Memory Enhancement
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Swarfmaker
Dec 2, 2010, 4:32:11 PM12/2/10
to Alzheimer's Medicines Supplements and Treatments
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....@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. di...@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.
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 any supplement
"cocktail" for people struggling with neurodegenerative diseases.
Exercise:
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:
Do a search for these topics:
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
+ 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....@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. di...@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.
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 any supplement
"cocktail" for people struggling with neurodegenerative diseases.
Exercise:
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:
Do a search for these topics:
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
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