Alzheimer's? Why?

[Michaelangelica]

Glutamaic system in Alzheimers'

Another example is memantine, our newest tool in the struggle against Alzheimer's disease. This drug appears to be effective because it has a low affinity for the N-methyl-D-aspartate (NMDA) glutamate receptor.
Because it has only a low affinity, it only has an effect when the glutamate system is hyperactive and potentially neurotoxic, so it slows the progression of cell death in Alzheimer's disease.
This is in stark contrast to drugs that have a high affinity for the NMDA glutamate receptor, such as ketamine or dextromethorphan, which can interfere with the overall functioning of the glutamate system and in some cases mimic schizophrenia to the point of precipitating psychosis.

Medscape Psychopharmacology Today: All the Things They Taught Us That Were Wrong

Check out also schizophrenia, Clinical depression, austism and MSG Chain letter meme Hypography threads

PS Yet another very preventable reason.
Public Dental care in Australia is a disgrace with a 12 month waiting list for "emergencies" and a 2-3 year wait for any other work!

From

Does Tooth Loss Lead to Mental Decline? Or Vice-Versa? - Articles

[Michaelangelica]

And still another study listed 22 different categories of drugs that can cause symptoms that mimic Alzheimer's... plus 14 different over-the-counter drugs that can cause those symptoms!

Here's a typical scenario. A healthy person goes to the doctor for a checkup and is told his cholesterol or blood pressure is high. So he starts taking medication, which causes side effects.
This leads his doctor to give him a second drug to treat those side effects. But, of course, that second drug causes new side effects.
So the doctor prescribes a third drug to treat the side effects of the second one!

MORE AT:-
Care2 - This Common Misdiagnosis Can Land You In A Nursing Home!

Chew a Tree?

Chemical Compound Found In Tree Bark Stimulates Growth, Survival Of Brain Cells

The tree bark compound, known as gambogic amide, behaves much like Nerve Growth Factor (NGF), a molecule found in the brain. NGF binds to TrkA, a neuronal receptor, and activates neuronal signaling.
It is known that the loss of TrkA density correlates with neuronal atrophy and severe cognitive impairment such as that associated with Alzheimer's disease.

Because gambogic amide also binds to TrKA and activates neuronal signaling, the researchers believe it may have potential as a therapeutic treatment in people affected by neurodegenerative disease, such as stroke, Alzheimer's disease and peripheral diabetic neuropathies.

Gambogic amide is derived from gambogic acid, a major ingredient of gamboges, a brownish-orange resin exuded from the Southeast Asian Garcinia hanburryi tree.
The resin has been used in that area of the world for thousands of years to treat cancers without any reported toxicity to noncancerous cells.

ScienceDaily: Chemical Compound Found In Tree Bark Stimulates Growth, Survival Of Brain Cells

[Michaelangelica]

Mini-strokes Linked To Uric Acid Levels

Science Daily — Researchers at Johns Hopkins have found that high-normal uric acid (UA) levels may cause barely detectable mini strokes that potentially contribute to mental decline in aging adults.

Diet, exercise and drugs like allopurinol (all of which lower UA levels) could eventually be of value in reducing this risk, especially for those with additional risk factors such as diabetes, obesity and hypertension, the researchers say. But they caution that it would be premature to try this now.

In a study published in the Oct. 2 issue of Neurology, lead author David Schretlen, Ph.D., of the Department of Psychiatry at The Johns Hopkins University School of Medicine, linked UA levels to high volumes of so-called white matter hyperintensities (WMH), which are small dead areas of the brain that occur when brain cells are deprived of oxygen. Lack of oxygen due to clots or burst blood vessels in the brain are hallmarks of classic large strokes.

"Over a lifetime, it is common to have a small number of these mini strokes and not even notice," says Schretlen, "but as the overall volume of WMH increases, the damage can seriously disrupt how quickly we think and how effectively we learn and remember information."

The role of UA is best known in gout, where buildup of the fatty acid creates pain and disability in the feet and toes. However, UA appears to play contradictory roles in the brain, says Schretlen. For example, UA is a powerful antioxidant that might even protect against Parkinson disease and Alzheimer disease, possibly because antioxidants destroy oxygen free radicals that damage tissue.

