Alzheimer's Disease Symptoms Reversed in Mice

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Scientific American

 

A cancer drug given to mice eliminates brain-damaging proteins, leading to improved cognition within days, but will it work in humans?

By Gary Stix

 

A nearly 13-year-old skin cancer drug rapidly alleviates molecular signs of Alzheimer's disease and improves brain function, according to the results of a new mouse study being hailed as extremely promising. Early-stage human clinical trials could begin within months.

In the study, published online February 9 by Science, researchers from Case Western Reserve University in Cleveland and colleagues used mice genetically engineered to exhibit some of the symptoms of Alzheimer's. Most notably, the mice produced amyloid beta peptides—toxic protein fragments that gum up neurons and lead to cell death—and showed signs of forgetfulness.

Amyloid beta (red areas) peptides clear from the brain of an Alzheimer's mouse after three days of treatment with a cancer drug (right image). Source: AAAS/Science
The Case Western team, led by Gary Landreth, decided to try the drug bexarotene (Targretin), approved in 1999 for cutaneous T cell lymphomas. The team chose this drug because of its long experience working with proteins in the nucleus of brain cells that can induce biochemical processes that affect amyloid beta.
Landreth and his colleagues fed bexarotene to the demented mice, and with just a single dose it lowered the most toxic form of the amyloid beta peptide by 25 percent within six hours, an effect that lasted for up to three days. Mice that were cognitively impaired by the amyloid buildup resumed normal behaviors after 72 hours: They began to crinkle toilet paper placed nearby to make nests, a skill lost as amyloid increased in their brains.
"We have successfully reversed all of the known pathological features and behavioral deficits found in mouse models of Alzheimer's disease," Landreth says. "Never before has anyone observed clearance of amyloid plaques with such speed in mouse models."
Other Alzheimer's researchers hail the work. "I think this is extremely promising," says Samuel Gandy, a professor of neurology and psychiatry at Mount Sinai School of Medicine and associate director of the hospital's Alzheimer's Disease Research Center. "One of the drugs that has been on our wish list for 25 years is a drug that would clear existing amyloid deposits."
"Landreth's paper is impressive," adds Kenneth Kosik, a neuroscientist at the University of California, Santa Barbara. "The effects in mice, including some restoration of cognitive abilities, are dramatic."
Neural sanitation
In a field littered with drug failures, the study offers hope that the strategy of clearing the brain of the toxic peptide can work. Bexarotene does not do so directly, however; instead, it activates retinoid receptors on brain cells that increase production of a fat-protein complex, apolipoprotein E, that helps rid excess amyloid in the fluid-filled space between neurons. It also appears to enhance another cleanup process, called phagocytosis.
Bexarotene functions differently than an amyloid-clearance approach using monoclonal antibodies, which are further down the drug development pipeline. These antibodies bind directly to amyloid and then remove it, but they have sometimes caused fluid to fill brain tissue. Bexarotene may be less likely to cause such swelling. "I think the fact that we're inducing a natural process by turning on these receptors doesn't lend itself to water on the brain," says Paige Cramer, Landreth's graduate student who performed much of the research. Unlike bexarotene, which is taken orally, monoclonals are more troublesome to administer, because they must be delivered intravenously, and if they receive U.S. Food and Drug Administration approval, they would likely be significantly more expensive.

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Alzheimer’s Advance: Gene Could Help to Clear Brain Plaques Responsible for the Disease

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Time

 

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.

(MORE: New Research on Understanding Alzheimer’s)

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.

(MORE: First Genes Linked to Higher Risk of Alzheimer’s Disease Among African-Americans)

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.

(MORE: Genetic Markers May Predict Increased Risk of Alzheimer’s)

That clearance could be the key to alleviating some of the worst symptoms of the disease, experts say, since most people make amyloid protein but for some reason it starts to accumulate as we age. “What we discovered is that CD33 is a key switch so when the switch is off, and it is deactivated, there is more clearance of [amyloid,]” says Tanzi. “If we can now find drugs that inactivate CD33 it should allow more clearance of [amyloid] by the microglial cells.”

His group is already screening compounds to find those that might block CD33 from turning rogue, but the search will have to balance compounds that do a good job of keeping CD33 honest without compromising its ability to seek and destroy real invaders, as it was designed to do. “It’s something we have to keep an eye on for sure,” says Tanzi of the possibility that a CD33 blocker to treat Alzheimer’s could compromise immune functions and make patients more vulnerable to infections or other health issues.

But the discovery could be an important step toward finally developing an effective Alzheimer’s drug treatment, since clearing amyloid plaques could be critical in addressing the deposits of amyloid that mushroom throughout the brain as the disease progresses. “We just need to take advantage of the housekeeping functions of CD33 and entice them to stay helpful and not go crazy,” says Tanzi.

MORE: Two Studies Find Promising New Ways to Detect Alzheimer’s Earlier

 

Alzheimers takes away emotions

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newsfix.ca

A study has revealed that Alzheimer’s not only causes cognitive decline and memory loss, but also takes emotions out of those who suffer from the terrible disease.
Researchers from the University of Florida have been doing a great deal of work on Alzheimer’s disease and dementia to see the various ways in which it will impact its victims.
One interesting thing that they found is that Alzheimer’s can actually suck the emotions right out of people, to the point where they will respond differently to things once the disease has developed when compared to before the disease.
The study was carried out by having a group of patients with Alzheimer’s experience ten different negative pictures, and ten different positive pictures.
The idea was to see how they would react when it comes these pictures, and how Alzheimer’s would impact their reaction.
Researchers stated that the Alzheimer’s patients, within their brains, realized what their emotions were, but they were different when compared those who did not have Alzheimer’s.
Emotions could vary depending on the case and the patient, but from this study those who have Alzheimer’s are not able to actively display their emotions the same way healthy people can.
The study has been published in the Journal of Neuropsychiatry and Clinical Neurosciences

Anona for Alzheimer's

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weartv.com

 

Alzheimer's disease eats away at the mind and the memory.

