News and Research Updates on Parkinson's Disease. Articles will be posted in reverse chronological order with the newest items first.

Please visit the original website for more information about these articles.

An excellent resource for following Alzheimer's Disease news and research updates is Yahoo! News Full Coverage...

[This message was edited by Casey on December 19, 2002 at 09:43 AM.]

Yes we do,every nite,& at 2 pm central time.

Lynne, do y'all still hold the chats?

If you do, there are probably some here who may be interested.

Thanks!

Would you like talking with others who have AD.Go to alzinfo.org
We chat at 2 & 8 pm central times.

Cell Insight May Lead to New Drug Targets

Agents against Alzheimer's, Parkinson's, diabetes are possible, researchers say.

By E.J. Mundell
HealthDay Reporter

THURSDAY, Feb. 10 (HealthDay News) -- After combing through thousands of candidates, researchers say they've identified a compound that can protect, in a whole new way, cells threatened by disease.

The breakthrough may pave the way to drugs that fight illnesses such as Alzheimer's, Parkinson's disease, diabetes and a host of viral infections, the scientists said.

"That's why there's so much interest in this paper," said lead researcher Junying Yuan, a professor of cell biology at Harvard University Medical School.

Her team's findings are published in the Feb. 11 issue of Science.

Almost every illness involves the death of an excessive number of body cells due to stresses from both inside and outside the cell. Biologists call one of the most potent forms of cellular stress "endoplasmic reticulum (ER) stress."

"The endoplasmic reticulum is a tiny organ near the cell's nucleus," Yuan explained. "It's responsible for making proteins that are then exported up to the outside of the cell."

In neurodegenerative diseases such as Alzheimer's, Parkinson's and Lou Gehrig's disease, as well as in other illnesses, outside pressures can cause this cellular organ to malfunction.

"It's very sensitive to stress, which affects its ability to fold the proteins -- they need to be folded a certain way for transport," Yuan said. When this misfolding occurs, proteins start "backing up" in the endoplasmic reticulum, "like a room getting full of junk," she said.

"There's increasing thought, in a number of places, that neurodegenerative diseases are, at their foundation, diseases of protein folding," added Bill Thies, vice president for medical and scientific affairs at the Alzheimer's Association. Finding ways to stop the misfolding of proteins in cells "could be broadly applied to a lot of these diseases, including Alzheimer's, Parkinson's disease, ALS [Lou Gehrig's disease], and others," he said.

For decades, cell biologists and medical researchers have looked for ways to protect cells from ER stress caused by disease. One way is through drugs that inhibit kinases -- cellular compounds that add phosphates to proteins, a necessary step in the transport process.

But kinases have their opposite -- phosphatases, which go to work stripping phosphate from these proteins.

Interrupting either kinase or phosphatase activity stops the steady transport of proteins, giving clogged endoplasmic reticulums a bit of "breathing room."

"The 'junk' stops building up," Yuan explained. "So, inhibiting these processes can really protect cells."

Because there are hundreds of different kinases, "it's been relatively easy to make compounds to inhibit any one of them," Yuan said.

But finding a phosphatase inhibitor has proven a lot harder.

"That's because our genome only makes five or six kinds of phosphatases," Yuan said. "So, the problem has been to control the specificity -- how do we control that this particular phosphate is stripped off a protein, but not that one?"

Her team believes it has found the first such compound to do so -- a small molecule they called salubrinal. After looking through 19,000 candidate compounds, the researchers report that salubrinal appears to target only one specific cellular phosphotase complex.

Article

LATEST LAB-LEVEL ALZHEIMER’S TREATMENT LINES EVOKES HOPE
Priyanka
Date : NOV 02, 2004

The news that researchers have hit upon a strategy to prevent or treat Alzheimer’s disease has come as good news for the Alzheimer’s patients across the world. Even though the US medical fraternity is testing this strategy at the laboratory, but the news has evoked some hope for the patients fighting hard with this disease.

Till now all that is known about cause of Alzheimers disease is that it is due to accumulation of plaques and tangles of abnormal amyloid protein in the brain. These are known as amyloid beta, which has the capability to attack the nerve cells. The scientists are looking for a method that can stop amyloid beta aggregation and formation of plaques. Recently, the scientists from Stanford University Medical School in California have envisioned a Trojan horse strategy.

