Friday, 11 January 2013

Accepted model for brain signaling flawed

A new study out January 10 in the journal Science turns two decades of understanding about how brain cells communicate on its head. The study demonstrates that the tripartite synapse -- a model long accepted by the scientific community and one in which multiple cells collaborate to move signals in the central nervous system -- does not exist in the adult brain.
(Credit: Image courtesy of University of Rochester Medical Center)

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Friday, 21 September 2012

The Neuroscience of Idle Minds

This article explains how the brain is active when at rest and considers the implications of this. 

There is a myriad of activity occurring in our brains, even as we sleep. It is important to distinguish, however, between brain activity and conscious thoughts. Just because a person is having (or thinks he is having) no conscious thoughts, or even if he is unconscious, there is still masses of activity flowing through his brain. 

I think they will find that while our brains rest - whilst we are lounging idly on the sofa, for example - our brains are consolidating memories formed throughout the day. So, it's probably best to take a break after studying and do nothing, rather than watch TV, or socialise, even. 

I also reckon memories aren't, as previously thought, merely set pathways through which a current flows which make up a conscious recall of a stimulus. I think they can change, and perhaps 'exist' in many places at once, constantly being reformed and manipulated through processes such as neuroplasticity. 

It is also suggested that the brain can reuse past experiences to 'prime' connections which may be useful in the current situation. For example, if we are crossing a busy road, not only would we be consciously aware that we are in danger, but the motor sections of our brain would be primed so that we are more prepared to dodge that oncoming bus. 

I particularly like the analogy: 
If your car is ready to go, you can leave faster than if you have to turn on the engine.
The brain is surprising similar to any other machine; yet vastly different and infinitely complex.  

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Monday, 10 September 2012

Did Your Brain Make You Do It?

There seems to be a phenomenon prevalent across much of Western society. People don't like to accept responsibility for their own actions when they've done something wrong. They'd much rather say it that their actions were due to "a complex sequence of chemical reactions within my brain", over which they, supposedly, had no control, and therefore it's not their fault - they're innocent. Of course, the premise is true - we, and all our actions, are the result of various biochemical reactions throughout our bodies. However, that doesn't mean that they're not in our control. That's loosely analogous to saying, "Oops, my car lost control and killed someone - but it was the road conditions; there was nothing I could do." (Yes, it makes no sense)

But what about if our driver had lost control, but instead of killing someone, had collided with another car and changed it's course, when that other car would otherwise have hit a pedestrian? It's unlikely then that the driver would attribute the events to road conditions out of their control. No, they would claim it was their own fast thinking, bravery and heroism that saved the pedestrian's life.

It's nothing new, this phenomenon. It's part of a standard sixth-form psychology course, dubbed 'situational factors' vs 'dispositional factors', or 'self-serving bias'.

However, this likely only applies to Western societies - more collectivist societies would likely attribute their errors to themselves (that is, if they knew that their every move is the result of the workings of the brain). That is because they have a more utilitarian approach; they care more about the good of the society than the consequences they themselves may face. 

My point is, it's a cultural phenomenon, not a neuroscientific one. It's about whether people see themselves as a living being forming a part of a group of living beings for which they are partly responsible; or as an individual biological organism reacting with other individual biological organisms. Of course, both views are true - thus, neither are valid as an argument. You can never say "my brain made me do it" and you can never say "it was my fault, not my brain's", since both are equally true. It just depends how you look at it. 

Pointless argument, really. 

(N.B. I'm referring to adults here, not adolescents whose brains may or may not have fully developed self-control abilities. But this poses a further question - who decides what "fully developed self-control abilities" are? All brains are different, ergo, people have varying "self-control abilities". Do people turn 18 and suddenly reach a baseline level of self-control?)

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Wednesday, 22 August 2012

Common parasite that lives in the bodies of 10 - 20% of Americans linked to a sevenfold higher risk of attempted suicide
Testing positive for a common parasite that lives in the bodies of 10 - 20% of Americans is linked to a sevenfold higher risk of attempted suicide, according to new research.

I found this article pretty interesting since it furthers the hypothesis that depression is a biological disorder with real, physiological, biochemical roots. It proposes that inflammation and other effects within the brain caused by a common parasite which up to 1 in 5 people host can lead to a drastically increased "risk of attempted suicide".

However, I would like to know exactly what this means. The supposed "risk" is measured on a "suicide assessment scale" - but surely the risk of suicide is something which is subjective to each person. Also, the perception of the "risk of suicide" in the subject could vary greatly depending on the background and/or mental health of the person evaluating the risk.

