Thread: Alzheimer's Vaccine

http://www.torontosun.com/2012/06/07...er%27s+vaccine

Researchers in Sweden have developed a vaccine that helps improve the symptoms of people with mild to moderate Alzheimer's disease.

The study, published in Lancet Neurology, says this is a breakthrough in the search for a cure to the dementia disease.

The researchers noted the vaccine focuses on the amyloid precursor protein, which resides in the outer membrane of nerve cells and that, instead of being broken down, can form a harmful substance called beta-amyloid, which accumulates as plaques and kills brain cells.

In the second clinical trial in humans, the researchers found 80% of patients developed their own protective antibodies against beta-amyloid without suffering any side-effects over the three years of the study.

The researchers now want to use the vaccine, called CAD106, in a larger clinical trial to see if they get the same results.

For those who prefer to analyze the data on their own...

http://www.thelancet.com/journals/la...140-0/fulltext

Methods
We did a phase 1, double-blind, placebo-controlled, 52-week study in two centres in Sweden. Participants, aged 50—80 years, with mild-to-moderate Alzheimer's disease were entered into one of two cohorts according to time of study entry and then randomly allocated (by use of a computer-generated randomisation sequence) to receive either CAD106 or placebo (4:1; cohort one received CAD106 50 μg or placebo, cohort two received CAD106 150 μg or placebo). Each patient received three subcutaneous injections. All patients, caregivers, and investigators were masked to treatment allocation throughout the study. Primary objectives were to assess the safety and tolerability of CAD106 and to identify the Aβ-specific antibody response. Safety assessment was done by recording of all adverse events, assessment of MRI scans, physical and neurological examinations, vital signs, electrocardiography, electroencephalography, and laboratory analysis of blood and CSF. Patients with Aβ-IgG serum titres higher than 16 units at least once during the study were classified as responders. This study is registered with ClinicalTrials.gov, number NCT00411580.

Findings
Between August, 2005, and March, 2007, we randomly allocated 31 patients into cohort one (24 patients to CAD106 treatment and seven to placebo) and 27 patients into cohort two (22 patients to CAD106 treatment and five to placebo). 56 of 58 patients reported adverse events. In cohort one, nasopharyngitis was the most commonly reported adverse event (10 of 24 CAD106-treated patients). In cohort two, injection site erythema was the most commonly reported adverse event (14 of 22 CAD106-treated patients). Overall, nine patients reported serious adverse events—none was thought to be related to the study drug. We recorded no clinical or subclinical cases of meningoencephalitis. 16 of 24 (67%) CAD106-treated patients in cohort one and 18 of 22 (82%) in cohort two developed Aβ antibody response meeting pre-specified responder threshold. One of 12 placebo-treated patients (8%) had Aβ-IgG concentrations that qualified them as a responder.

So, 74% overall met the pre-specified threshold, but we should expect a 1/12 margin of error, based on the placebo-treated patients.

That lowers the overall incidence in CAD106-treated patients to just under 68% (or more specifically, 187/276).

This is excellent news. Phase II trials were a resounding success, which means on to phase III trials. Roughly 2000 people, spanning a 2 year period to confirm the results of phase II, and then they'll be widely available.

Very, very good news for the roughly 32 million people who will be effected, by the time it is approved.

Alzheimer's gender-biased gene found...

Alzheimer's gene found to affect women over men
Wednesday, June 13, 2012 - A gene that's been known for two decades as the largest inheritable risk for developing Alzheimer's disease mostly affects the brains of women, not men, according to a team of researchers from Stanford and UCSF.

The gene variant known as APOE4 is the most common genetic risk factor for Alzheimer's - only about 15 percent of people carry the gene, but it's found in more than half of all Alzheimer's patients. The variant was first connected to Alzheimer's in 1993, but doctors and scientists for the most part have been unaware of any gender differences, despite early studies that showed an increased risk for women with the gene. The new research, which is being published Wednesday in the Journal of Neuroscience, looked at two biological indicators - or biomarkers - associated with Alzheimer's disease: decreased activity in a brain network related to memory, and increased levels of the tau protein in spinal fluid. Women with the APOE4 gene were more likely to test positive for both markers than men who had the gene and women who didn't have the gene.

