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"Give with a free hand, but give only your own."
 -- J.R.R. Tolkien The Children of Hurin
Memory Enhancement

I have nothing to sell you but hope, and that I give you for free.

The "Gerbil food cocktail"

+ Choline [how much?  From eggs, lecithin, or as a supplement]
+ Uridine monophosphate [how much or from what alternative source? Brewer's yeast? Orotates?]
+ DHA [How much?  From fish oil]

[Without having any further guidance on how much of each and how often, and until we have more information, all we can do is go by supplement manufacturer's recommended dosages.]

DHA: Fish oil

Choline: Choline or "citi-choline" supplements, lecithin.

Uridine: Sugar beets, molasses (from sugar beets), tomatoes (0.5 to 1.0 g uridine per kilogram dry weight), brewer’s yeast (3% uridine by dry weight)[3], beer (from the yeast), broccoli, "orotates", organ meats (liver, pancreas, etc.).

I'm going to use fish oil, lecithin, and brewer's yeast for myself. I will use the recommended dose on the label.

Interestingly, for anyone battling depression, I found lots of articles from about 2006 saying that a combination of DHA (fish oil) and uridine was about as effective as Prozac.

Better than Prozac
Treating depression with common food components might be as effective as using traditional drugs.
By Jason Feirman,
Psychology Today
published on March 01, 2005 - last reviewed on February 13, 2007
...Membrane fluidity may be especially important for mitochondria, the little energy factories found inside all cells of the body, including nerve cells. Omega-3 acids seem to boost the flexibility of mitochondrial membranes while uridine delivers raw material for the mitochondrial furnace...
http://www.psychologytoday.com/articles/200503/better-prozac

Here's a thread about this that appeared on the Alz.org message board back in July of 2008:

http://alzheimers.infopop.cc/eve/forums/a/tpc/f/762104261/m/4081064272?r=4531016513#4531016513

Here are the links to the articles and the associated journal article:

Get Smart About What You Eat And You Might Actually Improve Your Intelligence

ScienceDaily (July 3, 2008)
New research findings published online in The FASEB Journal provide more evidence that if we get smart about what we eat, our intelligence can improve. According to MIT scientists, dietary nutrients found in a wide range of foods from infant formula to eggs increase brain synapses and improve cognitive abilities... In the study, gerbils were given various combinations of three compounds needed for healthy brain membranes: choline, found in eggs; uridine monophosphate (UMP) found in beets; and docosahexaenoic acid (DHA), found in fish oils. Other gerbils were given none of these to serve as a baseline. Then they were checked for cognitive changes four weeks later.
http://www.sciencedaily.com/releases/2008/07/080702150706.htm

Cocktail Therapy For Alzheimer's Disease? Works for Gerbils

ScienceDaily (July 9, 2008) — A dietary cocktail that includes a type of omega-3 fatty acid can improve memory and learning in gerbils, according to the latest study from MIT researchers that points to a possible beverage-based treatment for Alzheimer's and other brain diseases... The cocktail has previously been shown to promote growth of new brain connections in rodents.

"It may be possible to use this treatment to partially restore brain function in people with diseases that decrease the number of brain neurons, including, for example, Alzheimer's disease, Parkinson's, strokes and brain injuries."

The researchers found that normal gerbils treated with the mixture--a combination of DHA (a type of omega-3 fatty acid), uridine and choline--performed significantly better on learning and memory tests than untreated gerbils...

http://www.sciencedaily.com/releases/2008/07/080708155604.htm

Dietary uridine enhances the improvement in learning and memory produced by administering DHA to gerbils.
Sarah Holguin, Joseph Martinez, Camille Chow, and Richard Wurtman.  FASEB Journal, July 7, 2008 DOI: 10.1096/fj.08-112425
http://dx.doi.org/10.1096/fj.08-112425

The following article says that uridine does not come from the diet, but is produced by the liver.  Hmmmm.  Other sources say you can get uridine in the diet from things like sugar beets and brewer's yeast.