Here a small bifunctional molecule has been created that would bind with the amyloid beta and prevent the formation of plaques and tangles. The scientists have confirmed that this molecule has helped in reducing the neurotoxicity significantly. Clinical application of this newly devised approach to Alzheimer’s is still nowhere in site for the benefit of patients as this has to undergo several medical tests at the laboratories.

The medical researchers and chemists at the Harvard Medical School in Boston will also approve the new lines of treatment underway in New York.

Article

Dementia Diagnostics Made Evidence-Based: A Critical Evaluation of Cognitive Assessment Tools in Clinical Dementia Diagnostics

Intro:

Diagnostic tests for dementia have historically been validated in specialty memory clinic populations with a high prevalence of dementia. In the general elderly population, with a prevalence of 5% to 10%, there is a need for valid short tests with high predictive value. This article summarizes the currently available neuropsychological tools for diagnosing and predicting early dementia in a primary care population.

Medscape article Sign up is free to read.

'Alzheimer's Gene' Affects Even Healthy Seniors

Causes problems with prospective memory, researchers discover

MONDAY, Jan. 24 (HealthDayNews) -- Even if they're healthy, older people with the higher-risk genotype for Alzheimer's disease can suffer major problems with prospective memory -- the ability to remember what they need to do in the future, such as take medications or make a doctor's appointment, a new study says.

People who carry the high-risk e-4 allele on both of their ApoE genes are eight times more likely to develop Alzheimer's as non-carriers. People with the high-risk allele on only one ApoE gene are three times more likely to develop Alzheimer's than non-carriers, according to the research.

University of New Mexico researchers studied a group of 32 healthy, dementia-free adults between 60 and 87 years old. Half of them carried the e-4 allele and half did not.

The study participants were asked to do a prospective memory task that required them to remember to write a specific word when they saw a target word. Far more often than the non-carriers, the e-4 carriers forgot to remember to write down the specified word when they were supposed to, meaning they forgot to do what they meant to do, when they meant to do it.

The findings counter the prevailing view that the e-4 allele has only subtle, undetectable effects on a carrier's cognition, the researchers said.

In light of the study results, doctors might consider helping even healthy e-4 carriers to improve their prospective memory, the study authors said. The study also suggests that testing prospective memory may prove useful as an early diagnostic tool for Alzheimer's disease (AD).

Article

Test May Help Detect Alzheimer's Earlier

Tue Feb 1, 8:43 AM ET Health - AP

A highly sensitive new test could lead to a different way to diagnose people with Alzheimer's disease, possibly helping find the illness in its early stages when there might be time for treatment.

While as many as 4 million Americans are thought to suffer from the memory-destroying illness, the only way to diagnose it definitively is by studying brain tissue during an autopsy.

It is important to have some way to diagnose the disease while the patient is still alive, especially during its early stages, so experimental treatments can be evaluated, and to catch it at a time when the disease might be treatable.

"If you can't diagnose it, you're not going to have a therapy for it," said Chad A. Mirkin of Northwestern University.

Many companies have experimental therapies, he said, "But those therapeutics aren't very good if you can't definitively diagnose and follow a disease," explained Mirkin, a lead researcher — along with William L. Klein — on a team that developed the new test, which can detect small amounts of proteins in spinal fluid.

The team's findings are reported in Tuesday's issue of Proceedings of the National Academy of Science.

The new test, called a bio-barcode assay, is 100,000 times to 1 million times more sensitive than other available tests, Mirkin said in a telephone interview.

It was first used last year in testing for a marker for prostate cancer, and Mirkin said he invited other investigators to suggest subjects for further testing

Klein, also at Northwestern, had done research associating Alzheimer's with a protein in the brain called amyloid-beta-derived diffusable ligand, or ADDL, Mirkin said.

So the research team set out to try and detect ADDL in spinal fluid.

They got samples of the spinal fluid of 30 people, 15 who had Alzheimer's disease and 15 who did not.

The researchers found at least some ADDL in all the patients, which Mirkin said is an indication that everyone may have a baseline level of the protein.

"What was really encouraging," he said, is that the concentration of ADDL increases as the disease gets worse, so the progression of the illness could be followed.

"Do we have a new diagnostic for Alzheimer's?" Mirkin said. "That's a bit premature."

The method needs to be repeated and tested on more patients, he said. Also tests need to be done to see if high levels of ADDL occur in other memory loss diseases.