Path to new research

The findings will not have any immediate clinical impact - very few people are encouraged to learn their APOE4 status because there is no treatment for Alzheimer's. But the results could open a torrent of new research possibilities, such as studying the relationship between hormones and Alzheimer's, or looking for other gender differences that could be making women with the gene more vulnerable, scientists said. "We haven't been able to get much insight into how APOE is affecting increased risk. This might be a big clue," said Dr. Michael Greicius, medical director of the Stanford Center for Memory Disorders and senior author of the study.

The older study of the APOE4 gene found that women with one copy of the gene were four times more likely than anyone without the gene to develop Alzheimer's; men with a single copy had no increased risk. Both men and women, however, were up to 14 times more likely to develop Alzheimer's if they had two copies of the gene. But that's a rare combination - only 2 percent of the population has two copies. The APOE4 gene, along with other genetic risk factors for Alzheimer's, has become increasingly important in research for treating the disease. Genetic research can help scientists better understand what causes Alzheimer's and it may lead to treatments that target specific biological mechanisms of the disease. For example, scientists might find a connection between sex hormones and the gene or a genetic mutation tied to the X chromosome that interacts with APOE4, Greicius said.

Hope for early signs

The gene connection also could help scientists identify people who are showing early biological signs of developing Alzheimer's, years before they suffer memory problems. One of the major barriers to developing treatments has been identifying patients in the earliest stages of Alzheimer's, before the disease has caused too much damage to repair. If scientists know to look for certain genes associated with Alzheimer's and know to look for certain biomarkers, they may be able to stop the disease progression, or at least slow it down. In theory, it would be similar to identifying a patient with high cholesterol decades before he suffers a heart attack, said Maria Carrillo, senior director of medical and scientific relations with the Alzheimer's Association. "Studies like this open up all kinds of questions, and we can ask them at the earliest molecular changes," Carrillo said.

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Anti-Alzheimer's gene found...

Scientists find anti-Alzheimer's gene mutation
12 July`12 - Scientists have found a genetic mutation they say protects against Alzheimer's disease and holds promise for a possible treatment for this form of dementia.

More than five percent of people over the age of 60 in the Western world are believed to suffer from dementia, about two-thirds of which is due to Alzheimer's disease. Scientists in the United States and Europe reported in the journal Nature that they had found a gene coding mutation, A673T, that protects against both Alzheimer's and cognitive decline in elderly people who do not have the disease. "This is a mutation in a gene that makes a protein that people have believed for a long time is involved in Alzheimers," geneticist Kari Stefansson of the Icelandic medical company deCODE genetics and lead author of the paper, told AFP. "What this mutation does is to make the protein less harmful."

If you had the rare mutation, you were between five and seven times less likely to develop the disease than the general population, said Stefansson -- "a very strong protection". Probing the genetic data of some 1,800 Icelanders, the scientists also found that people between the ages of 80 and 100 who did not have Alzheimer's disease but carried the mutation had much better cognitive function than those without it.

He added there had been a lot of research in the past two decades into manipulating the amyloid precursor protein, APP, to treat Alzheimer's -- an incurable and progressive disease characterised by memory loss and dementia. The disease involves an accumulation of amyloid plaques in the brain. "This mutation could possibly represent a target for treatments to prevent Alzheimer's disease," a Nature press summary added.

http://news.yahoo.com/scientists-ant...151901443.html

See also:

Alzheimer's 'early signs timeline developed'
11 July 2012 - Protein plaques in the brain indicate Alzheimer's disease

Scientists have assembled a "timeline" of the unseen progress of Alzheimer's before symptoms appear. A team at Washington University School of Medicine looked at families with a genetic risk of the disease. Writing in the New England Journal of Medicine, they say signs appeared up to 25 years before the expected onset of the disease. UK experts said the ability to detect Alzheimer's early would give the best chance of successful treatment.

'Key changes'

The 128 people in the study, from the UK, US and Australia, had a 50% chance of inheriting one of three mutations that are certain to cause early Alzheimer's, which often develops in people's 30s and 40s - much earlier than the more common form of Alzheimer's which generally affects people in their 60s. Those who carry the mutations will go on to develop the disease. The researchers looked at the age the participants' parents were when they developed the disease - and therefore how many years it was likely to be before they too showed symptoms. They underwent blood and spinal fluid tests as well as brain scans and mental ability assessments.

The earliest change - a drop in spinal fluid levels of the key ingredient of Alzheimer's brain plaques - can be detected 25 years before the anticipated age of disease onset, they suggest. At 15 years, raised levels of tau, a structural protein in brain cells can be seen in spinal fluid - and shrinkage can also be detected within parts of the brain. Changes in the brain's use of the sugar glucose and slight memory problems become apparent 10 years before symptoms would appear, they suggest. Researchers also tested other members of the families without the inherited mutations - and found no changes in the markers they tested for.

