Saturday, 30 March 2013

Smart drug movie - Limitless (Movie Trailer Official) - YouTube



Uploaded on 21 Dec 2010
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Bradley Cooper and Robert De Niro star in Limitless, a paranoia-fueled action thriller about an unsuccessful writer whose life is transformed by a top-secret "smart drug" that allows him to use 100% of his brain and become a perfect version of himself. His enhanced abilities soon attract shadowy forces that threaten his new life in this darkly comic and provocative film.

Aspiring author Eddie Morra (Cooper) is suffering from chronic writer's block, but his life changes instantly when an old friend introduces him to NZT, a revolutionary new pharmaceutical that allows him to tap his full potential. With every synapse crackling, Eddie can recall everything he has ever read, seen or heard, learn any language in a day, comprehend complex equations and beguile anyone he meets—as long as he keeps taking the untested drug.

Soon Eddie takes Wall Street by storm, parlaying a small stake into millions. His accomplishments catch the eye of mega-mogul Carl Van Loon (De Niro), who invites him to help broker the largest merger in corporate history. But they also bring Eddie to the attention of people willing to do anything to get their hands on his stash of NZT. With his life in jeopardy and the drug's brutal side effects taking their toll, Eddie dodges mysterious stalkers, a vicious gangster and an intense police investigation as he attempts to hang on to his dwindling supply long enough to outwit his enemies.

Aniracetam Cognitive Enhancers Unlock Limitless Potential - YouTube



Uploaded on 25 Jan 2012
http://w34.us/amz/B006ICFUCW Aniracetam is marketed as a cognitive enhancer, but probably anti-anxiety medication is a fairer term. It doesn't make me smarter, just more focused and less distracted. That does let me do more "smart" things, and be more productive, and sleep better, and generally have a higher quality of life, but it wasn't like I instantly hand photographic memory.

Aniracetam has drastically improved my quality of life, but I am not a doctor, so review your medications with your physician before you changes to your prescriptions.
 

Brain's Use of 'Alternative Energy' May Be Related to Alzheimer's - Dana Foundation

By Jim Schnabe - February 23, 2011
How does amyloid beta protein (A-beta) harm cells in Alzheimer’s disease? Why is this harm concentrated in certain brain regions? Researchers don’t know, but two studies published in the Oct. 12, 2010, edition of the Proceedings of the National Academy of Sciences suggest a plausible explanation.

According to the studies, the regions where A-beta deposits are seen in the brains of people with Alzheimer’s closely match the regions that normally rely heavily on less-efficient but faster processes of energy production in cells. The studies’ authors propose that A-beta in its disease-driving forms might impair these processes, and thus might principally harm the brain regions that most depend on them.

“It really opens up a lot of questions,” says Pierre Magistretti, a neurobiologist and brain metabolism researcher at the Ecole Polytechnique Federal in Lausanne, Switzerland, who wasn’t involved in the research. Magistretti is a vice-chairman of the European Dana Alliance for the Brain.

“It suggests that we should expand our view of what the cell-biological problem in Alzheimer’s might be,” says Marcus Raichle, a neurologist and neurobiologist at Washington University at St. Louis who was senior author of one of the two papers. Raichle is a member of the Dana Alliance for Brain Initiatives.

Glycolysis for speed

The basic energy-molecule used by living cells is adenosine triphosphate (ATP). Adult cells usually make it in a multi-step process that includes the simple sugar glucose and oxygen and leaves water and carbon dioxide as byproducts. But there are faster, less-efficient ways of turning glucose into ATP, and some cellular processes in the brain depend on them. These faster processes, which don’t require oxygen, account for only 10–15 percent the adult brain’s use of glucose and are used more extensively by fetal cells and cancer cells, and by muscle cells during intense exercise.

Raichle has been researching brain metabolism for several decades, including developing functional imaging technology that tracks the brain’s use of glucose and oxygen. In a paper in Science in 1988, he and his colleagues found that these non-oxygen-consuming uses of glucose in the brain increase temporarily when brain activity increases. “The question of what is really going on there has been lingering in the back of my mind since then,” he says.

