The key to long life will most likely be found in those that live the longest. Scientists at Albert Einstein College of Medicine of Yeshiva University have taken this idea to heart and have been working on the Longevity Gene Study. It was theorized that individuals who live a long time must possess some beneficial genes that “buffer” against more harmful genotypes.

The study gathered over 1200 individuals all of Ashkenazi Jewsish descent. Since these individuals originated from a founder group of about 30,000 people, the genetic diversity is fairly small. This makes it easier to identify genes that confer longevity to their owners.

More after the jump.
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Apologies for the lack of activity. I’ve been up to my ears in drywall and paint these last few days

Autism or autistic symptoms affect roughly 1 in 500 people and yet is still a relative mystery. A new study from the New York State Institute for Basic Research in Developmental Disabilities sheds some light on the growth and proliferation of neurons in autistic individuals. It was theorized that external growth factors in serum from autistic children would affect the growth of neuronal progenitor cells, thereby simulating early neurogenesis in autistic individuals. Neuronal prgenitor cells were grown in serum from autistic children and age-matched controls, giving some interesting results.

Results and details after the jump.
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Glial cells have been regarded for years as the poor, red-headed step child to neurons in the brain. It has generally been considered that glial cells serve as support structures for neurons. The general analogy used relates glial cells to be the “glue” that holds neurons together. Glial cells perform many important (if mundane) tasks such as mopping up excess ions and recycling neurotransmiters. Glial cells also provide physical support for neurons, guide axon/dendrite growth, maintain a stable cocktail of chemicals in the fluid surrounding the brain and coat axons in myelin.

Glia, however, has always been assumed to take a backseat when the “real” work of the brain happened, watching from the sidelines as the flashy neurons communicated with eachother. Recent research may finally bring glial cells off the sideline and give them some credit they deserve. More details after the jump.

…These data indicate that glia contribute actively to the transfer and storage of information in the central nervous system. The findings reviewed above, however, are only beginning to scratch the surface of what will be an explosion of findings related to glial modulation of brain function

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Epilepsy and glaucoma could be a thing of the past. Well, that could be a bit sensationalistic but research coming out of Purdue University is showing some promise. A recent press release highlights three astounding projects. One measures epileptic brain activity while a seizure is occurring, another dispenses GABA neurotransmitters to calm localized seizures. The last measures pressure buildup in glaucoma patients.

Details after the jump.
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Scientific American just posted an article about a study correlating learning language to mathematical statistics.

Cognitive scientist Bob McMurray of the University of Iowa set up a relatively simple mathematical model of word learning on a commonly available spreadsheet, assessing the potential to learn each of some 200 words. He set a numerical threshold at which a given word would be considered learned, operating under the assumption that it would take kids time to learn each word, they could pick up multiple words at the same time, and that some words were more difficult to process.

Color me doubtful. It looks to me like they are applying a simple mathematical to an overly complex subject and calling correlation causation. Why I disagree after the jump.
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People have remarked in recent years that obese individuals behave like drug addicts. A new study by the University Bordeaux has shown that sweets are infact addictive. And surprisingly, more addictive than cocaine. Both act on the brain’s dopamine reward system and tend to induce addictive traits in users.

But don’t start railing lines of sugar. I’ve heard it causes a terrible headache. More details on the study after the jump.

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Researchers have found that a mutation in the ADRA2B gene improves the recall of emotional memory. This specific mutation of ADRA2B deletes three amino acids from the encoded protein. This mutation affects the behavior of noradrenaline receptors.

The research team tested this gene mutation by genotyping 435 young adults. These participants were shown a series of pictures. The pictures were one of three emotional categories: neutral, positive and negative. After viewing all the pictures for 4 seconds each, participants were asked to write a description of what they had seen. Participants with the ADRA2B mutation recalled up to 80% of the emotional images while those without the mutation recalled on average 40%.

The team believes the mutation is as common as 30% in Caucasians and 12% in Africans. The study also contacted people suffering from Post-dramatic Stress Disorder. Those with the mutation recalled their negative emotional memories more vividly than those without the mutation.

On the flip side, Retrospectacle recently posted an interesting article on a new drug, propranolol, which “blocks the action of epinephrine on both β1- and β2-adrenergic receptors”. The drug weakens and removes emotional attachment to past memories. Participants are asked to vividly recall their traumatic memory and are then administered the drug. I would theorize that recalling a memory is somewhat similar pharmacologically to experiencing it the first time and thus the beta-blocking capabilities of propranolol minimizes the “resaving” of the memory. Of course, this is wild speculation and I have zero direct evidence to support my theory

It is believed that propranolol works because of the interaction between norepinephrine and glucocorticoids. Glucocorticoids are released by the adrenal cortex during emotional arousal and are believed to consolodate and strengthen new memories. It was theorized that glucocorticoid release was triggered by norepinephrine.

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Tiny brain no obstacle to French civil servant

A man with an unusually tiny brain managed to live an entirely normal life despite his condition, caused by a fluid buildup in his skull, French researchers reported on Thursday.

Scans of the 44-year-old man’s brain showed that a huge fluid-filled chamber called a ventricle took up most of the room in his skull, leaving little more than a thin sheet of actual brain tissue.

Wow. The human brain never ceases to amaze me at its ability to survive even the most extreme conditions.

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