Prof Clive Ballard, director of research at the Alzheimer's Society, said: "This important research highlights that key changes in the brain, linked to the inherited form of Alzheimer's disease, happen decades before symptoms show, which may have major implications for diagnosis and treatment in the future. "These findings are a good indicator that there may be key changes in the brain happening early in people who develop non-hereditary Alzheimer's disease, but we can't be sure. Further research into this complex condition is needed to confirm a definite link."

And Dr Eric Karran, director of Research at Alzheimer's Research UK, said: "These results from people with the inherited form of Alzheimer's seem to be very similar to the changes in the non-genetic, common form of the disease. "It's likely that any new treatment for Alzheimer's would need to be given early to have the best chance of success. "The ability to detect the very earliest stages of Alzheimer's would not only allow people to plan and access care and existing treatments far sooner, but would also enable new drugs to be trialled in the right people, at the right time."

http://www.bbc.co.uk/news/health-18796309

Uncle Ferd gonna start takin' aspirin so he don't go goofy like Granny...

Aspirin may 'slow elderly brain decline', study finds
4 October 2012 - Could taking an aspirin a day slow brain power decline?

An aspirin a day may slow brain decline in elderly women at high risk of cardiovascular disease, research finds. Around 500 at risk women, between the ages of 70 to 92, were tracked for five years - their mental capacity was tested at the start and end of the study. Those taking aspirin for the entire period saw their test scores fall much less than those who had not. The Swedish study is reported in the journal BMJ Open.

Dr Silke Kern, one of paper's authors, said: "Unlike other countries - Sweden is unique, it is not routine to treat women at high risk of heart disease and stroke with aspirin. This meant we had a good group for comparison." The women were tested using a mini mental state exam (MMSE) - this tests intellectual capacity and includes orientation questions like, "what is today's date?", "where are we today?" and visual-spatial tests like drawing two interlinking pentagons.

No self-medication

But the report found that while aspirin may slow changes in cognitive ability in women at high risk of a heart attack or stroke, it made no difference to the rate at which the women developed dementia - which was also examined for by a neuropsychiatrist. Dr Simon Ridley, head of research at Alzheimer's Research UK, said: "The results provide interesting insight into the importance of cardiovascular health on cognition, but we would urge people not to self-medicate with aspirin to try to stave off dementia.

"The study reports no benefit from aspirin on overall dementia rates in the group, and previous trials investigating the potential of drugs like aspirin for dementia have been negative." Dr Kern added: "We don't know the long term risks of taking routine aspirin. For examples ulcers and serious bleeds may outweigh the benefits we have seen. More work is needed. We will be following up the women in this study again in five years."

http://www.bbc.co.uk/news/health-19819065

New study shows way to detect Alzheimer's earlier...

Alzheimer's detected decades before symptoms
5 November 2012 - Researchers have found some of the earliest signs of Alzheimer's disease, more than two decades before the first symptoms usually appear.

Treating the disease early is thought to be vital to prevent damage to memory and thinking. A study, published in the Lancet Neurology, found differences in the brains of an extended Colombian family predisposed to develop an early form of Alzheimer's. Experts said the US study may give doctors more time to treat people. Alzheimer's disease starts long before anyone would notice; previous studies have shown an effect on the brain 10-15 years before symptoms.


The shrunken brain of an Alzheimer's patient compared with a healthy one

It is only after enough brain cells have died that the signs of dementia begin to appear - some regions of the brain will have lost up to 20% of their brain cells before the disease becomes noticeable. However, doctors fear so much of the brain will have degenerated by this time that it will be too late to treat patients. The failure of recent trials to prevent further cognitive decline in patients with mild to moderate Alzheimer's disease has been partly put down to timing.

Early start

A team at the Banner Alzheimer's Institute in Arizona looked at a group of patients in Colombia who have familial Alzheimer's. A genetic mutation means they nearly always get the disease in their 40s. Alzheimer's normally becomes apparent after the age of 75. Brain scans of 20 people with the mutation, aged between 18 and 26, already showed differences compared with those from 24 people who were not destined to develop early Alzheimer's. The fluid which bathes the brain and spinal cord also had higher levels of a protein called beta-amyloid.