But, the researchers said in their paper, the work provides a "potential reliable detection method for diagnosing" Alzheimer's Disease.

In addition, Mirkin said, the researchers are hoping to use the new test to search for proteins and other chemicals that can offer early diagnoses of other diseases, ranging from cancers to AIDS to mad cow.

ADDLs are small soluble proteins. To detect them the researchers used nanoscale particles that had antibodies specific to ADDL. Some particles were magnetic and some of gold with strings of DNA attached.

The antibodies bind to the ADDL, sandwiching the protein between the two particles. They are then removed from the solution magnetically and the hundreds to thousands of DNA strands attached to the gold particles serve as a barcode because they can be used to label the specific target with standard detection methods.

Dr. Samuel Gandy, who was not part of the research team, said the report is impressive but needs to be repeated with larger numbers of subjects.

If the test can, in fact, correlate the presence of ADDLs with brain function, "this is good news indeed for identifying who is at risk for Alzheimer's and potentially for following the effectiveness of many new anti-amyloid medicines that are now in clinical trials," said Gandy, vice chair of the National Medical and Scientific Advisory Council of the Alzheimer's Association and director of the Farber Institute for Neurosciences at Thomas Jefferson University in Philadelphia.

Article

Cardiovascular Risk Factors at Midlife Increase Dementia Risk

NEW YORK (Reuters Health) Jan 24 - The presence of cardiovascular risk factors -- diabetes, hypertension, high cholesterol and smoking -- in middle age is strongly associated with late-life dementia, investigators in California report in the January 25th issue of Neurology.

"What is bad for the heart is also bad for the brain," lead investigator Dr. Rachel A. Whitmer said in an interview with Reuters Health. "Future research needs to figure out what the mechanisms are."

Dr. Whitmer, of Kaiser Permanente Division of Research, Oakland, and her colleagues correlated the results of health evaluations conducted between 1964 and 1973, when patients were between 40 and 44 years old, and the diagnosis of dementia between 1994 and 2003. The 8845 subjects were members of an HMO and had equal access to medical care. Dementia was documented among 721 individuals at ages 66 to 82.

Medscape article. Sign up to read there is free and they don't bug you with emails.

Ces, thank you so much, this is an excellent group of articles.I have been following this review of the convention , held this summer in Phila.The University of Pittsburgh has been top notch in their research.

Gene Therapy Improves Alzheimer's in Mouse Study

Mon Jan 17, 5:40 PM ET Health - Reuters

NEW YORK (Reuters Health) - Gene therapy might one day be an effective treatment for Alzheimer's disease, new experiments in mice suggest.

The study found that gene delivery of a human protein called apolipoprotein E2 (apoE2) helped cut down amyloid-beta deposits in the brains of mice. The deposits are the hallmark of Alzheimer's disease.

"Gene therapy offers the opportunity to influence the progression of this horrible disease," Dr. Inder M. Verma, who led the study, told Reuters Health.

Apolipoprotein E latches on to fats and clears them from the bloodstream. It is also found in the brain, where it is thought to perform a similar function by getting rid of unwanted substances.

People produce different forms of apolipoprotein E, and studies have shown that those with apoE2 tend to be protected against Alzheimer's disease, whereas those with apoE4 are more likely to develop the disease.

Verma, who is based at The Salk Institute in La Jolla, California, and his colleagues investigated whether gene delivery of apoE2 could directly affect the deposits of amyloid-beta in mice that had been genetically altered to develop Alzheimer's disease.

ApoE2 gene therapy resulted in a 30 percent to 50 percent reduction in amyloid-beta in the mice's hippocampus, a region of the brain that helps control memory.

Article

FRIDAY, Jan. 7 (HealthDay News) -- Hope is not a word often used in discussions of treatments for Alzheimer's disease.

But, many of the professionals who attended the ninth international conference on Alzheimer's Disease in Philadelphia last year predicted a viable treatment within the next 10 years.

"Our goal of delaying the disabling symptoms and eventually preventing Alzheimer's is a feasible objective that we now believe the research community can achieve in the next decade," said Sheldon Goldberg, president and CEO of the Alzheimer's Association.

Excerpt from further on...

Gandy is among the researchers who see that the key to Alzheimer's may lie with the diagnosis and treatment of plaques and other abnormal protein aggregates called "tangles" in the brain. The main component of plaques, a toxic protein fragment called beta-amyloid, is a primary suspect in the death of brain cells, which causes the mental deterioration that is the hallmark of the condition.