One must also bear in mind that the sample only included 84 people - 54 attempted suicide patients and 30 controls. All were adults. I'd expect to see a sample of at least a few hundred for a study like this.

Nonetheless, this paves the road for a whole new area of study - the physiological effects of parasites on the brain and the psychological impact of these effects.

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Thursday, 24 May 2012

Doubts regarding research suggesting that “A Very Sugary Diet Makes You Stupid”

Read the article(s):

I have some doubts about the conclusions reached in this research.
“As a control, the animals were fed on standard rat feed for five days before the fructose diet started. They were also trained on a maze twice per day and tested to see how well they performed. They also placed visual markers in the maze to help the rats remember their way around.”
 Gomez-Pinilla recounts his experience of testing the rats after six weeks on the sugary diet:
    “The second group of rats navigated the maze much faster than the rats that did not receive omega-3 fatty acids … The DHA-deprived animals were slower, and their brains showed a decline in synaptic activity. Their brain cells had trouble signaling each other, disrupting the rats’ ability to think clearly and recall the route they’d learned six weeks earlier.”

Maybe, rather than omega-3 fatty acids negating a negative effect of fructose on synaptic activity, omega-3 combined with fructose may have enhanced activity and protected from damage to the synapses, leading to the rats’ increased performance in the maze tests.

“Our findings suggest that consuming DHA regularly protects the brain against fructose’s harmful effects …”

The researchers appear to have arrived at the conclusion that fructose (in abundance?) may have negative effects on cognitive activity and memory. I don’t believe that the results of this experiment necessarily point to this conclusion.

Both groups of rats were fed fructose, with the second group also being fed omega-3 fatty acids in the form of flaxseed oil and docosahexaenoic acid (DHA)
There should have been a further control group which was not fed fructose at all, to compare the other two groups against. This would determine whether fructose had any effect on the rat’s brain and performance in the maze tests, prior to investigating any effect that omega-3 fatty acids may have in “negating” this effect. Instead, the researchers gave fructose solutions to both groups of rats.

The UCLA article also suggests that the first group of rats, who did not receive omega-3 fatty acids, may have developed a resistance to insulin:  

"The DHA-deprived rats also developed signs of resistance to insulin, a hormone that controls blood sugar and regulates synaptic function in the brain. A closer look at the rats’ brain tissue suggested that insulin had lost much of its power to influence the brain cells."
"He suspects that fructose is the culprit behind the DHA-deficient rats’ brain dysfunction. Eating too much fructose could block insulin’s ability to regulate how cells use and store sugar for the energy required for processing thoughts and emotions."

I believe that this is the more appropriate route for the experiment to proceed. However, it is unclear whether it is fructose itself that is responsible for the DHA-deprived rat’s lower performance, or an interaction between insulin and fructose in the absence of omega-3 fatty acids.

More research should be done to determine an effect of fructose on the rats’ brain and performance, compared against a baseline, control group of rats who are not fed fructose solutions.

Nonetheless, it is known that omega-3 fatty acids protect the brain and enhance cognitive function and memory. However, it is not correct to conclude from this article that fructose has any negative effect on the brain.

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Friday, 11 May 2012

Neurotransmitters Identified That Lead To Forgetting

Read the article:

Just some thoughts;

This also might be a strategy for developing drugs to promote cognition and memory – what about drugs that inhibit forgetting as cognitive enhancers?"

But surely forgetting is essential for normal day-to-day functioning? Remembering too much trivial information about your day would undoubtedly be undesirable, and maybe this “information overload” leads to some of the undesirable symptoms of savantism.

Also, considering dopamine’s known roles in the reward-pathways, perhaps savants get a “kick” out of learning excessive amounts of information, due to a faulty dopamine receptor/mechanism (DAMB), or an overactive dDA1?

Perhaps this research could have implications for dementia, too.

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Friday, 20 April 2012

The Future of Neuroscience: Changing The Brain to Enhance…

I thought I’d write a post concerning my disapproval of this article. It seems to be a running theme that I disagree with articles from PsychCentral.

“Changing The Brain to Enhance Well-Being, Happiness”

The article basically states what has been long known – that physical exercise, certain forms of psychological counseling (for some people) and meditation can all increase our well-being. That’s all well and good.

Then comes the part I don’t like: 

“The study reflects a major transition in the focus of neuroscience from disease to well-being.”