The researchers said differences could be detected "more than two decades before" symptoms would appear in these high-risk patients. Dr Eric Reiman, one of the scientists involved, said: "These findings suggest that brain changes begin many years before the clinical onset of Alzheimer's disease. "They raise new questions about the earliest brain changes involved in the predisposition to Alzheimer's and the extent to which they could be targeted by future prevention therapies."

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An Alzheimer's cure in time for the Baby Boomers?...

Antibody Therapy Clears Destructive Alzheimer’s Brain Plaques
December 07, 2012 - Scientists say they've developed a type of disease-fighting antibody that, in tests with laboratory mice, is able to clear away the destructive brain plaques, or protein deposits, believed to cause Alzheimer’s Disease. Researchers note that while several experimental drugs have shown promise in preventing plaque development, this new antibody therapy is the first to successfully remove existing plaques, suggesting a possible treatment for Alzheimer's patients.

By the time most people visit their doctors complaining of serious memory problems and cognitive decline, experts say their brains very likely are already riddled with sticky deposits of amyloid beta protein. These plaques are the hallmark of Alzheimer's, a progressive neurodegenerative disease that eventually leads to disability and death. According to Alzheimer’s Disease International, in 2010 there were an estimated 35.6 million people around the world suffering from various forms of dementia, including Alzheimer’s. Researchers at drug maker Eli Lilly report their experimental antibody therapy binds to and literally sweeps away existing plaques in a mouse model of Alzheimer’s. Their new antibody is part of a trend in so-called immunotherapy in which the body's immune system proteins, or antibodies, can be engineered to target and disable specific disease-causing molecules.

In Eli Lilly's neurodegenerative section, Ronald DeMattos works on new therapies to treat and prevent Alzheimer's disease. “What we’ve been able to demonstrate is that by treatment with this antibody that is very specific to binding to this deposited sticky material… we’re actually able to remove pre-existing clumps or plaque material,” he explained. In a healthy brain, the protein beta amyloid is normally broken down and eliminated by the body. But in people with Alzheimer’s, the dissolvable proteins accumulate and form hardened plaques. Researchers theorize that water-soluble beta amyloid washes over existing plaques, interfering with therapeutic attempts to eliminate the buildup.

Instead of genetically engineering a drug that targeted all of the beta amyloid in an experimental group of mice bred to have Alzheimer’s disease, DeMattos and colleagues developed an antibody that attached to and eliminated only the hardened plaque deposits. “The antibody is meant literally to enter the brain and help one’s own body facilitate the removal of this deposited plaque material. And it’s our hope that by doing so, we can hopefully mitigate some of the cognitive deficits that are attributed to the disease,” DeMattos said.

But it remains to be seen, DeMattos says, whether elimination of hardened Alzheimer’s plaques leads to memory improvements or stops the cognitive decline associated with the disease. Alzhiemer’s patients typically begin to develop beta amyloid deposits ten or more years before they are diagnosed, according to DeMattos, who says the ultimate goal would be to treat individuals before they develop signs of the disease. An article on a new antibody therapy for Alzheimer’s disease is published in the journal Neuron.

Source

Lilly Alzheimer's prevention drug to be studied...

Lilly drug chosen for Alzheimer's prevention study
Jan 18,`13: Researchers have chosen an experimental drug by Eli Lilly & Co. for a large federally funded study testing whether it's possible to prevent Alzheimer's disease in older people at high risk of developing it.

The drug, called solanezumab (sol-ah-NAYZ-uh-mab), is designed to bind to and help clear the sticky deposits that clog patients' brains. Earlier studies found it did not help people with moderate to severe Alzheimer's but it showed some promise against milder disease. Researchers think it might work better if given before symptoms start. "The hope is we can catch people before they decline," which can come 10 years or more after plaques first show up in the brain, said Dr. Reisa Sperling, director of the Alzheimer's center at Brigham and Women's Hospital in Boston.

She will help lead the new study, which will involve 1,000 people ages 70 to 85 whose brain scans show plaque buildup but who do not yet have any symptoms of dementia. They will get monthly infusions of solanezumab or a dummy drug for three years. The main goal will be slowing the rate of cognitive decline. The study will be done at 50 sites in the U.S. and possibly more in Canada, Australia and Europe, Sperling said.

In October, researchers said combined results from two studies of solanezumab suggested it might modestly slow mental decline, especially in patients with mild disease. Taken separately, the studies missed their main goals of significantly slowing the mind-robbing disease or improving activities of daily living.