Several years ago, Raichle informally examined brain-metabolism data taken during functional imaging experiments and noticed that these alternative uses of glucose seemed to vary considerably from region to region in ordinary brains. Also piquing his interest was the observation that the regions that relied the most on these alternate energy processes appeared to be the ones that make up the “default mode network,” a set of brain regions that are relatively active when a person is not engaged in any specific task.

Raichle and his fellow metabolism researchers pioneered research on the default mode network, but in recent years Alzheimer’s researchers have taken an interest too, because the regions that make up the network are also the ones that gather the most A-beta deposits. That connection prompted Raichle and his colleagues to set up a formal set of studies.

In one study of 33 young adults, the researchers mapped the levels of these non-oxygen burning uses of glucose in resting brains, using positron emission tomography (PET) scans. They found that the levels of “aerobic glycolysis”—a catchall term for these alternative processes—did vary throughout the brain, and corresponded closely to the default mode network. In the second study, the researchers found a strong correspondence between the more aerobic-glycolysis-dependent regions in these 33 young brains and the regions that had accumulated signs of A-beta plaques in brain-imaging of 39 elderly people. The plaques largely spared the regions that showed average or below-average aerobic glycolysis—even if their overall energy use was high, such as in the visual cortex.

One possible explanation for the finding is that these alternate glucose uses are especially vulnerable to disruption by A-beta. For example, Raichle points out that glucose-fuelled processes are used by helper cells known as astrocytes to keep concentrations of the neurotransmitter glutamate below toxic levels in the synapses of cortical neurons. In principle, disruption of these processes by A-beta could lead to the deaths of the neurons. Magistretti’s group recently showed that A-beta in its disease-causing forms does alter the metabolism of astrocytes, apparently putting them under stress and ultimately weakening the neurons they are meant to protect. “One of the things that astrocytes do is to remove A-beta from the extracellular space, and then somehow they have to degrade it, but this is an extra burden for them,” says Magistretti.

Recent studies also have linked Alzheimer’s to G3PD, an enzyme that among other functions is needed for glucose-fuelled glutamate management:  People with ordinary late-onset Alzheimer’s are more likely to have certain variants of G3PD, which may be less functional than normal; and A-beta clusters have been reported to cause G3PD to aggregate and become dysfunctional.

Magistretti suggests that one way to investigate further would be “to follow from an early age, in transgenic mice that overexpress A-beta, their glucose utilization and their A-beta deposits, and see how they develop over time.”

William Powers, a neurologist at the University of North Carolina whose own research has uncovered evidence of a similar abnormality in glycolysis in Huntington’s disease, suggests testing to see whether glucose use affects A-beta deposition rather than vice-versa. “This could be done in an animal model of Alzheimer’s by feeding a diet high in fat and low in carbohydrates, which will reduce glucose availability to the brain and decrease cerebral glucose metabolism,” he says.

Helping the brain use alternative fuel may ease symptoms of Alzheimer's

By (BPT) - March 11, 2013

(BPT) - Whether a patient faces a simple health problem, such as a head cold, or one as complex as Alzheimer’s disease, relieving the symptoms is often as important as resolving the issue itself. Yet for the more than 5 million Americans affected by Alzheimer’s, treating the symptoms is even more vital.
Some of the early signs of Alzheimer’s include memory loss that disrupts daily life, mood and personality changes, and difficulty solving otherwise simple daily tasks.

Alzheimer’s disease is the sixth-leading cause of death in the United States, according to the Alzheimer’s Association. Of the top 10 causes of death, it is the only one for which there is no cure or preventive measure. However, research suggests that addressing one early facet of the disease – decreased blood sugar in brain cells, also known as diminished cerebral glucose metabolism (DCGM) – may help relieve symptoms for certain people with mild to moderate Alzheimer’s.
In a healthy brain, glucose is the primary energy source. A brain affected by Alzheimer’s doesn’t process glucose into energy as efficiently as a healthy brain.

“Unlike other cells in the body that can metabolize fats as fuel, brain cells rely on glucose (sugar) for their primary energy source,” says Dr. Richard S. Isaacson, associate professor of clinical neurology and vice chair of education at the University of Miami’s Miller School of Medicine. "One aspect of Alzheimer’s is that it hinders the brain’s ability to use glucose, and this significantly affects brain function.”

