Air Pollution May Raise Dementia Risk

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Fisher Center for Dementia Research

Can dirty air be bad for the brain? A new study suggests that smog and other air pollutants may contribute to memory loss and dementia.

The findings, part of a large and ongoing study of nurses in their 70s, found that long-term exposure to air pollution may speed up cognitive decline in older adults. Women who lived in areas with the worst quality air scored lower on tests of memory and thinking than those who lived in cleaner areas.

Exposure to polluted air contributed to the equivalent of about a two-year decline in brain function, which might lead to an earlier onset of Alzheimer’s and other forms of dementia. That translates to about two million cases of Alzheimer’s over a 40-year period, the researchers estimate.

The report, from the Archives of Internal Medicine, is one of the few to study the effects of air pollution on brain health.

It is difficult to establish a direct link between environmental toxins and a disease like Alzheimer’s, because so many factors are involved, and correlation does not equal causation. But this study examined thinking skills over a four-year period and involved a large sample size of more than 19,000 women living in different parts of the United States.

The levels of pollution in the study linked to memory and thinking problems were typical of exposure levels found in many areas of the United States.

Other studies have linked air pollution to an increased risk of heart attacks and strokes. Cardiovascular problems have likewise been linked to dementia and poor brain health.

“Unlike other factors that may be involved in dementia, such as diet and physical activity, air pollution is something we can intervene on as a society at large through policy, regulation and technology,” said Jennifer Weuve, assistant professor at the Rush Medical College in Chicago and the principal investigator of the study. “If our findings are confirmed in other research, air pollution reduction is a potential means for reducing the future population burden of age-related cognitive decline, and eventually, dementia.”

Air pollutants contain chemicals and metals that become suspended in the air. Fine particles may be particularly damaging, reaching deep into the lungs and possibly even penetrating into the brain. Sources of such emissions include cars, diesel-powered equipment and various industrial processes.

In earlier studies, levels of beta-amyloid, a toxic protein that builds up in the brains of those with Alzheimer’s disease, were higher among residents of polluted cities. Another report, from Germany, found that older women who lived near busy roads did worse on memory and thinking tests than similar women who lived in rural areas. Exposure to so-called black carbon, a product of traffic, over the previous one to 11 years has been linked to worse cognitive function in a study from China.

Animal studies have recorded higher levels of brain inflammation in animals exposed to polluted air. Increasingly, scientists believe that inflammation may play a role in Alzheimer’s and heart disease.

By ALZinfo.org, The Alzheimer's Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer's Research Foundation at The Rockefeller University.

Source: Jennifer Weuve, Robin C. Puett, Joel Schwartz, et al: “Exposure to Particulate Air Pollution and Cognitive Decline in Older Women.” Archives of Internal Medicine, Vol. 172 (No. 3), pages 219-227, 2012.

Alzheimer's Diagnosis: More Tests Improve Chance Of Early Detection

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Huffington Post

Two or three tests are better than one, when it comes to predicting the onset of Alzheimer's disease, a new study suggests.

The research, published in the journal Radiology, shows that using more than one diagnostic test could better predict which people with mild cognitive impairment will go on to develop Alzheimer's disease.

"Misdiagnosis in very early stages of Alzheimer's is a significant problem, as there are more than 100 conditions that can mimic the disease. In people with mild memory complaints, our accuracy is barely better than chance," study researcher P. Murali Doraiswamy, MBBS, professor of psychiatry and medicine at Duke Medicine, said in a statement. "Given that the definitive gold standard for diagnosing Alzheimer's is autopsy, we need a better way to look into the brain."

The study, conducted by Duke Medicine researchers, included 97 people with mild cognitive impairment who were part of the Alzheimer's Disease Neuroimaging Initiative. Researchers had the study participants undergo the typical diagnostic procedures for Alzhiemer's -- which includes cognitive testing -- as well as three otherdiagnostic tests. They included magnetic resonance imagine (MRI), cerebrospinal fluid analysis and fluorine 18 fluorodeoxyglucose positron emission tomography (also known as FDG-PET).

