Can you believe that your brain is intrinsically unreliable? I can't, I implicitly trust it. I have no choice. In this news release they address one of the great mysteries of nervous function: is "noise" a byproduct of nervous function or does it serve some fundamental purpose?
I used to become very annoyed at people who likened brains to complicated computers. The analogy is so stupid it is hardly worthy of serious consideration yet Artificial Intelligence bods adopted it as a working assumption. They should stick to designing computer games because I'm bored with ones I've got.
As an "information processing" device, and I have great difficulty with that phrase but I won't go there, the brain represents a formidable challenge in understanding its function. This is because......
Saturday, July 3, 2010
Inhibition and Depression: GABA a hidden player?
Initially I was pleased to see this news release because it appeared concordant with my earlier post wherein I explored the angle of depression and arousal. Upon further reflection I realise there are some serious problems with the conclusions put forward in the news item.
Nonetheless this study represents a novel approach to the issue of depression. What they did was create a mouse with a defect in GABA A receptors. GABA A receptors are key receptors in inhibition. GABA is the major inhibitory neurotransmitter in nervous function and is strongly implicated in the etiology of epilepsy. Many drugs for epilepsy aim to increase GABA levels, though there is some recent research which suggest astrocyte release of glutamate may also be implicated in the condition. In relation to depression and arousal though the loss of GABA suggests the potential for excessive arousal. Most anxiety drugs also target GABA. Interestingly, depression and anxiety are often co-morbidities so perhaps GABA does play a role.
The problem I have with this study though is that knock out gene studies are very crude instruments. There is value in such studies but we need to be very careful in drawing too many conclusions from such studies. Why? Because we know next to zilch about how nervous systems function as a whole, so when we introduce such a gross morphological deficit there are potentially any number of possible reasons for the observed effects. So we must rely on the old scientific demand: more research is required.
Nonetheless this study represents a novel approach to the issue of depression. What they did was create a mouse with a defect in GABA A receptors. GABA A receptors are key receptors in inhibition. GABA is the major inhibitory neurotransmitter in nervous function and is strongly implicated in the etiology of epilepsy. Many drugs for epilepsy aim to increase GABA levels, though there is some recent research which suggest astrocyte release of glutamate may also be implicated in the condition. In relation to depression and arousal though the loss of GABA suggests the potential for excessive arousal. Most anxiety drugs also target GABA. Interestingly, depression and anxiety are often co-morbidities so perhaps GABA does play a role.
The problem I have with this study though is that knock out gene studies are very crude instruments. There is value in such studies but we need to be very careful in drawing too many conclusions from such studies. Why? Because we know next to zilch about how nervous systems function as a whole, so when we introduce such a gross morphological deficit there are potentially any number of possible reasons for the observed effects. So we must rely on the old scientific demand: more research is required.
Friday, July 2, 2010
Oils Aint Oils: EPA for Depression
One of the more remarkable features about depression is the number of therapies that have proved beneficial. I explored that issue in this post. This latest study highlights the importance of prostaglandin regulation in depression. This latest study, the largest ever trial on omega 3 fats in treating depression, demonstrates a careful delineation that helps clarify the role of omega 3's in treating depression. The nutshell is this: they focused on EPA, typically at 120mg in your fish oil tablets, and boosted that intake to a big 1000mg per day. That's a lot but given the role of EPA in regulating prostaglandin pathways makes good sense.
Thursday, July 1, 2010
Beatroot Juice for Blood Pressure?
Not really sure that eating lots of nitrates to control blood pressure is a good idea. As the news item states the nitrates are converted to nitric oxide, which is very important in inducing relaxation of the blood vessel muscles, thereby reducing blood pressure. There are 3 major enzymes for producing nitric oxide, iNOS,nNOS,eNOS. i=inducible, typically associated with inflammatory events, n=neuronal, nitric oxide being very important for neural transmission, 3=endlothelial NOS, that which helps the blood vessels relax. Nitric oxide concentrations are tightly regulated and with good reason: it is a potent free radical. Nitrates are a substrate for boosting nitric oxide, perhaps generally, so while it may help with blood pressure it may also upset nitric oxide regulation, induce inflammation, cause free radical damage, and over activate the immune responses, thereby setting the stage for atherosclerosis ... . I suspect it would be better to focus on arginine intake(esp. vs. lysine?) and the let the body work it out. The effect in the below study was within 24 hours, which suggests a strong response. All the more reason to worry.
Tuesday, June 29, 2010
Climate Change, Ecological Novelty, This is not the Age of Aquarius
Generally I prefer to stay away from debates about climate change. I try to perceive the issue in an ecological setting rather than some argument what is going to happen in 50 years if we don't or do do A or B. I have little confidence in our ability to predict the future but I often get the impression that arguments from sceptics and advocates appear predicated on the idea we can make reasonable predictions about future outcomes with sufficient degrees of confidence so as to justify actions A or B. Logically speaking we can't have such confidence, practically speaking if we try we learn something. We might even learn something useful but that's a long shot.
Tuesday, June 22, 2010
Can Diet Reverse Alzheimers?
Hope springs eternal, except when you're dead. (With no Arrow of Time is one eternally dead or eternally alive? Or am I in a box and if God happens to look inside will my fate then be decided? God, don't look!) On the internet there is a cure and conspiracy for everything. Such is the nature of human cognition, a ramshackle attack on reality that through brute force manages to get enough things right amidst the a multitude of errors and disasters. I read Camus in another life and I really must try to start forgetting him.