He cited a breakthrough by Dr. William E. Klunk and his colleagues at the University of Pittsburgh. They recently developed a compound known as Pittsburgh Compound-B (PIB) that sticks to amyloid plaques and makes them visible on positron emission tomography (PET) scans for the first time. According to Gandy, the ability to finally view, monitor and measure amyloid probably heralds the beginning of a new chapter in Alzheimer's research.

"Combined with advances in medications to rid the brain of amyloid plaques, this could very well result in a major breakthrough in our understanding of and successful treatment of Alzheimer's," Gandy said. "It will not only answer questions about how amyloid damages brain cells, but it will help us monitor whether and how well the new medications work."

According to Gandy, as PET technology becomes more widespread, it will be increasingly possible to test the hypothesis that amyloid is the primary culprit in Alzheimer's.

"Our inability to visualize or measure amyloid in the brain was a huge bottleneck for research," Gandy explained. "Now that there are both medications that can rid the brain of amyloid and a method of visually monitoring the amount of amyloid present and the effect of the medication on it, we're about to move past that bottleneck once and for all. We should know very soon whether amyloid is the right target or whether our focus on it has been a huge mistake."

Gandy admitted that the amyloid hypothesis isn't the only one being rigorously pursued by the medical community.

"There are other models -- potential explanations -- for what causes Alzheimer's," he said. "Some researchers are looking closely at abnormal oxidation and the role it may play in the aging of brain cells, for example. There is some evidence that the accumulated damage from oxidation could result in the cognitive impairments characteristic of this disease, just as oxidation affects the condition of other cells in the body."

Whole article.

Ces, I heard this opinion on a brief message in the news awhile back

Diabetes in Midlife Linked to Later Dementia

2 hours, 58 minutes ago Health - Reuters

By Anthony J. Brown, MD

NEW YORK (Reuters Health) - Middle-aged people with diabetes are nearly three times more likely to develop dementia in old age than people without diabetes, according to a new study.

Studies looking at a cross-section of the population have "tied diabetes to Alzheimer's disease (news - web sites) or dementia," Dr. Michal Schnaider Beeri, from Mount Sinai School of Medicine in New York, told Reuters Health. "Our study is special because it shows a strong association between these disorders over several decades."

The study involved 2600 subjects who participated in the Israeli Ischemic Heart Disease study in the 1960s and were still alive and available for follow-up in 1999. The subjects were between 40 and 65 years of age when the study began.

The mental status of 1892 participants was determined, and 652 were identified as possibly demented. This was confirmed in 309 subjects (16.3 percent).

Those with diabetes during the study were 2.83-times more likely to develop dementia than those without diabetes, the investigators report in the medical journal Neurology.

As for how diabetes might promote dementia, Beeri offered three possibilities.

First, excess glucose can create high levels of so-called "advanced glycation end products," and these have been linked to dementia and Alzheimer's disease in several studies, she said.

"These end products seem to stick to beta-amyloid and prevent its degradation," the researcher explained, referring to the abnormal protein that accumulates in the brain of people with Alzheimer's disease.

Rest of article.

Source: University Of Wisconsin-Madison

Date: 2004-09-13

Discovery May Halt Progression Of Alzheimer's
In a finding that may cause a dramatic shift in the way scientists and researchers search for a therapy for Alzheimer's disease, a team of researchers led by Jeff Johnson, an associate professor at the School of Pharmacy, has discovered that increased expression of a protein called transthyretin in the brain appears to halt the progression of the disease. The findings appear in the current issue of The Journal of Neuroscience.

"This work shows convincingly that if we can intervene in Alzheimer's pathology by introducing molecules and drugs into the brain and increase transthyretin levels, we could slow the progression of the pathology," says Johnson, who co-authored the report with Thor Stein, a former graduate student in UW's M.D./Ph.D. program who performed most of the experiments. "Even if patients have plaque formation in the brain, they still could have normal function."

For years, researchers have focused on creating an animal model that mimics the pathology of Alzheimer's disease to test potential therapies. By genetically engineering mice to express mutated genes from the families of patients with early-onset Alzheimer's disease, researchers produced several mouse lines that over-express the human amyloid precursor protein (APP), a protein involved in the disease development. While the mice developed plaque formation in their brains, they didn't develop the other hallmark of Alzheimer's disease -- neurofibrillary tangles, a leading indication that neural cells are dead or dying.