The study participants were followed for up to four years. Researchers found that the rate of misdiagnosis was highest when the study participants only received the typical cognitive testing -- 41.3 percent. However, that percentage went down with each additional test the person was given, with the lowest percentage of misdiagnosis occurring when all three tests were administered -- 28.4 percent.

And of all the tests, the FDG-PET seemed to add the most diagnostic value, the researchers noted.

According to the Alzheimer's Association, the earlier memory loss conditions are discovered, the better. That's because doctors are then able to know which medications to prescribe -- and not to prescribe -- early on, and patients can be aware of potential safety issues that may crop up.

Worries about dementia: How hospitalization affects the elderly

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Medical Xpress

Older people often worry about dementia and while some risks are known, for example alcoholism or stroke, the effects of illness are less clear. New research published in BioMed Central's open access journal Critical Care looks at illness requiring hospitalization and treatment in the intensive care unit (ICU) and finds that infection or severe sepsis, neurological dysfunction, such as delirium, or acute dialysis are all independently associated with an increased risk of a subsequent diagnosis of dementia.

This study was based on a random 5% of older (66 years or above) Medicare patients who were treated in intensive care in 2005 and whose health was followed for a further three years using Medicare claims data. Of the 25,368 patients included in the study 4,519 (17.8%) went on to receive a diagnosis of dementia during the three year follow up period. Patients with previous indications of cognitive impairment for whom dementia could have been an escalation of a pre-existing condition were excluded from the study. Increasing age was very strongly associated with diagnosis of dementia following ICU. The risk at 75 was more than double that of the 66 to 69 year olds. And this rose to more than five times the risk for those age 85 and older. Women had a marginally higher risk than men and, as other studies have shown, race was also important to risk. Length of stay in ICU was not a factor nor was the need for mechanical ventilation. Three factors related to the critical illness were independently associated with an increased risk of a diagnosis of dementia: a critical illness with the presence of an infection which increased to a higher risk with more severe infection such as severe sepsis, having acute neurologic dysfunction during critical illness, including anoxic brain damage, encephalopathy, and transient mental disorders, and finally acute renal failure requiring dialysis. This last risk was time-dependent and only increased the risk 6 months after the patient had been discharged from hospital. Dr Hannah Wunsch, from Columbia University Medical Center, lead author of the study commented, "Due to increasing life spans and better hospital care, millions of older people now survive a critical illness every year. Our study provides a greater understanding of the consequences of these hospitalizations on subsequent risk of receiving a diagnosis of dementia, and may allow for better planning and targeting future studies to high risk populations." More information: Risk factors for dementia after critical illness in elderly Medicare beneficiaries Carmen Guerra, Walter T Linde-Zwirble and Hannah Wunsch Critical Care (in press) Journal reference: Critical Care

Health roundup: Lonely more likely to develop dementia

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USA Today

Aging and loneliness: Older adults who feel lonely -- but do not necessarily live alone -- are more likely to develop memory loss and other symptoms of dementia, a Dutch study shows. The study doesn't prove the loneliness comes first: It's possible that people losing their mental sharpness react by withdrawing from social life and then report feeling lonely. But it's also possible that a lack of social stimulation and support speeds mental decline. (TIME)

Amarantus BioScience Licenses LymPro Alzheimer’s Disease Diagnostic Blood Test

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SUNNYVALE, Calif.– Amarantus BioScience, Inc. (OTCQB: AMBS), a biotechnology company discovering and developing treatments for diseases associated with protein misfolding and apoptosis, today announced that it has licensed the LymPro Alzheimer’s Disease Diagnostic Blood Test (LymPro) from Memory Dx, LLC (MDx), formerly known as Provista Life Sciences, Inc. LymPro originated from the University of Leipzig in Germany and has received over $3 million in research grants from the National Institutes of Health (NIH).