MIT Research Offers New Hope For Alzheimer's Patients
ScienceDaily (Apr. 27, 2006) — CAMBRIDGE, Mass.--MIT brain researchers have developed a "cocktail" of dietary supplements, now in human clinical trials, that holds promise for the treatment of Alzheimer's disease... he three compounds in the treatment cocktail - omega-3 fatty acids, uridine and choline - are all needed by brain neurons to make phospholipids, the primary component of cell membranes... the new research focuses on brain synapses, where neurotransmitters such as dopamine, acetylcholine, serotonin and glutamate carry messages from presynaptic neurons to receptors in the membranes of postsynaptic neurons... the researchers detected a large increase in the levels of specific brain proteins known to be concentrated within synapses, indicating that more synaptic membranes had formed... Synaptic membrane protein levels rose if the gerbils were.. fed all three compounds... Choline can be found in meats, nuts and eggs, and omega-3 fatty acids are found in a variety of sources, including fish, eggs, flaxseed and meat from grass-fed animals. Uridine, which is found in RNA and produced by the liver and kidney, is not obtained from the diet. However, uridine is found in human breast milk, which is a good indication that supplementary uridine is safe for humans to consume, Wurtman said...
http://www.sciencedaily.com/releases/2006/04/060427215901.htm


Nutrition and Alzheimer's disease: pre-clinical concepts.
Kamphuis PJ, Wurtman RJ.
Danone Research-Centre for Specialised Nutrition, Wageningen, The Netherlands. patrick.kamphuis@danone.com
Abstract
Eur J Neurol. 2009 Sep;16 Suppl 1:12-8.
...An Alzheimer's brain contains fewer synapses and reduced levels of synaptic proteins and membrane phosphatides. Brain membrane phosphatide synthesis requires at least three dietary precursors: polyunsaturated fatty acids, uridine monophosphate (UMP) and choline. Animal studies have shown that administration of these nutrients increases the level of phosphatides, specific pre- or post-synaptic proteins and the number of dendritic spines - a requirement for new synapse formation. These effects are markedly enhanced when animals receive all three compounds together. This multi-nutrient approach in animals has also been shown to decrease amyloid beta protein (Abeta) plaque burden, improve learning and memory through increased cholinergic neurotransmission and have a neuroprotective effect in several mouse models of AD. Whether these potential therapeutic effects of a multi-nutrient approach observed in animal models can also be replicated in a clinical setting warrants further investigation.
PMID: 19703215 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/19703215


Use of phosphatide precursors to promote synaptogenesis.
Wurtman RJ, Cansev M, Sakamoto T, Ulus IH.
Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. dick@mit.edu
Annu Rev Nutr. 2009;29:59-87.

Abstract

New brain synapses form when a postsynaptic structure, the dendritic spine, interacts with a presynaptic terminal. Brain synapses and dendritic spines, membrane-rich structures, are depleted in Alzheimer's disease, as are some circulating compounds needed for synthesizing phosphatides, the major constituents of synaptic membranes. Animals given three of these compounds, all nutrients-uridine, the omega-3 polyunsaturated fatty acid docosahexaenoic acid, and choline-develop increased levels of brain phosphatides and of proteins that are concentrated within synaptic membranes (e.g., PSD-95, synapsin-1), improved cognition, and enhanced neurotransmitter release. The nutrients work by increasing the substrate-saturation of low-affinity enzymes that synthesize the phosphatides. Moreover, uridine and its nucleotide metabolites activate brain P2Y receptors, which control neuronal differentiation and synaptic protein synthesis. A preparation containing these compounds is being tested for treating Alzheimer's disease.
PMID: 19400698 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/19400698


Synapse formation is enhanced by oral administration of uridine and DHA, the circulating precursors of brain phosphatides.
Wurtman RJ, Cansev M, Ulus IH.
Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
J Nutr Health Aging. 2009 Mar;13(3):189-97.