On the other hand, elevated UA accompanies diabetes, obesity and heart disease, and it is a well-known risk factor for stroke. One possible explanation of its seemingly contradictory nature is that, like a double-edged sword, UA is beneficial, but processes leading to its production can be harmful under some circumstances, says Schretlen.

ScienceDaily: Mini-strokes Linked To Uric Acid Levels

[Michaelangelica]

Don't you hate these pre-emtive press releases?
"Discovered the cure to Alzheimer's" (maybe perhaps in 20 years- if you give us lots of money for our research and BMWs.)
So many science press releases are like this.

Alzheimer's cold sore virus link
Cold sore
The cold sore virus has been linked to Alzheimer's disease
Evidence is building that the cold sore virus may be linked to Alzheimer's disease, an expert says.

In lab tests, Manchester University found brains infected with the herpes simplex virus, HSV-1, saw a rise in a protein linked to Alzheimer's.

Scientists believe the discovery could pave the way for a vaccine that may help prevent the brain disorder, New Scientist magazine reported.

But such a breakthrough was a long-time off, experts said.


We need to carry out much more work into this, but the problem is people are quite sceptical of a viral link
Dr Ruth Itzhaki, of Manchester University

The researchers infected cultures of human brain cells with the virus and found a "dramatic" increase in levels of the beta amyloid protein - the building blocks of deposits, or plaques, which form in the brains of people with Alzheimer's

BBC NEWS | Health | Alzheimer's cold sore virus link

[Michaelangelica]

Brain Exercise Can Enhance Memory, Thinking, In Older Adults

ScienceDaily (Nov. 20, 2007) — Doing the right kind of brain exercise can enhance memory and other cognitive abilities of older adults, according to new research.


Dr. Elizabeth Zelinski of the University of Southern California Andrus Gerontology Center presented data* from the IMPACT study (Improvement in Memory with Plasticity-based Adaptive Cognitive Training) – the largest study ever done on aging and cognitive training using a program available to the public.

Brain Exercise Can Enhance Memory, Thinking, In Older Adults

[Michaelangelica]

Alzheimer's Treatment: 'Cocktail' Of Compounds Improves Brain Function In Rodents

ScienceDaily (Nov. 29, 2007) — MIT researchers have shown that a cocktail containing three compounds normally in the blood stream promotes growth of new brain connections and improves cognitive function in rodents.
. . .
In the Brain Research paper, the MIT team reported that rodents given a cocktail of DHA (a type of omega-3 fatty acid), uridine and choline showed a greatly increased concentration of dendritic spines, which receive messages in the postsynaptic neuron. That indicates that synapse regeneration has occurred, which is unusual, Wurtman said.

Synapse regrowth could also prove an effective treatment for other brain diseases, such as Parkinson's, or for brain injuries, he said.

The researchers found that rodents who received the treatment performed much better on tests of cognitive ability

Alzheimer's Treatment: 'Cocktail' Of Compounds Improves Brain Function In Rodents

High Blood Pressure May Heighten Effects Of Alzheimer's Disease

ScienceDaily (Nov. 29, 2007) — Having hypertension, or high blood pressure, reduces blood flow in the brains of adults with Alzheimer's disease, according to a new study presented today at the annual meeting of the Radiological Society of North America.

High Blood Pressure May Heighten Effects Of Alzheimer's Disease

[InfiniteNow]

Why fish oil is good for you

UCLA researchers find anti-Alzheimer's mechanism in omega-3 fatty acids

It's good news that we are living longer, but bad news that the longer we live, the better our odds of developing late-onset Alzheimer's disease.

Many Alzheimer's researchers have long touted fish oil, by pill or diet, as an accessible and inexpensive "weapon" that may delay or prevent this debilitating disease. Now, UCLA scientists have confirmed that fish oil is indeed a deterrent against Alzheimer's, and they have identified the reasons why.

Reporting in the current issue of the Journal of Neuroscience, now online, Greg Cole, professor of medicine and neurology at the David Geffen School of Medicine at UCLA and associate director of UCLA's Alzheimer Disease Research Center, and his colleagues report that the omega-3 fatty acid docosahexaenoic acid (DHA) found in fish oil increases the production of LR11, a protein that is found at reduced levels in Alzheimer's patients and which is known to destroy the protein that forms the "plaques" associated with the disease.