LymPro was designed with the purpose of diagnosing Alzheimer’s in its mild to moderate stage, a population of patients currently being tested in numerous clinical studies with amyloid-beta targeting strategies. LymPro works by identifying immune-based biomarkers in the blood of Alzheimer’s patients, diagnosing Alzheimer’s and allowing physicians to definitively differentiate Alzheimer’s disease from other forms of dementia.  This patient-specific identification has the potential to become an invaluable tool for Alzheimer’s disease clinical trials, where there has been a well-documented history of patient recruitment errors related to inaccurate diagnosis of Alzheimer’s. LymPro has completed two Phase 1 clinical studies in over 80 patients, showing 98% sensitivity and 96% specificity for Alzheimer’s disease diagnosis.  LymPro is ready to move into a Phase 2 validation study.  If successful, LymPro can begin generating revenue as a laboratory developed test (“LDT”) within 18 months of study initiation through commercial sales and through sales to companies performing Alzheimer’s disease clinical research.

“We believe LymPro has significant clinical and commercial potential as a diagnostic blood test for Alzheimer’s disease,” said Gerald E. Commissiong, President and CEO of Amarantus. “It is clear that the path forward for treating Alzheimer’s disease is to identify and initiate therapeutic intervention as early as possible. If proven effective, LymPro could provide physicians with a lower-cost, minimally-invasive intervention and reduce the need for costly brain imaging scans.  This license expands our diagnostic pipeline and complements our strategic focus on neurodegenerative diseases. While we are not currently developing MANF for Alzheimer’s disease, we believe that the cost-effective definitive identification of earlier-stage patients will create a significant opportunity for Amarantus to evaluate the MANF Program as a disease-modifying treatment in this large, underserved therapeutic indication.”

Under the terms of the agreement, Amarantus has agreed to issue two million shares of restricted common stock to MDx, pay a development milestone upon successful completion of the Phase 2 validation study, as well as pay a nine percent royalty on sales. In addition, Amarantus has agreed to retain MDx to perform the necessary validation study to gain Clinical Laboratory Improvement Amendments (CLIA) certification for LymPro. Together, Amarantus and MDx will expand their relationships with large pharmaceutical companies, and will also seek additional grant funding for the further development of LymPro. Amarantus has the right to assign or sub-license LymPro to a third party of its choosing at any time.

“Amarantus represents an excellent partner for Memory Dx because of its scientific focus on protein misfolding and aggregation, which we believe will continue to be critical in developing disease-modifying treatments for Alzheimer’s,” said William E. Gartner, President and CEO of Memory Dx, LLC. “This agreement with Amarantus is the final step in the transition of Memory Dx from a diagnostic product developer into a contract CLIA lab focused on driving revenues. We look forward to working with Amarantus to advance LymPro and get it into the hands of physicians so we can help address the significant socioeconomic problems caused by Alzheimer’s disease.”

About Alzheimer’s Disease

It is estimated that over 5.4 million people in the United States suffer from Alzheimer’s disease and over 300,000 patients are diagnosed annually, with nearly one in eight older Americans affected by the disease. Alzheimer’s is the sixth leading cause of death in the United States. The estimated cost of unpaid care in the United States is estimated at over $210 billion annually and the total payments for care are estimated at over $200 billion annually, including $140 billion in cost to Medicare and Medicaid. It is estimated that these figures will double by 2050. Amarantus believes the market opportunity for an effective Alzheimer’s disease diagnostic far exceeds $500 million annually.[1]

About Amarantus BioScience, Inc.

Amarantus BioScience, Inc. is a development-stage biotechnology company founded in January 2008.  The Company has a focus on developing certain biologics surrounding the intellectual property and proprietary technologies it owns to treat and/or diagnose Parkinson’s disease, Traumatic Brain Injury and other human diseases.  The Company owns the intellectual property rights to a therapeutic protein known as Mesencephalic-Astrocyte-derived Neurotrophic Factor (“MANF”) and is developing MANF-based products as treatments for brain disorders. The Company also is a Founding Member of the Coalition for Concussion Treatment (#C4CT), a movement initiated in collaboration with Brewer Sports International seeking to raise awareness of new treatments in development for concussions and nervous-system disorders. For further information please visit www.Amarantus.com.

