Saturday
Apr222017

Bumblebees playing soccer – an example of behavioral flexibility and social learning in insects

Have you ever seen bumblebees playing soccer? In a recent study done by Loukola et al. [1], bumblebees were taught to transfer a ball in marked location and bees were rewarded after a successful performance. The aim of this study was not only to enjoy some nice playtime with bees but also to observe behavioral flexibility and social learning. Social learning is a phenomenon in which a new behavior is learned by the observation and imitation of others, whereas behavioral flexibility is considered to reflect one’s ability to change a pattern of behavior and create novel solutions to a problem. These features are thought to be common in mammals and birds, but are not well understood in insects.

By observing how bumblebees learned to play soccer, it was found that social learning is the best way for bees to learn the game [1].  Bees were not only copying the demonstrated ball transport method but also, were able to improve upon learned methods and develop more a convenient approach[1]. This kind of behavioral flexibility has not been noted before in insects, although behavior and cognition of insects has been widely studied [2,3]. But back to our first question; if you have not seen how a bee plays soccer, check out the videos from the supplementary material of Loukola et al. (http://science.sciencemag.org/content/355/6327/833), or see collected clips https://www.youtube.com/watch?v=ToZDCo51c_I

- JR 


References:

[1] Loukola OJ, Perry CJ, Coscos L, Chittka L. Bumblebees show cognitive flexibility by improving on an observed complex behavior. Science. 2017, 355(6327):833-836. doi: 10.1126/science.aag2360.

[2] Chittka L, Niven J. Are bigger brains better? Curr Biol. 2009, 19(21):R995-R1008. doi: 10.1016/j.cub.2009.08.023.

[3] Giurfa M. Cognition with few neurons: higher-order learning in insects. Trends Neurosci. 2013, 36(5):285-94. doi: 10.1016/j.tins.2012.12.011

Monday
Apr172017

An early event in Autism Spectrum Disorder: Increase in Brain Surface Area

Observations of increased brain size and head circumference in autism spectrum disorder (ASD) are certainly nothing new [1, 2], with previous work having suggested accelerated growth rates as potential early warning signs of risk of ASD [3]. However, an interesting study published in Nature reports additional evidence, including timing of this event and its relationship with behavioral symptoms [4].

 Hazlett and colleagues conducted a prospective anatomical MRI study of infants at high vs. low familial risk of ASD and found evidence that early post-natal hyper-expansion of cortical surface area may play a role in the development of ASD [4]. Furthermore, this cortical surface area increase (which was observed between 6-12 months) was linked with increases in total brain volume (at 12 - 24 months) and social deficits (at 24 months).

 In terms of potential underlying mechanisms the authors discuss previously suggested mechanisms such as increase proliferation of neural progenitor cells, increase in number of mini-columns and decreased pruning.

 - NRZ

 

 References

 - Piven, J. et al. An MRI study of brain size in autism. Am. J. Psychiatry 152, 1145–1149. 1995.

- Courchesne, E. et al. Unusual brain growth patterns in early life in patients with autistic disorder: an MRI study. Neurology 57, 245–254. 2001.

- Courchesne et al. Evidence of brain overgrowth in the first year of life in autism. JAMA. 2003.

- Hazlett et al . Early brain development in infants at high risk for autism spectrum disorder. Nature. 2017.

Wednesday
Apr052017

How should we be using exercise as a tool to protect our brains?

It is well-accepted that physical exercise is beneficial for your health, but researchers are still investigating how exactly these benefits translate in the brain.  Many studies have shown that aerobic exercise increases neurogenesis and improves cognitive performance, but the exact mechanism connecting these two observations is still unclear. Two recent publications have reported interesting results describing how exercise type, genetic variance, and external stress affect the brain. The experiments are both done in rodents, so take the results with a grain of salt.

What the best type of exercise I can do for my brain?

While most clinicians are likely to encourage any physical activity, Nokia et al investigated the effects of three different types of exercise on neurogenesis in the hippocampus, the region of the brain critical for memory, learning, and stress response. Rodent exercise research generally employs a running wheel to simulate aerobic exercise, but here the authors compared three different exercise regimens: 1) sustained aerobic endurance exercise (ie. Voluntary running wheel or motorized treadmill), 2) high-intensity interval training (speed intervals on treadmill) and, 3) anaerobic resistance training (ie. weighted climbing). Interestingly, the authors found markers of cell proliferation, maturation, and survival- all indicative of neurogenesis- were only significant in rats that had completed the endurance training, which included voluntary running on a running wheel 3 times per week for 6 weeks. Moreover, they found the effects were most significant in rats genetically predisposed to respond to physical exercise (ie. maximal running distance increased following 8 weeks of treadmill training as opposed to no change). Take home: Sustained aerobic exercise is the most effective training paradigm to promote hippocampal neurogenesis, especially if you are running voluntarily and genetically predisposed to show gains in aerobic fitness with training.