Abstract

OBJECTIVE: The loss of cortical and hippocampal synapses is a universal hallmark of Alzheimer's disease, and probably underlies its effects on cognition. Synapses are formed from the interaction of neurites projecting from "presynaptic" neurons with dendritic spines projecting from "postsynaptic" neurons. Both of these structures are vulnerable to the toxic effects of nearby amyloid plaques, and their loss contributes to the decreased number of synapses that characterize the disease. A treatment that increased the formation of neurites and dendritic spines might reverse this loss, thereby increasing the number of synapses and slowing the decline in cognition. DESIGN SETTING, PARTICIPANTS, INTERVENTION,

MEASUREMENTS AND RESULTS: We observe that giving normal rodents uridine and the omega-3 fatty acid docosahexaenoic acid (DHA) orally can enhance dendritic spine levels (3), and cognitive functions (32). Moreover this treatment also increases levels of biochemical markers for neurites (i.e., neurofilament-M and neurofilament-70) (2) in vivo, and uridine alone increases both these markers and the outgrowth of visible neurites by cultured PC-12 cells (9). A phase 2 clinical trial, performed in Europe, is described briefly.

DISCUSSION AND CONCLUSION: Uridine and DHA are circulating precursors for the phosphatides in synaptic membranes, and act in part by increasing the substrate-saturation of enzymes that synthesize phosphatidylcholine from CTP (formed from the uridine, via UTP) and from diacylglycerol species that contain DHA: the enzymes have poor affinities for these substrates, and thus are unsaturated with them, and only partially active, under basal conditions. The enhancement by uridine of neurite outgrowth is also mediated in part by UTP serving as a ligand for neuronal P2Y receptors. Moreover administration of uridine with DHA activates many brain genes, among them the gene for the m-1 metabotropic glutamate receptor [Cansev, et al, submitted]. This activation, in turn, increases brain levels of that gene's protein product and of such other synaptic proteins as PSD-95, synapsin-1, syntaxin-3 and F-actin, but not levels of non-synaptic brain proteins like beta-tubulin. Hence it is possible that giving uridine plus DHA triggers a neuronal program that, by accelerating phosphatide and synaptic protein synthesis, controls synaptogenesis. If administering this mix of phosphatide precursors also increases synaptic elements in brains of patients with Alzheimer 's disease, as it does in normal rodents, then this treatment may ameliorate some of the manifestations of the disease.

PMID: 19262950 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/19262950


Synapse Formation and Cognitive Brain Development: effect of docosahexaenoic (DHA) and other dietary constituents
R. J. Wurtman, Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences, Cambridge MA, 02139, USA;
Corresponding Author: R. J. Wurtman, Address: MIT, 43 Vassar St., 46-5023, Cambridge MA, 02139
Metabolism. Author manuscript; available in PMC 2009 October 1.
Published in final edited form as:
Metabolism. 2008 October; 57(Suppl 2): S6–10.
doi: 10.1016/j.metabol.2008.07.007.

PMCID: PMC2578826
NIHMSID: NIHMS71939

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2578826/



Dietary uridine enhances the improvement in learning and memory produced by administering DHA to gerbils.
Holguin S, Martinez J, Chow C, Wurtman R.
Massachusetts Institute of Technology, 43 Vassar St., 46-5023, Cambridge, MA 02139, USA.
FASEB J. 2008 Nov;22(11):3938-46. Epub 2008 Jul 7.

Abstract

This study examined the effects on cognitive behaviors of giving normal adult gerbils three compounds, normally in the circulation, which interact to increase brain phosphatides, synaptic proteins, dendritic spines, and neurotransmitter release. Animals received supplemental uridine (as its monophosphate, UMP; 0.5%) and choline (0.1%) via the diet, and docosahexaenoic acid (DHA; 300 mg/kg/day) by gavage, for 4 wk, and then throughout the subsequent period of behavioral training and testing. As shown previously, giving all three compounds caused highly significant (P<0.001) increases in total brain phospholipids and in each major phosphatide; giving DHA or UMP (plus choline) produced smaller increases in some of the phosphatides. DHA plus choline improved performance on the four-arm radial maze, T-maze, and Y-maze tests; coadministering UMP further enhanced these increases. (Uridine probably acts by generating both CTP, which can be limiting in phosphatide synthesis, and UTP, which activates P2Y receptors coupled to neurite outgrowth and protein synthesis. All three compounds also act by enhancing the substrate-saturation of phosphatide-synthesizing enzymes.) These findings demonstrate that a treatment that increases synaptic membrane content can enhance cognitive functions in normal animals.