Those results were not considered good enough to win the drug approval. So in December, Lilly said it would start another large study of it this year to try to confirm the hopeful results seen patients with mild disease. That is separate from the federal study Sperling will head. About 35 million people worldwide have dementia, and Alzheimer's is the most common type. In the U.S., about 5 million have Alzheimer's. Current medicines such as Aricept and Namenda just temporarily ease symptoms. There is no known cure.

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Uncle Ferd hopin' dey come up with sumpin' so he don't go goofy like Granny...

An Alzheimer's 'epidemic' could hit the USA by 2050
February 6, 2013 - The number of people with the brain disease could nearly triple during the next three decades.

A new government-funded report confirms what advocacy groups have been warning for years: The number of people in the USA with Alzheimer's disease will almost triple by 2050, straining the health care system and taxing the health of caregivers. Numbers are projected to rise from about 5 million now to 13.8 million. The disease robs people of their memory, erases personality and makes even routine tasks like dressing and bathing impossible. "We're going to need coordinated efforts for this upcoming epidemic,'' says lead author Jennifer Weuve, assistant professor of medicine at Rush Institute for Healthy Aging in Chicago. "People have trouble getting their heads around these numbers, but imagine if everyone in the state of Illinois (population 12.8 million) had Alzheimer's. I look around Chicago and can't imagine it.''

The study is published Wednesday in the journal Neurology. Researchers analyzed information from 10,802 black and white Chicago residents, ages 65 and older, from 1993 to 2011. Participants were interviewed and assessed for dementia every three years. Age, race and level of education were factored into the research. The projections are similar to a study done 10 years ago but include new data from the 2010 Census about death rates and future population rates. An upcoming study will examine the effect on health care costs, which are expected to exceed $2 trillion, according to the Alzheimer's Association. "These numbers are more credible because they involve new Census data,'' says Dallas Anderson, director of population studies and epidemiology of Alzheimer's disease at the National Institute on Aging. "If you know anyone who has Alzheimer's disease now, you know how dire this projection is for the nation.''

The three-fold increase is largely the result of the aging Baby Boomers, born between 1946 and 1964. The main risk for Alzheimer's is age. The population of people 65 and older is expected to more than double from 40.3 million to 88.5 million, according to the 2010 Census. "We've had great success in this country when we've decided to focus on a condition,'' Weuve says. "We've done it with good research in heart disease, cancer and HIV, but we are in our infancy when it comes to Alzheimer's research."

Alzheimer's is the only disease among the top six killers in the USA for which there is no prevention, cure or treatment. The government boosted funding last year and made prevention a 2025 goal. Funding for the disease was $606 million -- exceeding $500 million for the first time in 2012. But it trails other diseases: HIV at $3 billion and cancer at $6 billion. An additional $100 million for Alzheimer's research for 2013 is awaiting approval, the Alzheimer's Association says. "We need to put the pedal to the metal on research,'' says George Vradenburg, chairman of USAgainstAlzheimers, an advocacy group. "We need to find a way to prevent this terrible disease."

Former president RonaldReagan, who left office in 1989, disclosed in 1994 that he had Alzheimer's. Others include Robert Sargent Shriver, actress Rita Hayworth and singer Glen Campbell. In 2011, the University of Tennessee's legendary women's basketball coach Pat Summitt revealed she has Alzheimer's. The study was financed by the National Institute on Aging, National Institutes of Health and the Alzheimer's Association. "There is great urgency for meaningful, timely and comprehensive action," says Maria Carrillo, vice president of medical and scientific relations for the Alzheimer's Association.

Source

Uncle Ferd says dat must be what the doctor got Granny on `cause it ain't helpin'...

Baxter drug fails to slow Alzheimer's in big study
7 May`13 — Baxter International Inc. says that a blood product it was testing failed to slow mental decline or to preserve physical function in a major study of 390 patients with mild to moderate Alzheimer's disease.

The company says that people who received 18 months of infusions with its drug, Gammagard, fared no better than others given infusions of a dummy solution. Gammagard is immune globulin, natural antibodies culled from donated blood. Researchers thought these antibodies might help remove amyloid, the sticky plaque that clogs patients' brains, sapping memory and ability to think.