I think neuroscience is a great, fascinating subject which has a promising outlook for the near future, with beneficial applications such as the treatment of disease and the study of the human brain/mind. However, when we start using neuroscience to improve our “well-being”, we introduce a plethora of potential dangers and moral issues.

The goal is “to use what we know about the brain to fine-tune interventions that will improve well-being, kindness, altruism. Perhaps we can develop more targeted, focused interventions that take advantage of the mechanisms of neuroplasticity to induce specific changes in specific brain circuits.”

Not only is this sort of research reducing the time spent researching treatment for diseases such as Alzheimer’s and Parkinson’s (which is much more important at the current time) it also represents the start of a revolution – the designer-brain revolution. Digressing from the article (although relevant), it won’t be long until we can purchase “add-ons” to enhance our well-being, intellect, kindness, altruism etc. “Add-ons” could also be developed to add “additional-features” to the brain, much like add-ons for Firefox.

People will be purchasing these add-ons to enhance their ability; to gain the upper-hand and improve their lives. However, it can be dangerous to modify nature, especially when it comes to the brain. Since the brain is such a complex organ and is fundamental to our conscious existence, tinkering with it could be dangerous in both the short-term and long-term. Of course there will be years of testing before these add-ons are released, but every brain could react differently, and we might not know the long-term dangers until it’s too late.

More importantly, the moral implications are huge. I can imagine various religious groups objecting to the “designer-brain” revolution on the grounds that it is “playing God”. Although I’m not religious myself, I can see where they’re coming from. We are, in effect, tinkering with thousands of years of evolution. Sure, there are many ways in which the human brain/body can be improved for the better. This, however, is a far beyond therapeutic applications.

For a start, the first to get their hands brains on these “add-ons” will surely be the rich. Instantly, we can see that those in power with modified super-brains could leave us all slaves to the authority. Politics would undoubtedly see a shift to the right. However, once these “add-ons” become more readily available, anyone will be able to buy them. At first, it’ll require surgery to install them; but soon enough, you’ll be able to install them yourself at home. Also, much like add-ons for Firefox, there could be a whole market of 3rd-party add-ons (“Make Me Happy V1.0″, designed by “dodgydesigner666″ on “BrainBay”, for example). Whether illegal or not, a black market of brain add-ons would undoubtedly lead to numerous deaths. Plus, your purchased add-ons could be riddled with viruses which upload your thoughts/personal informations to a crook’s (or government’s) inbox. This might be taking the computer-brain analogy a little too far, but you see my point.

Back to the ethical implications, the “designer-brain” revolution could lead to a break-down of society. People would be purchasing these add-ons to “better” themselves intellectually. This would lead to a social divide between those who can access the add-ons (who would become super-intelligent, with the highest-earning careers) and those who can’t (who, well, wouldn’t). People might also purchase these add-ons to improve their well-being. I’m not sure how to put this, but that just doesn’t seem right. There are reasons we don’t always feel great. Negative emotions can be a positive thing – they can help us to realise errors we may have made, and thus we can begin to work on amending them. With these add-ons, we may not feel the need to amend our mistakes, and they’d be repeated. For example, if a person experiences negative emotions as a result of failure, these emotions will (eventually) give them the motivation to make the change, and work on amending their mistakes and achieving to the best of their abilities. Also, to me, achieving to the best of our ability is something we should have to work for. If one person can purchase an add-on to increase their chances of success, then of course that’s unfair on those who haven’t  purchased the add-ons, whether due to choice or not.

This brings me onto my next point. If people are purchasing these add-ons and becoming super-intelligent, sooner or later people will realise that they need to buy them in order to keep up. It doesn’t become a choice anymore, it becomes an obligation to artificially modify your brain. There comes a time when free-will is out the window. With everyone installing “add-ons” into their brains, who’s to say their designers couldn’t be paid to design the add-ons so that their users can be manipulated, and their personal information shared with crooks/the government? We like to think that these things couldn’t, and wouldn’t, happen – but in reality, of course they can.

As Dieter Birnbacher, a philosopher at the University of Düsseldorf in Germany, says: 

"There are risks in technological self-improvement that could jeopardise human dignity. One potential problem arises from altering what we consider to be “normal”: the dangers are similar to the social pressure to conform to idealised forms of beauty, physique or sporting ability that we see today. People without enhancement could come to see themselves as failures, have lower self-esteem or even be discriminated against by those whose brains have been enhanced”, Birnbacher says.