PMID: 18606862 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/18606862
Full text (free): http://www.fasebj.org/cgi/reprint/22/11/3938



Chronic administration of DHA and UMP improves the impaired memory of environmentally impoverished rats.
Holguin S, Huang Y, Liu J, Wurtman R.
Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences, 43 Vassar Street, 46-5023, Cambridge, MA 02139, USA.
Behav Brain Res. 2008 Aug 5;191(1):11-6. Epub 2008 Mar 18.

Abstract

Living in an enriched environment (EC) during development enhances memory function in adulthood; living in an impoverished environment (IC) impairs memory function. Compounds previously demonstrated to improve memory among IC rats include CDP-choline and uridine monophosphate (UMP). Brain phosphatidylcholine (PC) synthesis utilizes both the uridine formed from the metabolism of exogenous CDP-choline and UMP, and the choline formed from that of CDP-choline. It also uses the polyunsaturated fatty acid (PUFA) DHA, a precursor for the diacylglycerol incorporated into PC. DHA administration also improves cognition in young and aged rodents and humans; its effects on cognitively impaired IC rats have not been characterized. We have thus examined the consequences of administering DHA (300 mg/kg) by gavage, UMP (0.5% in the diet), or both compounds on hippocampal- and striatal-dependent forms of memory among rats exposed to EC or IC conditions for 1 month starting at weaning, and consuming a choline-containing diet. We observe that giving IC rats either dietary UMP or gavaged DHA improves performance on the hidden version of the Morris water maze (all P<0.05), a hippocampal-dependent task; co-administration of both phosphatide precursors further enhances the IC rats' performance on this task (P<0.001). Neither UMP nor DHA, nor giving both compounds, affects the performance of EC rats on the hidden version of the Morris water maze (P>0.05), nor the performance by IC or EC rats on the visible version of the Morris water maze (all P>0.05), a striatal-dependent task. We confirm that co-administration of UMP and DHA to rats increases brain levels of the phosphatides PC, PE, SM, PS, PI, and total brain phospholipid levels (all P<0.05), and show that rearing animals in an enriched environment also elevates brain PC, PS, and PI levels (all P<0.01) and total brain phospholipids (P<0.01) compared with their levels in animals reared in an IC environment. These findings suggest that giving DHA plus UMP can ameliorate memory deficits associated with rearing under impoverished conditions, and that this effect may be mediated in part through enhanced synthesis of brain membrane phosphatides.

PMID: 18423905 [PubMed - indexed for MEDLINE]PMCID: PMC2478743
http://www.ncbi.nlm.nih.gov/pubmed/18423905
Full text (free): http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2478743/?tool=pubmed

For the latest on this, do a search on PubMed http://www.ncbi.nlm.nih.gov/sites/entrez with the search terms Wurtman and uridine.

There was then some discussion about where one would get the various ingredients of the "cocktail".  Fish oil for DHA.  Choline can be had as a supplement.  The uridine was a problem.

Uridine as a supplement is difficult to find.  You wouldn't think so since it is used in most infant formulas.  Some people assert that anything with "orotate" in it will metabolize to uridine. Magnesium (Mg) Orotate would then be a good source of uridine and is readily available in health food stores or online at places like Amazon.com. Magnesium is advised widely for the AD brain. Moreover Mg. orotate can be used with DHA and choline.

A thread on the Alzheimer's Association message board called "The Ultimate Alzheimer's Cocktail" seems even more interesting:


http://alzheimers.infopop.cc/eve/forums/a/tpc/f/762104261/m/1891020913/p/1


Nutrient 'Cocktail' Appears to Improve Dementia Symptoms

FRIDAY, Jan. 8, 2010 (HealthDay News) -- A combination of three nutrients might help improve memory in Alzheimer's patients by stimulating the growth of new brain connections (synapses), a new study shows.