Forward Looking Statements

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Such statements include, but are not limited to, statements about the possible benefits of MANF therapeutic applications and/or advantages presented by Amarantus’ PhenoGuard technology, as well as statements about expectations, plans and prospects of the development of Amarantus’ new product candidates. These forward-looking statements are subject to a number of risks, uncertainties and assumptions, including the risks that the anticipated benefits of the therapeutic drug candidates or discovery platforms, as well as the risks, uncertainties and assumptions relating to the development of Amarantus’ new product candidates, including those identified under “Risk Factors” in Amarantus’ most recently filed Annual Report on Form 10-K and Quarterly Report on Form 10-Q and in other filings Amarantus periodically makes with the SEC. Actual results may differ materially from those contemplated by these forward-looking statements Amarantus does not undertake to update any of these forward-looking statements to reflect a change in its views or events or circumstances that occur after the date of this presentation.

[1] http://www.alz.org/alzheimers_disease_facts_and_figures.asp

Changes in Alzheimer's research

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UCSanDiego

For years Alzheimer’s researchers have focused on testing experimental drugs on patients who already have a diagnosis of Alzheimer’s and significant changes in cognition, memory and behavior. It has now become quite clear that researchers have been trying to treat the disease at too late a stage. They agree that they need to be focusing on the very earliest stage, what is called “prodromal AD,” when patients suffer little or no cognitive or memory loss but scans show that their brains contain beta amyloid, the sticky plaques that are the hallmark of the disease that destroy healthy neurons.

“In the past people with prodromal Alzheimer’s disease would not have been considered to have the disease,” says Michael Rafii, MD, PhD, director of the UC San Diego Health System Memory Disorders Clinic.  “Now, we recognize it as a condition where we may be able to intervene and possibly prevent it from progressing to full blown Alzheimer’s disease.”

Rafii compares the early intervention to heart disease. “Until cholesterol was discovered as the culprit that caused plaques in the arteries that ultimately blocked blood flow and caused heart attacks, heart disease was being treated only after someone suffered a heart attack, which people often did not survive,” he said, adding that once cholesterol was identified and drugs were developed to keep arteries free of cholesterol and dangerous plaques, heart disease rates and death from heart attacks plummeted.  The same, he says, can be said for Alzheimer’s disease.  “We’ve been attacking the problem too late.”

More studies are studying the disease at this early prodromal phase. The Scarlet Road Study, currently enrolling patients at UC San Diego Health System, is one such innovative study.

Scarlet Road, Rafii says, is a double-blind, placebo-controlled study that will test the effect of injections of an experimental drug, gantenerumab, or placebo on people who have prodromal Alzheimer’s disease. Gantenerumab is a new experimental drug made from human antibodies, a type of protein produced by the human immune system in response to a foreign substance such as a virus or bacteria. Antibodies protect the body from disease by attacking these substances and destroying them. Gantenerumab has been developed to attack the beta-amyloid plaques in the brain. In animal tests, antibodies like gantenerumab have been shown to remove plaques from the brain. In some cases, there has been improvement of the animals’ ability to think, make decisions, concentrate or remember, called “cognitive function.”

The UC San Diego study will run over a two and a half year period. One third of study participants will receive a low drug dose, one third will receive a moderate drug dose and the remaining group will receive the placebo. Most studies follow a 50/50 drug to placebo formula; in this study participants have a two in three chance of receiving the actual experimental drug. Neither the participants nor study staff will know who is receiving the study drug and who is receiving the placebo.

For further information on the Scarlet Road Study call 858-246-1300 or emailCAPmemory@ucsd.edu

Diabetes Drug May Restore Memory In Alzheimer's

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Medical News Today

Researchers in Canada have discovered a drug originally intended for the treatment of diabetes may restore memory in brain cells affected by Alzheimer's disease. In tests on animal brain cells, they found that AC253, a diabetes drug that never made it to market, restored memory to levels similar to those of normal cells. Trials could start in five years, should further tests succeed, says the team.