The plaques are deposits of a protein called beta amyloid that is thought to be toxic to neurons in the brain, leading to Alzheimer's. Since having high levels of LR11 prevents the toxic plaques from being made, low levels in patients are believed to be a factor in causing the disease.

Alzheimer's is a debilitating neurodegenerative disease that causes memory loss, dementia, personality change and ultimately death. The national Alzheimer's Association estimates that 5.1 million Americans are currently afflicted with the disease and predicts that the number may increase to between 11 million and 16 million people by the year 2050.

The researchers examined the effects of fish oil, or its component DHA, in multiple biological systems and administered the oil or fatty acid by diet and by adding it directly to neurons grown in the laboratory.

"We found that even low doses of DHA increased the levels of LR11 in rat neurons, while dietary DHA increased LR11 in brains of rats or older mice that had been genetically altered to develop Alzheimer's disease," said Cole, who is also associate director of the Geriatric Research Center at the Veterans Affairs Medical Center.

To show that the benefits of DHA were not limited to nonhuman animal cells, the researchers also confirmed a direct impact of DHA on human neuronal cells in culture as well. Thus, high levels of DHA leading to abundant LR11 seem to protect against Alzheimer's, Cole said, while low LR11 levels lead to formation of the amyloid plaques.

Fish oil and its key ingredient, omega-3 fatty acids (found in fatty fish like salmon), have been a mainstay of alternative health practitioners for years and have been endorsed by the American Heart Association to reduce the risk of cardiovascular disease.

Fatty acids like DHA are considered "essential" fatty acids because the body cannot make them from other sources and must obtain them through diet. Years of research have shown that DHA is the most abundant essential fatty acid in the brain, Cole said, and that it is critical to fetal and infant brain development. Studies have also linked low levels of DHA in the brain to cognitive impairment and have shown that lower levels may increase oxidative stress in the brains of Alzheimer's patients.

Based on the positive results, the National Institutes of Health is currently conducting a large-scale clinical trial with DHA in patients with established Alzheimer's disease. For those patients, Cole said, it may be too late in the disease's progression for DHA to have much effect. But he is hopeful that the NIH will conduct a large-scale prevention clinical trial using fish oil at the earliest stages of the disease — particularly because it is unlikely that a pharmaceutical company will do so, since fish oil in pill form is readily available and inexpensive.

Still to be determined, he said, "is what the optimal dose should be. It could be that a smaller amount might be helpful, especially in a place like the south of France, where people are already on a Mediterranean diet."

Here in the United States, though, where fish consumption is not very high, the dose may need to be higher.

"There's a deficiency of DHA to begin with," Cole said, "and this may contribute to the low LR11 seen in many Alzheimer's patients."

In addition to Cole, authors included Qui-Lan Ma, Bruce Teter, Oliver J. Ubede, Takashi Morihara, Dilsher Dhoot, Michael D. Nyby, Michael L. Tuck and Sally A. Frautschy, all of UCLA.

Funding for the research was provided by a grant from the National Center for Complementary and Alternative Medicine. The research was initiated with support from the National Institute on Aging.

The UCLA Department of Neurology encompasses more than a dozen research, clinical and teaching programs. These programs cover brain mapping and neuro-imaging, movement disorders, Alzheimer's disease, multiple sclerosis, neurogenetics, nerve and muscle disorders, epilepsy, neuro-oncology, neurotology, neuropsychology, headaches and migraines, neurorehabilitation, and neurovascular disorders. The department ranked No. 1 in 2005 and 2006 among its peers nationwide in National Institutes of Health funding.

For more information, visit UCLA Neurology.

[Michaelangelica]

My daughter told me yesterday that Terry Prattchett may have Alheimers

That is terrible, if true. He has a beautiful, creative (to the power of 10) mind. He is my favourite author. I go back and read and re-read his books always discovering new things.
I have only ever read one other fiction book more then once (Lord of the Rings)

Hazel Hawke, sharp, intelligent, generous ex- wife of our ex-prime minister also has Alzyheimers

[Monomer]

Cystatin C may help treat Alzheimer's

NEW YORK, Nov. 19 (UPI) -- Amyloid beta plaques, a hallmark of Alzheimer's disease, can be prevented by interacting with the protein cystatin C, U.S. and German researchers have found.