Uridine, choline and the omega-3 fatty acid DHA (all found in breast milk) are precursors to the fatty molecules that make up brain cell membranes, which form synapses... In a clinical trial, 225 Alzheimer's patients were given a cocktail of the three nutrients, along with B vitamins, phosopholipids and antioxidants. Patients with mild Alzheimer's showed improvements in verbal memory...
http://news.yahoo.com/s/hsn/20100108/hl_hsn/nutrientcocktailappearstoimprovedementiasymptoms

Could Drink, Souvenaid, Be A Cure For Alzheimer's?
Study Will Determine Whether Nutrient-Laden Souvenaid Can Head Off Memory Loss

CHICAGO (CBS) Jan 11, 2010 8:45 pm US/Eastern
... It looks like a simple juice box, but inside there's a mixture called Souvenaid that could help Alzheimer's patients head off memory loss and possibly even improve their memory... "Souvenaid" contains vitamins and nutrients, including Uridine, fish oil components and Choline...
http://cbs4.com/health/Souvenaid.Alzheimers.drink.2.1419881.html

Here is a Yahoo search on one of the key ingredients 'uridine':

http://news.search.yahoo.com/news/search?ei=UTF-8&c=&p=uridine

Some people claim that uridine is converted to CDP choline.  A supplement called Alpha GPC may be a superior acetylcholine precursor. If so, uridine may be redundant if you are already using Alpha GPC. However, uridine does appear to help with DNA synthesis which may warrant its use in addition to Alpha GPC.

Here are some links about a product with uridine.  This is just information, and in no way should be construed as an endorsement.

http://www.lef.org/Vitamins-Supplements/Item00921/Cognitex-with-Neuroprotection-Complex.html

You can read about CDP-choline, and Alpha GPC too:
http://search.lef.org/cgi-src-bin/MsmGo.exe?grab_id=0&page_id=4005&query=GPC&hiword=GPC%20
http://search.lef.org/cgi-src-bin/MsmGo.exe?grab_id=0&page_id=5875&query=GPC&hiword=GPC%20
http://search.lef.org/cgi-src-bin/MsmGo.exe?grab_id=0&page_id=8012&query=GPC&hiword=GPC%20
http://www.lef.org/magazine/mag2002/sep2002_cover_gpc_02.html
http://search.lef.org/cgi-src-bin/MsmGo.exe?grab_id=0&page_id=4906&query=CDP&hiword=CDP%20

I think an MCT oil regimen should be added to this "cocktail" for people struggling with neurodegenerative diseases.

Exercise:

How to cut your risk of memory loss
By David S. Martin, CNN
updated 11:35 AM EST, Wed November 9, 2011

...Growing the brain

Using new, more powerful MRI scanners, researchers have shown how even moderate exercise can actually increase the size of the hippocampus, the part of the brain responsible for forming memories, essentially turning back the clock and making the brain younger.

"We have found this treasure, this amazing phenomenon that the brain can grow," Fotuhi says.

After 50, the brain -- and the hippocampus -- typically begins losing volume. The hippocampus loses 1% of its volume every two years and accelerates up to 2% per year later in life. But this loss is not set in stone.

Dr. Arthur Kramer at the University of Illinois and his colleagues took 120 older adults and put half of them into an exercise group, which walked three days a week, and the other half on a stretching regimen.