Most researchers noticed this and continued to search for a way to create the perfect mouse model. Johnson had a different thought.

"I said to myself, everybody is trying to kill neurons in mice to create the Alzheimer's pathology," he explains. "And here we have a mouse that has amyloid deposition and plaques yet no neurons are dying. Let's try to figure out why these mice aren't getting the disease."

The answer was surprising, and could completely alter the way researchers think about treating Alzheimer's disease.

Johnson's research is based on the widely held amyloid hypothesis: When amyloid precursor protein (APP) is cut into pieces in the human brain, there are "good" cuts - proteins that help to protect neurons - and "bad" cuts, toxic beta-amyloid protein that, when present in large amounts, causes massive neural cell death, leading to cognitive function loss. In Alzheimer's patients, "bad-cut" proteins significantly outnumber "good cut" proteins.

Stein, under Johnson's supervision, analyzed the brains of the mice with plaque formation, and noticed something interesting: The levels of a pair of specific proteins, transthyretin and IGF-2, increased dramatically. Since transthyretin had been shown in test tubes to bind to the toxic beta-amyloid protein, Johnson and Stein hypothesized that in the mice, the transthyretin was preventing the "bad cut" toxic beta-amlyoid protein from interacting with the neuronal cells, thereby preventing tangle formation and subsequent neuronal cell death.

"Somehow, the adapted mechanism in the mice was due to the balance between the good cut and the bad cut," says Johnson. "The good cut product was causing the increase in transthyretin, which was balancing the toxicity of the beta-amyloid, or bad-cut protein."

Rest here.


One month later:


Source: NIH/National Institute Of Environmental Health Sciences

Date: 2004-10-25

Researchers Identify Brain Protein That Halts Progression Of Alzheimer’s
Researchers have identified a protein in the brain that halts the progression of Alzheimer’s disease in human brain tissue. The protein, known as “transthyretin,” protects brain cells from gradual deterioration by blocking another toxic protein that contributes to the disease process.

The National Institute of Environmental Health Sciences, a component of the National Institutes of Health, provided $1.25 million to University of Wisconsin-Madison scientists for the transthyretin study. The scientists will present their findings October 26 at the 34th annual meeting of the Society for Neuroscience in San Diego, Calif.

“The results of this study are promising,” said Kenneth Olden, Ph.D., director of the NIEHS. “More studies are needed to understand how transthyretin can be used in treating Alzheimer’s patients.”

Alzheimer’s disease progresses when a toxic protein, known as “beta-amyloid,” attacks the brain’s nerve cells involved in learning and memory. The beta-amyloid creates sticky plaques and tangles that gradually disable nerve cells, producing memory loss. Transthyretin appears to protect brain cells by intercepting the beta-amyloid and preventing it from interacting with the brain tissue.

“Based on the results of animal studies, we know that the disease process depends in large part on the delicate balance between the ‘good’ transthyretin protein and the ‘bad’ beta-amyloid protein,” says Dr. Jeff Johnson, associate professor at the University of Wisconsin’s School of Pharmacy and lead author on the study. “In Alzheimer’s patients, the ‘bad’ proteins significantly outnumber the ‘good’ proteins.”

Johnson discovered the effect of transthyretin while studying mice genetically engineered with defective genes taken from human patients with early-onset Alzheimer’s disease. As expected, the defective genes produced mice with higher-than-normal levels of the toxic beta-amyloid protein. These mice did not, however, exhibit symptoms of Alzheimer’s disease.

“We have a mouse whose brain is bathing in toxic beta-amyloid without exhibiting disease symptoms,” says Johnson. “We were all asking the same question – Why aren’t these nerve cells dying?”

Rest here.

Cathy

Certain NSAIDs Fail to Slow Progression of Alzheimer's Disease


***Certain NSAIDs Fail to Slow Progression of Alzheimer's Disease***

(This news release can be found on our web site at
http://www.alzheimers.org/nianews/nianews57.htm)

A new clinical trial finds that two non-steroidal, anti-inflammatory drugs (NSAIDs) do not slow
the rate of cognitive decline in people with mild to moderate Alzheimer's disease (AD). The
multicenter study, supported by the National Institute on Aging (NIA) and reported in the June
4, 2003, issue of the Journal of the American Medical Association (JAMA), is the first clinical
trial to prospectively test rofecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, and
naproxen, a non-selective NSAID, in people with AD.