Can exercise protect my brain?

Stress is known to negatively impact mood and impair memory, while simultaneously eliminating dendritic spines in the brain. Because exercise is known to improve memory function, Chen et al investigated whether exercise could rescue the negative effects of stress on behavior and spine stability. This study was carried out in mice who expressed fluorescent protein in their cortical neurons enabling in vivo transcranial monitoring of dendritic spine dynamics before and after exercise/stress intervention. Mice were physically stressed for 14days with or without one hour of continuous treadmill exercise, followed by behavioral testing, imaging, and brain protein/transcript quantification. The results showed that exercise not only prevented stress-induced anxiety and working memory loss, but also physically prevented spine elimination and enhancing survival of newly formed spines. The authors confirmed that the observed neuroprotective effects of exercise were conferred through the BDNF/TrkB pathway. Take home: Regular sustained aerobic activity can prevent the deleterious effects of stress on your brain.

Better get moving!

MMR

Chen et al. Treadmill exercise suppressed stress0induced dendritic spine elimination in mouse barrel cortex and improved working memory via BDNF/TrkB pathway. Transl Psychiatry (2017) 7, e1069.

Nokia et al. Physical exercise increases adult hippocampal neurogenesis in male rats provided it is aerobic and sustained. J. Physiol 594. (2016) pp 1855-1873.

Thursday
Mar302017

Schizophrenia and amyotrophic lateral sclerosis have more in common than we thought!

On the surface schizophrenia (SCZ) and amyotrophic lateral sclerosis (ALS) are quite different! SCZ is a chronic psychotic disorder that presents as a myriad of symptoms such as hallucinations and cognitive deficits, while ALS is a progressive neurodegenerative disorder that destroys motor neurons and downstream muscle movement. However, unexpected epidemiology links have emerged; higher than predicted rates of SCZ were discovered in relatives of ALS patients1 and polygenetic risk factors were identified in both patient populations2,3. Recently, McLaughlin et al. conducted a genome wide association study (GWAS) to compare polygenic risk factors between SCZ and ALS patients4. Association mapping of over 100,000 individuals identified a positive genetic correlation of 14%4. Interestingly, this correlation was specific to SCZ and was not found when comparing ALS to bipolar disorder, major depressive disorder, autism spectrum disorder, or Alzheimer’s disease. Supporting these results, authors found that SCZ polygenetic risk factors were significantly higher among ALS patients compared to healthy controls. Through this work novel ALS-associated genes were discovered, including genes with roles in axon connectivity and autoimmunity. The authors speculated that shared genetic risk factors between SCZ and ALS may converge on neural network dysregulation. The authors further suggested that therapeutic strategies beneficial for ALS may be beneficial for SCZ and vice versa.  

Given the shared genetic background and pathophysiological differences between SCZ and ALS, it is tempting to envision a role for epigenetic mechanisms in disease divergence. Moving forward it would be interesting to profile the occupancy of epigenetic enzymes on shared risk factor genes. It would also be interesting to compare in vivo epigenetic enzyme expression (for example with neuroepigenetic PET imaging!) in SCZ and ALS populations.

 

-TMG

1) Byrne, S. et al. Aggregation of neurologic and neuropsychiatric disease in amyotrophic lateral sclerosis kindreds: a population-based case–control cohort study of familial and sporadic amyotrophic lateral sclerosis. Ann. Neurol. 74, 699–708 (2013).

2) Schizophrenia Working Group of the Psychiatric Genomics Consortium. Biological insights from 108 schizophrenia-associated genetic loci. Nature 511, 421–427 (2014).

3) van Rheenen, W. et al. Genome-wide association analyses identify new risk variants and the genetic architecture of amyotrophic lateral sclerosis. Nat. Genet. 48, 1043–1048 (2016).

4) McLaughlin, R. et al. Genetic correlation between amyotrophic lateral sclerosis and schizophrenia. Nat. Communications 8:14774 (2017).

Friday
Mar242017

Everybody Makes Mistakes

Just when you thought you could beat cancer by staying healthy and maybe taking a wheatgrass shot here and there, science comes and tells you you’re wrong. A new study at Johns Hopkins found that DNA copying errors might cause some cases of cancer. These cancers occur more often than others and usually are prevalent most among patients that are relatively healthy. This study took a mathematical approach to how likely a cancer is to occur based on environmental factors, genes, or DNA replication errors. Cancer types that are most likely due to replication errors are colon, brain, bone, and pancreatic cancers. The more our cells divide, the greater the chance that errors will occur. This is problematic for a society that has an increasing lifespan. While this study does not say environmental factors are not detrimental, it does mean that many cancers are unavoidable if a healthy cell decides to be lazy during the replication process. Moral of the story: stop pretending like you enjoy wheatgrass shots and live a little. 

- LER

 

Source: https://www.sciencedaily.com/releases/2017/03/170323141403.htm

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