Science, please‪!‬ noreply@blogger.com (Anonymous)

Have you ever heard of nomofobia, a fear of not being able to check your phone regularly? Are you going crazy when forget your charger home? Have you ever freaked out because you reached an area without reception? Would you return and go home immediately because you left your phone home? You know what we are talking about. But is there an evidence for tools that we use regularly "grow" on us, furthermore, become the part of our body schema? The way we perceive our body is crucial for knowing our place in the world. Literally speaking, the information from our joints and muscles provide the baseline to coordinate our movements and actions. The so called proprioceptive set of stimuli arriving to the central nervous system is often not conscious, but always stored in comparison with other modalities such as visual information (looking in the mirror for eg.). This purely perceptive, on-line, plastic representation of our body is often referred to as 'body scheme' in neurology. The body schema is actually a working model, a helpful one, that can help anchor motor commands to the current position and state of the body. It is transient in nature, and its disturbance can lead extreme cases as described by Oliver Sacks (read on Oliver Sacks's terminal disease here): In that instant, that very first encounter, I knew not my leg. It was utterly strange, notmine unfamiliar. I gazed upon it with absolute non-recognition […] The more I gazed at that cylinder of chalk, the more alien and incomprehensible it appeared to me. I could no longer feel it as mine, as part of me. It seemed to bear no relation whatever to me. It was absolutely not-me – and yet, impossibly, it was attached to me – and even more impossibly, continuous with me . Oliver Sacks: A Leg to Stand On (1991) Body image, however, is the conscious concept about our body, that is "on the surface", it is the summation of the attitudes towards our body, thats one object of the environment. This knowledge is highly semantic and is closely related to our cognitive (I am fat), affective (I am ugly) and behavioural (self-punishing behaviours) interactions with our own self. In fact, as Mahler claims, having a body image is one of the first steps of having a self by differentiating ourselves from our mother.  (Longo et al, 2000).  But how can we connect all this concepts to what is actually happening in the brain? Neuroscientific research is mostly focused on the body scheme, since it is much easier to operationalize in primates. The concept of body map and somatotopic representation (A.K.A humunculus) is one of the first main findings of neuroscience, as it proves the premise of functional localisation in the brain. As Maravita and Iriki describes, the action-specificity of the body scheme (the fact that we fine-tune our movements compared to our position and previous movements) is pinned down to the frontoparietal network. More precisely, the receptive field of the neurons is "bimodal". For example, in a way that they respond with elevated firing rate to sensory and proprioceptive stimuli if it comes from the same "gestalt", the movement of the same limb or body part (interestingly that is not the case with fine movements, finger movement is encoded in a different way). Macaque selfie - strangely relevant to this post  How can we answer body schema-related questions in primates? One clever way of doing it is via tool use: the macaques were put in cages where it was impossible to reach the food that was put outside of the cage, unless they used a rake to pull the food towards themselves. After several days, the neurons of the frontoparietal network, that initially responded to the hand-related visual or proprioceptive information expanded to the rake, but only if the rake was used to grabbing food (only if the ACTION was functional).  source : http://tinyurl.com/oa4x8mz If you want to know how macaques and rakes can explain how you get anxious when your phone dies please li