The researchers write about their work in a paper published online in The Journal of Neuroscience on 28 November.

In a statement released on Tuesday, senior author Jack Jhamandas, a researcher with the Faculty of Medicine & Dentistry at the University of Alberta, says their discovery is "very important" because:

"... it tells us that drugs like this might be able to restore memory, even after Alzheimer's disease may have set in."

Estimates suggest in the next 30 years, 1,125,000 Canadians will be diagnosed with Alzheimer's disease.

Cells of people with Alzheimer's contain amyloid protein, which is found in particularly large amounts in cells from the memory and cognition parts of the brain. It is the presence of this protein that is believed to impair memory.

Last year, Jhamandas and his team showed that AC253 could block the toxic effects of amyloid protein that lead to brain-cell death.

For this latest study, they tested: read all about a Diabetes Drug May Restore Memory In Alzheimer's

Merck Makes A 'Speculative' Step Into Alzheimer's

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Forbes

Although several rivals have recently experienced setbacks with Alzheimer’s compounds, Merck hopes to defy the odds with plans to take a pill into a Phase II/III study with patients who suffer from mild-to-moderate stages of the disease. And while one analyst calls the move speculative, the decision underscores an ongoing willingness to place big bets on tackling Alzheimer’s, a market that may offer the pharmaceutical equivalent of a Powerball payoff.

To be specific, Merck (MRK) will test a beta-amyloid precursor protein site-cleaving enzyme, or BACE, inhibitor, which the drugmaker notes is the first drug with this type of mechanism to advance to this stage of clinical research. The Phase II portion of the new trial will enroll 200 patients and be completed by late 2013. The Phase III segment would then begin with 1,700 patients, and there is speculation that  second Phase III trial might also be attempted with only earlier-stage patients.

The decision comes after Bristol-Myers Squibb halted testing of an Alzheimer’s compound, and Pfizer and Johnson & Johnson gave up on their bapineuzumab compound, which failed to meet two Phase III primary endpoints in patients with mild-to-moderate stages of disease (read here). Eli Lilly, however, is proceeding with its solanezumab compound, which slowed cognitive decline in patients with mild disease, but showed no statistically significant reduction in functional decline (see this).

“Merck is committed to advancing the understanding and treatment of Alzheimer’s disease,” says Darryle Schoepp, a senior vp and head of neuroscience and ophthalmology at Merck Research Laboratories, in a statement. The trial, by the way, will study one of three oral doses of the compound, called MK-8931, which will be administered daily versus a placebo.

The effort underscores that a significant level of interest remains, at least among some researchers and executives, to study compounds in later-stage patients, despite the recent setbacks. For its part, Merck notes that its BACE inhibitor recently demonstrated a reduction in cerebral spinal fluid, or CSF, a biomarker, in a Phase I study. By contrast, Roche recently doubled the size of a trial testing a compound in patients with early-stage disease. And so one analyst, while noting that Merck may give Lilly a ‘run for its money,’ expresses caution.

In a research note, ISI Group analyst Mark Schoenebaum writes that Merck could end up on the same timeline to market as Lilly  if the FDA asks Lilly to do another confirmatory Phase III trial of its compound. If not, though, Merck would be about three years behind. He adds that the Merck drug “appears to prevent (almost entirely) the formation of new amyloid beta plaques in the brain.” The Lilly drug, however, leads to removal of existing plaques.

But while he called the 90 percent reduction in CSF “impressive,” Schoenebaum points out that “the meaning of bio-markers is no longer clear.” Why? The Pfizer and J&J compound had good biomarker data, but no clinical impact, while the Lilly data revealed some clinical impact despite very mixed biomarker data. And he continues, “we do not believe that Merck has any clinical efficacy data at this point upon which it is basing its Phase II/III decision. Thus, one must still view the Phase III as highly speculative.”

