds we produce can induce Parkinsonian symptoms. Let’s start by giving a brief overview of the systems involved before we attempt to answer that question.
The substantia nigra contains a collection of dopaminergic neurons that project to the striatum. Integrity of this pathway is essential for normal motor function, although this nigrostriatal system is capable of compensating for cell loss until it loses around 80% or more of its neurons. Loss of these neurons is one of the central features of Parkinson’s Disease, which for the most part has no known cause (idiopathic PD). There are some notable famous exceptions such as the boxer Muhammed Ali who likely had his triggered from repeated blows to the head, and a set of cases that developed in individuals exposed to MPTP, a byproduct of a street chemist’s failed attempt to produce a Demerol-like compound. MPTP is metabolized into MPP+, which is toxic to dopaminergic neurons and can cause a human to basically develop a PD-like disease after a few days of exposure.
Interestingly, some herbicides are now under scrutiny for a potential causal role in PD. One such example is Paraquat, which has a structure similar to that of MPP+

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