He stops short of saying that enhancement could “split” the human race, pointing out that society already tolerates huge inequity in access to existing enhancement tools such as books and education.

Everybody will enhance theirself to fit what they believe to be correct – what they believe is best for them and society. However, this would drastically affect relations between different cultures – some cultures will be much more advanced than others, and cultures would be much more separated than they are today. This would not only jeopardise international relations, but also the global economy.

I realise that some of my points may be a little far-fetched, but nonetheless, you can see my point. This is all potentially possible.

The world as we know it is changing. (Can you keep up? Buy the latest add-on to inhibit your anxieties and denial and induce a zombified state of acquiescence)

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Wednesday, 4 April 2012

What Your Facebook Account (doesn’t say) About Your Brain

Although I couldn’t find the original papers, after reading this article, I just had to say (write) something. It is the biggest piece of tosh I have read in a while, courtesy of the field of “psychology”.

The article suggests that people who have more friends on Facebook have a larger orbital prefrontal cortex. It then goes on to say that this region of the brain is involved in “complex cognitive processes”, thus implying that using Facebook is a “complex cognitive process”. While I don’t dispute that it is often difficult to keep track of “who is sleeping with whom, who is making alliances with whom”, I would by no means consider this a complex cognitive process. Yet the article appears to suggest some sort of relationship between the number of friends a person has on Facebook and “complex” cognition, suggesting that those with more “friends” are somehow smarter than those with fewer. I would argue on the contrary – those who spend more time on Facebook and less time doing something worthwhile (like complex cognitive processes) are less likely to be smart, surely.

Just a further point, before I go on, the article claims:

“Establishing and maintaining many social relationships requires a great deal of brainpower.”

It may indeed, in reality. I wouldn’t, however, say this was true of “virtual” friends on Facebook. If a person has over 1000 friends, say, on Facebook, are they really keeping track of every single one of them? I highly doubt it.

The article goes on to say that research has shown that monkeys and apes who live in large social groups tend to have larger brain size, specifically of the prefrontal cortex. This is probably true, but again, I point out that Facebook is NOT the same as normal socialising. It definitely isn’t the same sort of socialising the monkeys in the research were doing. Thus, this comparison is invalid.

Furthermore, the article says that:

“…people with larger social networks (including the number of friends on Facebook) also have a larger amygdala (a brain region involved in emotion regulation).”

This seems to imply that people with more friends on Facebook are somehow more emotionally active. I would argue the exact opposite. From my experience, those with many friends on Facebook (>1000) are less emotionally active. They probably have a shallow knowledge of these “friends”, adding them after meeting them once at a party, and then never speaking to them again. How much do they actually communicate with these people, on an emotional level? Not much, I would argue. Besides, I would consider those with a large number of Facebook friends somewhat shallow, trying to show off their “popularity” to their 7364 “friends“.

I don’t know, maybe my dislike for Facebook has influenced my opinions, being a Twitter user myself. Personally, I don’t have many Facebook friends (around 100), since I feel this makes my experience on Facebook more personal. I have more meaningful virtual contact with my friends, rather than being bombarded with “relationship statuses” from people I barely know.

So, does this mean I have a smaller orbital prefrontal cortex? Am I less intelligent as a result? Or do I have a smaller amygdala? Am I less emotional?

I don’t think so.

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Tuesday, 20 March 2012

Antioxidants Appear No Help for Alzheimer's

Antioxidant supplements don't appear to have an impact on cerebrospinal fluid (CSF) biomarkers related to Alzheimer's disease, a clinical trial determined.

The combination of vitamin E, vitamin C, and alpha-lipoic acid did not lower levels of the amyloid and tau proteins that make up the plaques and tangles seen in the brain with Alzheimer's disease, Douglas R. Galasko, MD, of the University of California San Diego, and colleagues found.

The combination did reduce CSF levels of the oxidative stress biomarker F2-isoprostane by 19% but raised a safety concern with faster decline in cognitive scores, they reported online in the Archives of Neurology.

The popular antioxidant coenzyme Q (CoQ) had no significant impact on any CSF measures in the Alzheimer's Disease Cooperative Study antioxidant biomarker trial.

Oxidative damage is widespread in the brain in Alzheimer's disease and contributes to neuronal damage, Galasko's group explained.

Some prior observational evidence has pointed to lower Alzheimer's risk with an antioxidant-rich diet, although prevention trials with supplements have had mixed results, they noted.