Indeed, there is increasing belief that, to be truly effective, a drug will have to combat the disease in its earliest stages, before signs of dementia appear. Although the biomarker data is encouraging, as Schoenebaum points out, this is far from a reliable predictor. Merck obviously needs the data to get to Phase III, but a payout is far from clear. The odds, in fact, may yet wind up resembling a ballooning Powerball kitty.

New evidence links repeat concussions to permanent brain injury

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Examiner

n a study published in the December 3 issue of the journal Brain, researchers from Boston University School of Medicine reported that examination of deceased athletes’ brains showed that most had signs of chronic traumatic encephalopathy (CTE), an Alzheimer’s-like condition, after sustaining repeated head injuries.

The study “extends our knowledge concerning the spectrum of the clinical and pathological abnormalities associated with CTE,” said Ann McKee, MD, lead researcher, professor of neurology and pathology, director, neuropathology core, at Boston University School of Medicine, and co-director of the Center for the Study of Traumatic Encephalopathy, in a December 3 news release.

An accumulation of blows
As reported in the Boston Globe, the study was based on brain samples taken posthumously from 85 donors who had histories of repeated head injuries. This new research adds to the mounting evidence linking CTE to repeated hits to the head in such sports as football and hockey. CTE is a progressive degenerative disease whose symptoms include memory loss, paranoia, confusion, impaired judgment, impulse control issues, depression, and dementia.

Among those in the study, 80 percent – 68 men, ages 17 to 98 and nearly all of whom played sports – showed evidence of CTE. Of the 85 donors, 50 were football players, including such NFL stars as Dave Duerson, Cookie Gilchrist and John Mackey. Also in the group were six high school football players, nine college football players, seven professional boxers and four NHL hockey players.

The four stages of CTE
Researchers interviewed families of the brain donors to learn more about the behaviors they exhibited as the disease progressed. In stage I, CTE victims suffered headaches and had trouble concentrating. In stage II, victims were depressed, had explosive tempers and short-term memory problems. Victims in stage III had cognitive impairment and difficulty with planning, organizing and handling multiple tasks. By final stage IV, full dementia was present.

In addition, the study found that damage to the brain was far more extensive in athletes who played professional contact sports and died after the age of 50. These patients were also more prone to severe memory loss and personality changes before they died.

The volume of cases in the study “allows us to see the disease at all stages of severity and how it starts and spreads in the brain, which gives us an idea of the mechanism of the injury,” McKee told the New York Times.

Protecting young football players
The study’s results are sure to renew calls for more restrictions like the Massachusetts concussion law which prohibits young football players who have sustained concussions from returning to a game on the same day of injury.

Robert Cantu, MD, study co-author, clinical professor of neurosurgery at Boston University School of Medicine and co-director of the Center for the Study of Traumatic Encephalopathy, told the Boston Globe he would like to see tackle football replaced by flag football for all children under the age of 14. He also favored high school teams limiting contact practices to once a week during the regular season.

“There’s no talk of setting up formal rules for limiting contact practices,” said Paul Wetzel, spokesperson for the Massachusetts Interscholastic Athletic Association. “But most football coaches will tell you two or three games into the season, they’re limiting contact practices to avoid injuries.”

Can chocolate make you smarter?

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East Side News

The regular warnings about chocolate and their negative impacts on people’s health may all be refuted by this study. A recent paper showed that a regular intake of cocoa (one of the main ingredients of chocolate) can help improve the mental functions in elderly people, and reduce the risks of mild cognitive impairment, a precursor to dementia and other forms of dementia diseases. Other studies revealed that mice and snails who ate chocolate had improved their memory capabilities.

Franz Messerli of Columbia University performed a study in which he counted the number of nobel laureates per 10 million population with the amount of chocolate consumed in that country. The number of nobel prize winners was to be used as a general indicator of the country’s intelligence level.. The P value was 0.0001, which means there is a 1/10,000 probability of the graph showing no correlation. The only country that didn’t quite follow the trend was Sweden because Sweden has a very high number of nobel laureates but consumes much less chocolate. However, because Sweden is the country that donates and evaluates the Nobel Prizes, Messerli has a theory that “‘the Swedes might have a slightly patriotic bias.’”