Sit back and listen to our podcast !!!! Will baby blood hit the anti-aging market? Is the young blood transfusion the new omega 3 / golgi berries for the prevention of cognitive decline? Stanford and Harvard scientists claim so. A new wave of interest was drawn from an old, yet neglected medieval medical technique, where two circulatory systems, one old and one young, were connected in order to refresh the old brain and facilitate its healing and rejuvenating mechanisms. The method, now fancily called heterochronic parabiosis, has recently been brought back to scientific focus for one simple reason: it looks like its working. source: http://tinyurl.com/qcr9bwy The neurological decline and associated cognitive deterioration experienced during healthy ageing as well as neurodegeneration is one of the biggest mysteries in neuroscience. It seems like we cannot point out a single, culpable black sheep from the several factors that accounts for the progressive decline in the end of life. Rather, it is more likely that there is a cascade of "little things going wrong" that leads to the decline in overall performance. This is exactly why counteracting or slowing down this progress is not an easy task.  It is not surprising that a method offering an all-purpose "cure" against old age will rob the bank, especially if it can have headlines such as Vampire therapy of ageing, and put Fifty shades of grey ads in the corner. 2014 was the year of young blood. I mean, apart from the season finale of True Blood, Katsimpardi and colleagues (2014) stitched an old and a young mouse together to connected their circulatory systems. This was not only beneficial for the vascularisation of the old brain compared to the young one but also upregulated the neurogenesis in one of the areas of the brain known for its role in the memory formation, the hippocampus. Pretty fascinating stuff, because it implies that we can now fight ageing in two ways: 1) better circulation in the brain (hence more food and oxygen to the neurons, and less probability of a stroke) and 2) more neurons in the area that is most likely to be the correlated with the contextual memory (decline). However, there is a rather big jump between the experimental evidence and literature review of possible candidate mechanisms to put behind all these effects. The authors finally pulled out the chocolate sprinkle (see the podcast) of growth factors called GDF11 to test on their parabionts. However, GDF11 is, according to my knowledge, too big a protein to cross the blood brain barrier (its concentration was not measured, it was only administered in the brain as a separate experiment). This does not mean that it cant account for a lot of circulatory beneficial effects, but I cant necessarily see the direct connection with the neurogenesis. The authors themselves highlight overall effects saying  This suggests that neural stem cells exposed to young systemic factors increase their ability to proliferate and differentiate into neurons. (highlighting by me if you cant tell form the shade of purple immediately :P) Hhmmm...anyway... Are these newborn neurons functional parts of the network; can we correlate their operation with physiological and behavioural improvement? Stanford suggested that we can. This paper is an old-school, all rounder evaluation of the vampire approach, so much so that they are not even stitching the bellies together, just transfusing the serum of young mouse to older ones. Clever move, not just because it helps the PR part (stitching together old people with babies, not my dream advert for rejuvenation therapy), but it also makes the implementation easier. They also started by looking for the 'it' factor of rejuvenation by performing a genome-wide microarray analysis of the old and young hippocampi in the parabiont mice. They found a rather good chocolate sprinkle called Creb (cyclic AMP response element–binding protein), that is known for regulating game-changer

Is there really anything we can do to prevent cancer; are we better packing it up and conceding that at some point we will all succumb to the emperor or all maladies? A well reported paper by the media last week in the journal, Science, does appear to have suggested this, and is surely a rude surprise to cancer researchers globally (including myself)! The paper in question found that 2/3 of the lifetime risk of developing cancer could be explained by only the random errors that accumulate overtime when cells replicate. This is indeed a shocking finding, but lets unpack it a little and see whether it is really saying all it has been reported as in the media - hint, it is not! Recent article reports cancer is due to mostly stochastic errors in cell divisions. Lung cancer, however,  falls out of this category, hence it cannot be explained solely by the luck factor. source :http://tinyurl.com/okdtt3w Firstly, the study accounts for 31 cell-types in its analysis and measured the association with the corresponding physiological location, a far cry from having considered cancer as a whole. In fact, common cancers such as breast or prostate were omitted. Explicitly, the study took stem cells (the basic building block for cells of all types) from these organs and estimated the number of cell replications that a particular organ would likely undergo in a single lifetime. The premise is that different organs will require different rates of cell replication just for the mainantance of the baseline function. Each time a cell replicates there is a certain probability that an error will occur that may or may not lead to cancer, and so organs that duplicate more should be more likely to observe cancer risk - and this is what they observed by correlating the estimate of cell replication with lifetime risk. However, lets quickly remember an old adage "correlation does not equal causation". It is difficult to suggest that this correlation is anything more than a very plausible association, and it is certainly not appropriate to suggest that this correlation rules out factors that we can affect like diet and lifestyle. More skepticism should also be given to the result as it didn't include the most common cancers that would be household concerns like prostate and breast, and so suggesting as the media did that cancer as a whole is stochastic is wholly misleading - such descriptions of cancer as one homogenous entity is just flat out incorrect, and will I'm sure be the topic of a future post! We should note also that the study inferred mutation rates that likely lead to cancerous cells from the estimated number of cell divisions, and did not explicitly measure said mutations. While this is an acceptable method for a paper, it is so only in the knowledge that average mutation rates will not be useful for predicting individual cell DNA mutations, and further, not all mutations lead to cancer - so we cannot say that these cell replications will predict with a large degree of accuracy which cell will have which mutation, and whether it will be cancerous. The final passage of the paper discusses how this correlation can be useful when deciding how to direct research funding and public policy. They use a clustering algorithm to group the cell types they used into two categories: largely driven by random mutations, and largely not driven by random mutations. The suggestion is that research should be directed to discovering modifiable risk factors (diet and lifestyle, etc) for only those cancers where they will be likely to be found. In the light of the caveats I raise with interpreting their findings, I hope it will not be a surprise that I am worried greatly by their claim that the single correlation should drive policy! Cancer is an umbrella term for a set of very complex and harmful diseases, and research should be driven by a more robust set of results with careful analysis than these. For our podcast discussing this article look here: https://