After a year, the group that walked had better memory than at the start of the study. More than that, MRI scans showed that hippocampal volume increased, on average, by 2%, effectively making their brains a year or two younger. The brains of the group that stretched continued to age...
http://www.cnn.com/2011/11/09/health/keeping-brain-young-memory/index.html

Attention, Couch Potatoes! Walking Boosts Brain Connectivity, Function

ScienceDaily (Aug. 27, 2010) — A group of "professional couch potatoes," as one researcher described them, has proven that even moderate exercise -- in this case walking at one's own pace for 40 minutes three times a week -- can enhance the connectivity of important brain circuits, combat declines in brain function associated with aging and increase performance on cognitive tasks.
http://www.sciencedaily.com/releases/2010/08/100826141327.htm

Natural Compound And Exercise Boost Memory In Mice

ScienceDaily (May 30, 2007) — A natural compound found in blueberries, tea, grapes, and cocoa enhances memory in mice, according to newly published research. This effect increased further when mice also exercised regularly... The compound, epicatechin, is one of a group of chemicals known as flavonols and has been shown previously to improve cardiovascular function in people and increase blood flow in the brain.
http://www.sciencedaily.com/releases/2007/05/070529174815.htm


Walk Much? It May Protect Your Memory Down the Road

ScienceDaily (Oct. 13, 2010) — New research suggests that walking at least six miles per week may protect brain size and in turn, preserve memory in old age, according to a study published in the October 13, 2010, online issue of Neurology®, the medical journal of the American Academy of Neurology... The study found that people who walked at least 72 blocks per week, or roughly six to nine miles, had greater gray matter volume than people who didn't walk as much, when measured at the nine-year time point after their recorded activity. Walking more than 72 blocks did not appear to increase gray matter volume any further.

By four years later, 116 of the participants, or 40 percent, had developed cognitive impairment or dementia. The researchers found that those who walked the most cut their risk of developing memory problems in half...
http://www.sciencedaily.com/releases/2010/10/101013164703.htm


Walking Slows Progression of Alzheimer's

ScienceDaily (Nov. 29, 2010) — Walking may slow cognitive decline in adults with mild cognitive impairment (MCI) and Alzheimer's disease, as well as in healthy adults, according to a study presented November 29 at the annual meeting of the Radiological Society of North America (RSNA). "We found that walking five miles per week protects the brain structure over 10 years in people with Alzheimer's and MCI, especially in areas of the brain's key memory and learning centers," said Cyrus Raji, Ph.D., from the Department of Radiology at the University of Pittsburgh in Pennsylvania. "We also found that these people had a slower decline in memory loss over five years."... The findings showed across the board that greater amounts of physical activity were associated with greater brain volume. Cognitively impaired people needed to walk at least 58 city blocks, or approximately five miles, per week to maintain brain volume and slow cognitive decline. The healthy adults needed to walk at least 72 city blocks, or six miles, per week to maintain brain volume and significantly reduce their risk for cognitive decline...
http://www.sciencedaily.com/releases/2010/11/101129101914.htm

The question is, do people not walk because they are having problems of some sort that make it difficult?  In that case, not walking or not exercising is a symptom of the disease.

Neurogenesis:

See also Curcumin
         Lithium
         Prozac
         Stem Cell
         Aphanizomenon flos-aquae (AFA)
         Brain-derived Neurotrophic Factor (BDNF)
         GCSF (granulocyte-colony stimulating factor)

Other news:

Promising Drug Candidate Reverses Age-Related Memory Loss in Mice

ScienceDaily (Oct. 13, 2010) — Researchers at the University of Edinburgh report a new experimental compound that can improve memory and cognitive function in aging mice. The compound is being investigated with a view to developing a drug that could slow the natural decline in memory associated with aging.

In a study published in the Journal of Neuroscience, the team reports the effects of a new synthetic compound that selectively blocks 11beta-HSD1 on the ability of mice to complete a memory task, called the Y maze.

"Normal old mice often have marked deficits in learning and memory just like some elderly people. We found that life-long partial deficiency of 11beta-HSD1 prevented memory decline with aging. But we were very surprised to find that the blocking compound works quickly over a few days to improve memory in old mice suggesting it might be a good treatment for the already elderly."