This study has an extremely high correlation, but as most know, correlation does not necessarily mean causation. Although it seems very likely that chocolate may be an important factor in the number of Nobel Prize winners in a country, more studies must be performed to consider other factors that would probably play a more crucial role in this process.

Psoriasis drug may halt or reverse Alzheimer's disease

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LA Times

A biological medication already widely used to treat plaquepsoriasis may be able to slow the accumulation of amyloid plaques in the brain that are the hallmark of Alzheimer's disease, a new study has found. The same study found that in older mice with established Alzheimer's, this treatment approach, which suppresses the brain's immune reaction to beta amyloid, brought a marked improvement in cognitive function and may even halt or reverse early signs of Alzheimer's.

The new study was published this week in the journal Nature Medicine.

Conducted by researchers in Switzerland and Germany, the study offers a glimmer of hope in the thus-far discouraging search for a therapy that could halt or reverse the inexorable process of neuronal loss and mental decline that affects some 35-million people worldwide. It also strengthens evidence for the long-suspected role of inflammation in the development of Alzheimer's disease.

The authors of the study suggest that researchers should immediately launch clinical trials of ustekinumab — a biologic drug already approved by the Food & Drug Administration for the treatment of plaque psoriasis (and marketed as Stelara) — on patients with mild cognitive impairment or very early Alzheimer's disease. They called agents that shut down specific immune responses — medications tested in auto-immune disorders such as psoriasis, Crohn's disease and multiple sclerosis — "the ideal candidate for the initiation of clinical trials" for Alzheimer's.

"This kind of research is a step forward in identifying potential human targets for drug action," said Dr. Lon Schneider, director of pharmacological research at USC's Alzheimer's Disease Research Center, who was not involved with the current study.

At the same time, Schneider cautioned against drawing too much hope from the latest research. In animal models of Alzheimer's disease, he said, interventions that seem to work for mice "have not translated to humans," he said. And even when an existing drug appears promising, he added, researchers are far from knowing what dose or form of administration will be safe and effective for humans.

"Using the drug off the shelf may not be either" safe or effective, he warned.

The latest research focuses on the role of the immune system in the degenerative process at the heart of Alzheimer's. Looking at the cerebrospinal fluid of 39 human subjects with established Alzheimer's disease and 20 healthy control subjects, the researchers showed that the accumulation of beta-amyloid in the brain may set off an immune reaction — including the release of two proteins known as interleukin-12 and interleukin-23.

These two chemicals, collectively called IL-12/23, send forth a signaling molecule called P40 that increases inflammation across the brain. Past research suggests that in brains where P40 is in plentiful supply, beta-amyloid particles that are circulating form plaques. Those plaques, in turn, disrupt signaling throughout the brain and appear to  cause the decline in memory and mental function so familiar to the loved ones of those with the devastating disease.

Researchers have sought to suppress IL-12/23 by different means. But among the most successful so far have been the injection of antibodies that shut down P40's signal. When the authors of the study injected P40 antibodies and an inactive control substance into young mice who were genetically programmed to develop Alzheimer's disease, they saw a distinct difference: At about middle age, the mice that got the P40 antibodies had 31% less beta-amyloid plaque in their brains than their peers who got the placebo.

The researchers also sought to test the effect of suppressing P40 in rats with established Alzheimer's disease. They implanted mini-pumps that for 60 days infused P40 antibodies directly into the brains of older rats with full-blown Alzheimer's. Another group of such rats got a placebo infusion. The treated mice performed far better than those who got the placebo in tests of memory and cognitive function. And while the treated mice still had amyloid plaques, there was far less beta-amyloid in their brains available to form new ones.

See recent reports of other drugs that have generated hope for Alzheimer's disease:

A hint of success in treating Alzheimer's raises ethical quandary; and

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