“DCGM is an early feature of Alzheimer’s disease, represented by region-specific declines in brain glucose – or energy – metabolism,” Isaacson says. “DCGM correlates with both the cognitive decline and the pathology associated with Alzheimer’s. Research suggests that addressing DCGM may help mitigate symptoms for some patients.”

Providing brain cells with an alternative energy source may help ease the effects of DCGM, while enhancing memory and cognitive function in Alzheimer’s patients. One prescription-only medical food aims at helping Alzheimer’s patients by addressing DCGM – Axona by Accera, Inc.

The easy-to-mix, once-daily drink is currently the only prescription therapy for patients with mild to moderate Alzheimer’s that addresses the link between the brain’s inability to process and use glucose with the degenerative symptoms of Alzheimer’s by providing the brain with an alternative energy source. The liver digests and metabolizes Axona to produce the naturally occurring compounds – ketones– that the brain can use as an alternative energy source. Patients or caregivers mix the powder with other liquids or foods and take it once a day in conjunction with commonly prescribed Alzheimer’s medications.

“More research is necessary to determine the exact reasons why DCGM can have profound effects on cognition over the long term,” Isaacson says. “When blood glucose drops rapidly, significant decline in cognitive function occurs and may be accompanied by confusion, coma and even brain death.”
While Axona is not a cure for Alzheimer’s, it can help some patients mitigate the symptoms of the disease. Doctors and caregivers of patients using Axona have reported patients appear more alert and engaged in daily activities and conversations. “If you or a family member experience symptoms such as poor short-term memory, changes in behavior and difficulty with language, see your doctor for a full evaluation,” says Isaacson.

To learn more about Alzheimer’s disease, visit www.alz.org, the website of the Alzheimer’s Association. For more information on DCGM and Axona, visit www.about-axona.com.

Fructose Affects Your Brain Very Differently than Glucose

Fructose Affects Your Brain Very Differently than Glucose

Startling NEW Evidence: This Drink Causes Your Neurons to Stagnate for 20 Minutes...

February 28, 2011 | 216,539 views | + Add to Favorites

Aniracetam (& episodic memory) - Nootropic Review - YouTube


 

Published on 27 May 2012
Review of the nootropic/cognitive enhancing drug Aniracetam.
Aniracetam is of the racetam family of drugs, the most famous of which is Piracetam. It does not elect any psychoactive effects such as being a stimulant, but is purported to improve memory and overall cognitive function.

I believe it did have an effect, but was extremely mild and arguably non-demonstrable. I would rate Aniracetam 5/10
 
 
 

How Much Glucose Does the Brain Really Need? | Mark's Daily Apple

We now know that the oft-repeated “your brain only runs on glucose!” is wrong.

I’ve mentioned it before, and anyone who’s taken the time to get fat-adapted on a low-carb Primal eating plan intuitively knows that your brain doesn’t need piles of glucose to work, because, well, they’re using their brain to read this sentence.
LowRes2
Obviously, you eventually adapt and find you have sufficient (if not much improved) cognition without all those carbs. That said, some glucose is required, and that’s where people get tripped up. ”Glucose is required” sounds an awful lot like “your brain only uses glucose” which usually leads to “you need lots of carbs to provide that glucose.” And that’s the question today’s edition of “Dear Mark” finds itself attempting to answer: how much glucose is required?

Let’s get to it.

Hi Mark,
I have a little problem. Even though I’m able to function at work, maintain conversations, and go about my daily life without having segments of my brain suddenly stop working while eating Primal, my friends are worried about my brain. All they know is that the brain needs glucose. What can I tell them? How much glucose does my brain actually require to keep working?
Thanks,
Frank
I wouldn’t be too hard on your friends. They mean well and it’s a common misconception. Instead of chiding them, rubbing their faces in the knowledge that you can function quite adequately on a high-fat diet, educate them.