Patients with moderate disease and those with a gene that raises risk of Alzheimer's who were taking the higher of two doses in the study seemed to benefit, although the study was not big enough to say for sure. "The study missed its primary endpoints, however we remain interested by the prespecified sub-group analyses" in groups that seemed to benefit, Ludwig Hantson, president of Baxter's BioScience business, said in a statement. Gammagard is already sold to treat some blood disorders, and the results of the Alzheimer's study do not affect those uses. About 35 million people worldwide have dementia, and Alzheimer's is the most common type. In the U.S., about 5 million have Alzheimer's. Current medicines such as Aricept and Namenda just temporarily ease symptoms. There is no known cure.

Excitement about Gammagard grew last summer, when researchers reported at a medical conference that the drug had stabilized Alzheimer's disease for as much as three years in four patients who had been receiving the highest dose of it for three years in the study. People typically go from diagnosis to death in about eight years, so to be stable for so long was considered remarkable. The new results on the full group of study participants are disappointing, said the study's leader, Dr. Norman Relkin, head of a memory disorders program at New York-Presbyterian Hospital/Weill Cornell Medical Center. "The bar was set very high" for the drug to show improvement, and "there does appear to be a signal" that it helped the two-thirds of patients in the study who had the apoE4 gene that raises the risk of developing Alzheimer's, as well as those with moderate versus mild disease, Relkin said.

No new side effects were seen in the study. About 5 percent of patients on the drug had a rash and decreases in hemoglobin, which carries oxygen in the blood. There were 17 serious reactions, 12 in the drug group and five in the placebo group. Full results will be presented in July at an Alzheimer's conference in Boston. Meanwhile, other studies are under way to test drugs earlier in the course of the disease. An experimental drug, Eli Lilly & Co.'s solanezumab, showed some promise in that setting in an earlier study. Shares of Baxter fell $2.53, or 3.6 percent, to $67.78 in morning trading.

Baxter drug fails to slow Alzheimer's in big study

See also:

Alzheimer’s Advance: Gene Could Help to Clear Brain Plaques Responsible for the Disease
April 26, 2013 - Mapping out how an Alzheimer’s gene works could lead to new treatments.

So far, nearly two dozen genes scattered across four chromosomes have been linked to an increased risk of Alzheimer’s disease. But identifying such genetic risk factors doesn’t mean that researchers fully understand how they contribute to cognitive decline and dementia. And that understanding is often crucial to turning genetic information into effective treatments. Now a group of scientists report in the journal Neuron that they have pieced together the back story of one gene, known as CD33, that could lead to exciting new ways of removing the amyloid plaques that build up in the brains of Alzheimer’s patients and cause so many problems with memory and cognitive functions.

Dr. Rudolph Tanzi, director of the genetics and aging research unit at Massachusetts General Hospital and professor of neurology at Harvard Medical School, and his team first identified CD33 in 2008, and at the time, he says, “We had no idea what this thing did. And in the [scientific research] literature, little was known about it. So we started from scratch.” Beginning with studies of the where the gene was expressed, he found that a subset of brain cells known as microglia seemed to show high levels of CD33, which makes receptors that pop up on the surface of the cells to bind to neuronal debris, including the residue of inflammatory reactions, and dead and dying nerve cells. CD33 functions as a molecular housekeeper, patrolling the nervous system for any material that doesn’t belong and could impair normal brain function. That includes the deposits of amyloid protein that build up in the brains of Alzheimer’s patients, eventually forming sticky plaques that compromise normal nerve function before destroying them.

But when Tanzi’s team looked at the brains of patients who had died of Alzheimer’s, they found that CD33 also had a darker side. In patients with a higher burden of amyloid plaques, CD33 also appeared in excess. And so did tons of dead neurons. “At some point, as the amyloid is making the cells sick, and forming tangles as lots of neurons are dying, the microglia put on their battle gear and turn radical, killing whatever they think is attacking the brain,” says Tanzi. “The result is friendly fire, and they start to kill so many neurons that the microglia are now detrimental; they are no longer clearing but they’re rounding up nerve cells and shooting out free radicals and causing a lot of damage.”

Instead of engulfing and removing the amyloid, microglia armed with CD33 were targeting healthy nerves instead. To confirm that, Tanzi’s team conducted a series of tests with cells in culture and in animals, and found that when microglia were stripped of CD33, they went back to performing their housekeeping duties as expected, sniffing out amyloid and pulling the protein out of circulation. Mice genetically engineered to develop Alzheimer’s plaques but without CD33 showed lower levels of amyloid plaques in their brains than animals with the gene, suggesting that the CD33 was clearing the protein away.

Read more: http://healthland.time.com/2013/04/2...#ixzz2Sf07lYuR