Their study included 78 adults with mild to moderate Alzheimer's randomly assigned to double-blind treatment over 16 weeks with the combination of 800 IU vitamin E, 500 mg vitamin C, and 900 mg of alpha-lipoic acid once a day; CoQ alone at a dose of 400 mg three times a day; or placebo.

Vitamins C and E act as antioxidants by controlling dangerous free radicals produced when oxygen reacts with certain molecules, while alpha-lipoic acid spurs production of many antioxidant enzymes in the body. CoQ is an antioxidant that helps protect mitochondria from oxidation.

Serial CSF specimens collected from 66 of the participants showed only small changes from baseline.

Beta-amyloid 42, which accumulates to forms plaques in the Alzheimer's brain, declined by 8 pg/mL from a baseline of 190 pg/mL with the antioxidant combination and by 15 pg/mL from a baseline of 185 in the CoQ group, but neither was a significant difference from placebo.

Tau protein, which forms neurofibrillary tangles in the brain with Alzheimer's, fell by 23 pg/mL with the antioxidant combination from a baseline of 123 and by 9 pg/mL from a baseline of 109 in the CoQ group, but again neither differed from changes with placebo.

Levels of tau phosphorylated at a specific site (P-tau181) likewise declined slightly over the study period for the two antioxidant groups but without a significant difference from placebo.

The one significant change was in CSF levels of the oxidative marker F2-isoprostane, which is stable oxidized arachidonic acid.

The vitamin C and E plus alpha-lipoic acid group saw a 7 pg/mL reduction in F2-isoprostane from a baseline of 38 over the 16 weeks of treatment (P=0.04). The other groups showed no change.

"It is unclear whether the relatively small reduction in CSF F2-isoprostane level seen in this study may lead to clinical benefits in Alzheimer disease," the group cautioned.

Cognition, measured with the Mini-Mental State Examination, didn't improve in any of the groups. In fact, the decline in scores appeared accelerated in the antioxidant combination group, with a change of -4.6 points over the 16 weeks compared with -2.3 to -2.4 in the other two groups.

The researchers highlighted that as a potential safety concern that needs further careful assessment if longer-term trials are considered. The antioxidants were otherwise well tolerated.

Function, as measured on the Alzheimer's Disease Cooperative Study Activities of Daily Living Scale, didn't change in any group.

Galasko D, et al "Antioxidants for Alzheimer disease: a randomized clinical trial with cerebrospinal fluid biomarker measures" Arch Neurol 2012; DOI:10.1001/archneurol.2012.85.

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Promising new research on Huntington's disease

Huntington's disease is a dreaded and debilitating congenital neurological disorder. There are little successful treatments and no cure. But a special type of brain cell forged from stem cells could help restore the muscle coordination deficits that cause the uncontrollable spasms characteristic of the disease.

"This is really something unexpected," Su-Chun Zhang, a University of Wisconsin-Madison neuroscientist said.

Zhang and his colleagues at the UW-Madison Waisman Center have learned how to make large amounts of GABA neurons from human embryonic stem cells, which they sought to test in a mouse model of Huntington's disease. The goal of the study, Zhang notes, was simply to see if the cells would safely integrate into the mouse brain. To their astonishment, the cells not only integrated but also project to the right target and effectively reestablished the broken communication network, restoring motor ability. It showed that locomotion could be restored in mice with a Huntington's-like condition.

What researchers found was intriguing, because GABA neurons reside in one part of the brain, the basal ganglia, which plays a key role in voluntary motor coordination. But the GABA neurons exert their influence at a distance on cells in the midbrain through the circuit fueled by the GABA neuron chemical neurotransmitter.

"This circuitry is essential for motor coordination," Zhang said, "and it is what is broken in Huntington patients. The GABA neurons exert their influence at a distance through this circuit. Their cell targets are far away."

That the transplanted cells could effectively reestablish the circuit was completely unexpected: "Many in the field feel that successful cell transplants would be impossible because it would require rebuilding the circuitry. But what we've shown is that the GABA neurons can remake the circuitry and produce the right neurotransmitter."

The study suggests that it may one day be possible to use cell therapy to treat Huntington's, but also because it suggests the adult brain may be more malleable than previously believed.

Zhang stresses that while the new research is promising; working up from the mouse model to human patients will take much time and effort. But for a disease that now has no effective treatment, the work could become the next best hope for those with Huntington's.

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