How much glucose the brain requires depends on the context. There’s not one single answer.
If you’re on a very high fat, very low carb diet – like a traditional Inuit diet – your brain will eventually be able to use fat-derived ketones for about 50-75% of its energy requirements. Most ketones are produced in the liver, but astrocytes in the brain also generate ketones themselves for use by neurons. You think we’d have that kind of set up in our brains if ketones weren’t useful to have around? If all we could do was burn glucose up there, what would be the point of even having localized ketone factories? Anyway, since the brain can use about 120 grams of glucose a day (PDF), that means you’d still need at least 30 grams of glucose while running on max ketones.

If you’re merely on a lower carb diet – staying under 150 grams per day or so – or eating medium chain triglycerides (coconut oil, MCT oil) to directly generate ketones, you’ll have access to ketones without being in full-blown ketosis, and your brain will be accessing some of them for energy. Take the story of Dr. Mary Newport, who lessened her husband’s Alzheimer’s symptoms simply by adding a couple tablespoons of coconut oil to his regular diet. The MCTs in the coconut oil were converted to ketones, which his brain began using. You’ll probably need more than 30 grams of glucose, but you won’t need the full 120 grams on a lower carb Primal way of eating (especially if you eat some coconut).

If you’re involved in strenuous exercise, your brain will be running primarily on lactate. Yep, lactate – that unwanted metabolic byproduct of muscle metabolism. During exercise, when the muscles are using up most of the available glucose to lift things and move a bunch of intelligent primate flesh through three dimensional space, and where inadequate oxygen (hence breathing hard) leads to incomplete glucose and pyruvate breakdown and increased lactate levels, the brain will draw upon lactate as a direct energy source. Not only that, but lactate appeared to make the brain run more efficiently, more snappily, and when both are available, the brain prefers lactate over glucose. Other research has found that the brain also prefers lactate in the hours and days immediately following a traumatic brain injury. I’m not sure how much glucose the brain requires when it’s accessing lactate, but it’s definitely fewer than 120 grams.

Of course, even when you need some glucose, that glucose needn’t necessarily come from dietary carbohydrate. It can famously come from gluconeogenesis, the process by which the liver converts amino acids into glucose. It can also come from glycerol, a byproduct of fat metabolism. In deep fasting situations, glycerol can contribute up to 21.6% of glucose production, with the rest presumably coming from gluconeogenesis. The glycerol can come from both dietary fat and adipose tissue (the authors of that glycerol fasting study even suggest that fasting burns body fat in order to provide glycerol for glucose production), while the amino acids can come from dietary protein (if you’re eating) or muscle (if you’re starving).

Overall, recent research into the metabolic demands of brain slices (“living” pieces of brains isolated and used for research) shows that incorporating other energy substrates – ketones, lactate, or even pyruvate – into the glucose solution improves oxidative metabolism and neuronal efficiency. Before you say “but this was in vitro, my brain’s not sliced up and submerged in a weird syrupy solution,” know that the whole point of the study was to better replicate the conditions of the kind of real, actual, living, thinking brains we find in human heads. The authors note that the glucose-only solution normally used to fuel brain slices in other studies is limited, because “in the intact brain, complex machinery exists that coordinates energy substrates delivery and adjusts energy substrate pool composition to the needs of neuronal energy metabolism.” In other words, glucose solution is an easy, dependable way to fuel brain slices, but it’s an incomplete representation of how brains work in heads. The authors conclude that “in slices as well as in vivo, the ability of glucose to maintain energy metabolism is limited and neuronal energy supply should be supported by other oxidative substrates.” 

So, a healthy, efficient brain is one that draws on several different fuels. A healthy, efficient brain is one that uses ketones (and perhaps lactate and other fuels) to spare some glucose. A complete reliance on glucose indicates an underachieving brain, a brain that could do so much better, a brain that could really use a coconut milk curry and some intense exercise every now and again. As far as we can tell, then, the absolute physiological minimum is 30 grams of glucose. I wish I could provide hard numbers for some of the other contexts beyond near carnivory (like basic 150 grams carbs Primal eating with coconut or maybe figuring out how to rely on lactate fueling), but the numbers don’t really matter in practice. What matters is that our brains don’t need the full 120 grams of glucose, especially if we’re following a Primal Blueprint eating plan.

I hope that helps.


Read more: http://www.marksdailyapple.com/how-much-glucose-does-your-brain-really-need/#ixzz2P4JFeOCp