The investigators, led by principal investigator Paul S. Aisen, M.D., of Georgetown University
Medical Center, Washington, D.C, randomly assigned the study's 351 participants to one of three
treatment groups: rofecoxib, naproxen, or placebo. Cognition was measured before and after
treatment by scores on the Alzheimer's Disease Assessment Scale, a test evaluating memory,
attention, reasoning, language, and orientation. After 12 months of treatment, both the
rofecoxib and naproxen groups showed cognitive declines similar to those found in the placebo
group. While the results do not eliminate the possibility of a very small beneficial effect,
analysis indicates that it is highly unlikely that naproxen or rofecoxib treatment reduces the
one-year rate of cognitive decline, even by as much as one-third.

Although the study failed to show a treatment benefit in people who already have AD, NSAIDs
still could prove to be effective in preventing the disease, says Neil Buckholtz, Ph.D., chief
of the NIA's Dementias of Aging Branch. An NIA-supported prevention trial of NSAIDs is
on-going.

In an editorial in the same issue of JAMA, neuroepidemiologist Lenore Launer, Ph.D., of the
NIA's Laboratory of Epidemiology, Demography and Biometry, points out that the individuals
participating in this study met specific criteria and the outcome could be different, and
possibly beneficial, in another group of people with AD or in those at risk for the disease.

The study was conducted at 40 centers nationwide organized under the Alzheimer's Disease
Cooperative Study (ADCS), a consortium of academic and other research centers supported by the
NIA to coordinate and facilitate the clinical testing of compounds to prevent AD or delay the
onset of its symptoms. The NIA, part of the National Institutes of Health (NIH) at the U.S.
Department of Health and Human Services, was the primary funder of the trial, with additional
support provided to Georgetown University by the National Center for Research Resources, also
part of the NIH.

The rationale for the study was based on previous findings that inflammation is a central
feature of AD. The disease is an irreversible progressive brain disorder that occurs gradually
and results in memory loss, behavior and personality changes, and cognitive decline.

The NIA is the lead federal agency conducting and supporting research on AD and the aging
brain. Its Alzheimer's Disease Education and Referral (ADEAR) Center website offers information
on age-related memory change, including a list of clinical trials testing possible therapies
for AD, at http://www.alzheimers.org. The public may also contact ADEAR at 1-800-438-4380.

NOTE:****You are currently subscribed to the NIA News e-mail alert list. To unsubscribe to this
or other ADEAR lists, go to: http://www.alzheimers.org/maillist.htm
To avoid unauthorized addition or deletion of names to our lists, the ADEAR Center does not
honor subscribe/unsubscribe requests sent via e-mail.******
.
.
.
.
.
.

Use today wisely,
It's the only one we get.

Oh, for so short a time,
we are on loan to each other.

Jim

[This message was edited by Jim Kallio on June 06, 2003 at 05:40 AM.]

Jim K :

Thanks for posting all the Sites re research, as you say some news some not.

Thanks I am forwarding them to my daughters.

Eleanor

Some News--some not...

Credit source for this information I have here

http://new-www.adrc.wustl.edu/archives/html/alzheimer/2003-05/msg01227.html

Articles are here-------->>>>>>>>>.

http://www.forbes.com/2003/05/29/cx_mh_0529alzheimers.html ,,,,,,,,,,,,,,Pharmaceuticals Use Widening For Alzheimer's Drugs


http://www.forbes.com/2003/02/28/cx_mh_0228wyeth.html-------->>>>>>>>>Pharmaceuticals Wyeth's Confusing Alzheimer's News



http://www.forbes.com/2003/02/03/cx_mh_0203elan.html----->>>>>>>.Pharmaceuticals Elan Readies New Assault On Alzheimer's


http://www.forbes.com/2002/11/06/cx_mh_1106jama.html------>>>>>>>Pharmaceuticals Can Estrogen Drugs Prevent Alzheimer's?
.
.
.
.
.
.
.
..

.
.
.

Use today wisely,
It's the only one we get.

Oh, for so short a time,
we are on loan to each other.

Jim

[This message was edited by Jim Kallio on June 05, 2003 at 09:01 PM.]