In our time, studies like this point to strategies that *may* help us. All things considered, it will not be a matter of single strategies or golden elixirs, but rather a lifestyle that incorporates a variety of strategies to minimise the risk of dementia.
If the only significant history of human thought were to be written, it would have to be the history of its successive regrets and its impotences.
The Myth of Sisyphus, page 24I seriously doubt there can ever be a cure of Alzheimers. (At the end of this post though I do suggest one idea that is worthy of serious consideration.) By the time diagnosis is made the damage tends to be extensive. Take Parkinsons Disease as an example, the individual can lose up to 60% of the neurons in the substantia nigra before symptoms arise. In dementias generally, by time of diagnosis a vicious physiological cycle of destruction has become established and at present there is no obvious solution to that problem. There is an increasingly detailed understanding of these processes and in time it will be possible for individuals to institute strategies that can seriously arrest the progression of even advanced dementia; though at that stage of dementia I'd rather take a bullet than pills. Such treatment expectations however are for another generation.
In our time, studies like this point to strategies that *may* help us. All things considered, it will not be a matter of single strategies or golden elixirs, but rather a lifestyle that incorporates a variety of strategies to minimise the risk of dementia.
Saturday, June 19, 2010
Can we all Possess Savant Like Skills?
My friend in New York sent me a link addressing the work of Alan Snyder who for many years has been arguing that within all of us reside hidden talents that can be unmasked through inhibiting certain regions of the brain. He goes so far as to state that this ability can constitute genius, more on that latter. While I have a number of problems with the various assumptions embedded in the ideas of Snyder and his team I also acknowledge that most laypeople operate from the same assumptions and as do many professionals. Nonetheless the perspective of Snyder may have utility and so in the spirit of "News ideas are like seedlings, easily trampled", let's play the game and see what we can learn ...
at
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Thursday, June 10, 2010
Peter Carey You Pretentious Dumbass
Who are these dinosaurs who think they can determine the true measure of intelligence? At the Sydney Writers' Festival one of Australia's most prominent "literary novelists", Peter Carey, whines about how we are turning into a nation of idiots. As regards to the purported dumbing down of our culture I addressed that in this post. Peter Carey might want to learn something about the vagaries of statistical analyses the douchebag. He might also wish to remember that the earliest recorded instance of someone complaining about the younger generation goes back to the Assyrians.
Tuesday, June 8, 2010
New Targets for Anti-Depressants?
This post is very long (3850 words) and very difficult. It is a preliminary investigation of the idea that depression arises from chronic sustained arousal leading to amine depletion and various other physiological changes.
This news release from Science Daily highlights a new pharmacological approach to treating depression. The nutshell is this: there is a class of proteins in our brains called RGS proteins which inhibit the signalling of various neurotransmitters. By manipulating the RGS protein that inhibits serotonin signalling we can treat depression. Most current anti-depressant drugs attempt to increase the levels of serotonin or norepinephrine. Unfortunately there are now some studies emerging which indicate these current anti-depressants can increase the risk to develop a range of disorders, from kidney problems to cataracts. Generally the risk profiles are low but given the very widespread use of anti-depressants it could constitute a considerable public health cost. Which raises an interesting question: if we place our faith in these statistical analyses then is the government entitled to extract an "pharmaceutical externality tax" to address the health risks and subsequent costs associated with drug side effectss? Yeah, like that'll ever happen. We'll develop a new class of anti-depressants, and wait 30 years before we know about the associated risks ... .
My unalloyed cynicism aside, what caught my interest about this research is the reference to RGS proteins. It reminded me I read in 1999:
This news release from Science Daily highlights a new pharmacological approach to treating depression. The nutshell is this: there is a class of proteins in our brains called RGS proteins which inhibit the signalling of various neurotransmitters. By manipulating the RGS protein that inhibits serotonin signalling we can treat depression. Most current anti-depressant drugs attempt to increase the levels of serotonin or norepinephrine. Unfortunately there are now some studies emerging which indicate these current anti-depressants can increase the risk to develop a range of disorders, from kidney problems to cataracts. Generally the risk profiles are low but given the very widespread use of anti-depressants it could constitute a considerable public health cost. Which raises an interesting question: if we place our faith in these statistical analyses then is the government entitled to extract an "pharmaceutical externality tax" to address the health risks and subsequent costs associated with drug side effectss? Yeah, like that'll ever happen. We'll develop a new class of anti-depressants, and wait 30 years before we know about the associated risks ... .
My unalloyed cynicism aside, what caught my interest about this research is the reference to RGS proteins. It reminded me I read in 1999:
Article:
Upregulation of RGS7 may contribute to tumor necrosis factor-induced changes in central nervous function
Journal: NATURE MEDICINE • VOLUME 5 • NUMBER 8 • AUGUST 1999
Friday, May 28, 2010
Immune Driven Psychopathology in Mice?
It all began way back in the 19th century. "Sickness Behavior" was observed in humans and farm animals. As that Wiki article goes on to explain, there are some interesting similarities between sickness behavior and depression. This has been an active area of research for many years now. One key article is this one from 2003. This strange and puzzling linkage between the nervous systems and immune systems has been evidenced by the following:
- Shizophrenia is associated with differing rates of cancer and autoimmune disease from others.
- Epileptics also have altered immunological responses, this possibly driven by hippocampal - fornix - PVN networks(guess).
- Traumatic brain injury can induce a variety of physiological changes, from altered melatonin production to variations in circadian cortisol secretion.
at
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