Lead author Efrat Levy of the New York University School of Medicine said two animal studies may open the door to new treatments for Alzheimer's disease that mimic the effects of cystatin C.

The first study, by Levy and researchers at the Nathan S. Kline Institute for Psychiatric Research and New York University School of Medicine, and the second study with Levy and colleagues in the laboratory of Dr. Mathias Jucker at the Hertie-Institute for Clinical Brain Research in Tubingen, Germany, used genetically engineered mice to produce human cystatin C and abundant amounts of amyloid beta plaques in their brains.

The protein cystatin C bound to the soluble, non-pathological form of amyloid beta in these mice, and inhibited the aggregation and deposition of amyloid beta plaques in the brain, Levy said.

Both studies are published online in advance of the December print issue of the journal Nature Genetics.

[Michaelangelica]

Now this bastard of a disease is getting personal.
What can be done?
More money for research?

Why does it attack such intelligent vibrant people with so much to offer the world?
Terry Pratchett has more ideas and more weird neuron connections to bizarre useless information than anyone on this planet.
He is a most neglected and undervalued writer even if he sells more books than anyone else he is still stupidly seen as a cult thing.
He has created his own unique and wonderful "genre" and people can't put him in a box.
BUT THIS IS TERRIBLE

*** Discworld Monthly ***
*** Issue 129: January 2008 ***

Table of Contents:

1. Editorial
2. News
3. Readers' Letters
4. DiscTrivia
5. Review: Hogswatch Event 2007
6. Competitions
7. Review: Guards! Guards! 24th November 2007
8. The End
--------------------------------------------------------------------
1. Editorial

Welcome to issue 129 and the start of a shiny new year. Unless you
live on another planet you can't have missed the news that Terry has
been diagnosed as having a rare form of early onset Alzheimers.
Below is what Terry wrote about it on 11th December 2007.


AN EMBUGGERANCE

Folks,

I would have liked to keep this one quiet for a little while, but
because of upcoming conventions and of course the need to keep my
publishers informed, it seems to me unfair to withhold the news. I
have been diagnosed with a very rare form of early onset
Alzheimer's, which lay behind this year's phantom "stroke".

We are taking it fairly philosophically down here and possibly with
a mild optimism. For now work is continuing on the completion of
Nation and the basic notes are already being laid down for Unseen
Academicals. All other things being equal, I expect to meet most
current and, as far as possible, future commitments but will discuss
things with the various organisers. Frankly, I would prefer it if
people kept things cheerful, because I think there's time for at
least a few more books yet )


PS I would just like to draw attention to everyone reading the
above that this should be interpreted as 'I am not dead'. I will,
of course, be dead at some future point, as will everybody else.
For me, this maybe further off than you think - it's too soon to
tell. I know it's a very human thing to say "Is there anything I can
do", but in this case I would only entertain offers from very
high-end experts in brain chemistry.


Then due to the high amount of traffic he was receiving he updated
the news with the following on the 12th December.

AN UPDATE

Folks,

My good friend Sandra Kidby of PJSM Prints
[http://www.pjsmprints.co.uk] is allowing me to use her website
because I am proverbially too busy to run one of my own. We have
hardly the time even to read the thousands of messages that have
come in here, let alone reply to them, but thank you all.

Could I make a small comment, however? Lots of people are sending
me plot ideas. Please, I have a lot of ideas. There is no shortage
of ideas and ideas sent to me, even with the very best of
intentions, are carefully filleted out of the correspondence before
they even get to me. I know they are sent in an effort to help, and
I appreciate this, but I advise you not to waste your time.

I am also getting a lot of requests for interviews. I am not giving
any because everything I have got to say or that can be said is in
the bulletin below. There is no point in saying it again, but in a
different order.

Can I remind everybody that I still aten’t dead, even today.

Thanks again for all your good wishes.


Discworld Monthly of course wishes Terry all the best and hopes that
the world will soon leave him alone a bit so that he can get on with
what he enjoys doing most which is writing books

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