"These results provide proof-of-concept that this class of drugs could be useful to treat age-related decline in memory. We previously showed that carbenoxolone, an old drug that blocks multiple enzymes including 11beta-HSD1, improves memory in healthy elderly men and in patients with type 2 diabetes after just a month of treatment, so we are optimistic that our new compounds will be effective in humans. The next step is to conduct further studies with our preclinical candidate to prove that the compound is safe to take into clinical trials, hopefully within a year."
http://www.sciencedaily.com/releases/2010/10/101012173222.htm


New Drug May Help Rescue The Aging Brain

ScienceDaily (Mar. 31, 2008) — As people age, their brains pay the price — inflammation goes up, levels of certain neurotransmitters go down, and the result is a plethora of ailments ranging from memory impairment and depression to Alzheimer’s and Parkinson’s. But in a long-term study with implications to treat these and other conditions, researchers have found that an experimental drug, taken chronically, has the ability to stem the effects of aging in the rat brain.

The drug, temporarily designated S18986, interacts with AMPA (short for α- Amino-3-hydroxy-5- methylisoxazole-4- propionic acid, or ampakine) receptors in the brain. These receptors transmit excitatory signals in the brain, and researchers were interested in experimental AMPA-receptor drugs (such as S18986) for their neuroprotective abilities and for the way they temporarily boost memory. But rather than investigating the compound’s short-term effects, Alfred E. Mirsky Professor Bruce McEwen and his lab members made a far longer commitment: The scientists studied the drug’s impacts on middle-aged to elderly rats and found that, when administered daily over four consecutive months, it appeared to improve memory and slow brain aging... When compared to control animals that had received only sugar water, the drugged rats were not only more active and better at memory tests, but their brains showed physical signs of slowed aging. Neurons in the forebrain that produce acetylcholine, a neurotransmitter known to play a role in learning and memory, had 37 percent less decline. Dopamine-producing neurons, which are responsible for sustaining activity and motivation levels, slowed their decline by 43 percent. Levels of inflammation in the brain were also significantly lower. “Every marker we chose to look at seemed to indicate there was some preservation of function during aging with chronic treatment,” Hunter says. The drug appears to slow aging’s effects throughout the entire brain...
http://www.sciencedaily.com/releases/2008/03/080330183235.htm


Learn More Quickly by Transcranial Magnetic Brain Stimulation, Study in Rats Suggests

ScienceDaily (Jan. 29, 2011)

..."In general, the activity of the cells drops as a result of a low-frequency stimulation, i.e. with one magnetic pulse per second. At higher frequencies from five to 50 pulses per second, the activity of the cells increases. This rhythm is based on the natural theta rhythm of four to seven Hertz which can be observed in an EEG,"...
http://www.sciencedaily.com/releases/2011/01/110128121629.htm

Let's hear it for multitasking!  I hate that word when I see it in job descriptions.  To me, what it means is that management can't make up its mind, so they have their employees jumping from task to task to task.  Multitasking is the consequence of bad management.  You can't think two thoughts at the same time.  Not even computers can work on more than one task at the same time unless they have multiple processors, but then, each one is only working on one task at a time.  Clever operating systems fool you into thinking that a computer is doing many tasks at the same time, when in fact what they are doing is swapping tasks in and out so fast that it just looks like it.  There is an enormous amount of computer dead time between human keystrokes on a keyboard, so they send the processor off to do a hundred or so other things while it waits for your finger.  But this article says that switching tasks helps you focus.  That may be, but I think it must be left up to your own "processor" to decide what "diversions" are most appropriate, otherwise, like a freight train, your thought get derailed and it takes great (inefficient) effort to get things back on track.

Brief Diversions Vastly Improve Focus, Researchers Find

ScienceDaily (Feb. 8, 2011) — A new study in the journal Cognition overturns a decades-old theory about the nature of attention and demonstrates that even brief diversions from a task can dramatically improve one's ability to focus on that task for prolonged periods... "We propose that deactivating and reactivating your goals allows you to stay focused," he said. "From a practical standpoint, our research suggests that, when faced with long tasks (such as studying before a final exam or doing your taxes), it is best to impose brief breaks on yourself. Brief mental breaks will actually help you stay focused on your task!"
http://www.sciencedaily.com/releases/2011/02/110208131529.htm

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Updated: October 14, 2010
Inception: January 23, 2010