Some doctors are now prescribing a "medical food" as part of their treatment. But not everyone who works with Alzheimer's patients thinks it will help.

Draw some water, pour in the powder, stir, and voila. That's all it takes to make this milkshake neurologist Doctor Gerald Calegan is prescribing to some of his patients.

"It's a medical food that is approved for treating Alzheimer's disease."

The "medical food" is called Axona.

According to doctors, the treatment that contains a derivative of coconut oil helps fuel the brain with ketones, an alternative brain fuel to glucose which is what those suffering from Alzheimer's are losing.

"Just sip on it for a few minutes after you eat breakfast and it's shown to improve memory scores in patients with Alzheimer's disease."

While Axona was approved by the FDA back in 2009, some are still skeptical as to how effective it is in treating Alzheimer disease.

"People will try anything when they have a terminal disease."

Barbera Autin is the executive director for Alzheimer's Services in Baton Rouge. Her mother recently succumbed to the disease and says some under stress might be tempted to try something new.

"As the disease progresses, it's as though the person regresses to almost infancy. Where they need 24 hour care. So it demands so much attention from the caregiver it just wears them out."

But her organization and some other critics aren't ready to recommend the use of medical foods like Axona in place of long standing medications for Alzheimer's just yet.

In the meantime, Doctor Calegan says it's working, and is impressed by his patients' improvement.

"Remembering a grandchild's birthday, being able to remember a doctor's appointment, knowing that you're taking your medicines properly. those things make a big difference.""Medical food" being prescribed by some doctors to treat Alzheimer's

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Alzneimer's Association

 

Hello!

You're invited to watch the new PBS documentary Age of Champions for free April 18th – 28th at ageofchampions.org/premiere.

Age of Champions tells the story of five competitors who sprint, leap, and swim for gold at the National Senior Olympics. You'll meet a 100-year-old tennis champion, 86-year-old pole vaulter, and rough-and-tumble basketball grandmothers as they triumph over the limitations of age.
This opportunity is brought to you by the Alzheimer's Association event, The Longest Day^®, along with the filmmakers of Age of Champions. We hope that you, your colleagues, friends and family will be able to use this resource as a positive and entertaining tool for promoting a healthy and active lifestyle. Please extend this viewing invitation by forwarding this email.
After being inspired by the film, register to join us on June 21, 2013, for The Longest Day, as together we honor those living with Alzheimer's disease and their caregivers. The Longest Day is about patience, strength and endurance – but it's also about a challenge. On The Longest Day, do something you love – or try something new – to advance the cause. For people facing Alzheimer's disease, this challenge is every day. For you, it's just one.
Organize a team for this sunrise-to-sunset event and raise funds and awareness for Alzheimer's care, support and research. Learn more at alz.org/thelongestday.

Thank you and enjoy the film!

The Longest Day Team

President’s Budget Proposed Increase for Alzheimer’s Disease Research

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CureAlzheimer'sFund

 

Good, but never enough until Alzheimer’s is gone!
The President states in the budget message for the National Institutes of Health that the proposed budget delivers on the "... Administration's commitment to enhance investment in Alzheimer's research" by adding approximately $80 million to the current year’s amount. This commitment which moves Alzheimer’s research from about 1.6% of the NIH budget to about 1.8% includes, "... investments in basic research on the fundamental causes and mechanisms of disease ..."
Cure Alzheimer's Fund is encouraged by President Obama's Fiscal Year 2014 budget and its commitment to ending Alzheimer's disease. Although we all agree that much more needs to be done and that much more money needs to be allocated to research, Cure Alzheimer's Fund applauds and welcomes the additional funds for Alzheimer's disease research in the budget.
Cure Alzheimer's Fund is gratified by the Administration's stated belief that research into the causes of Alzheimer’s disease is a key to preventing the disease because this has been the guiding principle at Cure Alzheimer's Fund since its founding. This principle is embodied in the Cure Alzheimer’s Fund Research Roadmap which focuses on finding and prioritizing the genes that affect risk for the disease followed by an understanding of the biological processes that propagate the pathology.
Increases in the budget for the National Institute of Aging and the National Institute of Neurological Diseases and Stroke are most welcome. However, we are also concerned about the proposed cut at the National Institute of Mental Health which has committed significant funding to Whole Genome Sequencing for Alzheimer’s in which Cure Alzheimer’s Fund researchers are taking part and which will provide critical data for drug discovery and development to Alzheimer’s researchers around the world.
Cure Alzheimer's Fund realizes this is the beginning of the budget and appropriation process, but it is hopeful that Congressional champions of preventing Alzheimer's disease will lead their colleagues in supporting the Administration's increases to Alzheimer's disease research funding. Cure Alzheimer's Fund will continue to work closely with Congress and the Administration to do all we can to end Alzheimer's disease.

Study uncovers key factor in Alzheimer's progression

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Medical Xpress

 

A new study from researchers at the University of Florida may have uncovered a critical factor that drives the relentless progression of Alzheimer's disease ― a discovery that could eventually slow its progression.

 For more than 15 years, scientists have known that two types of brain lesions form in patients with Alzheimer's disease, one type of lesion forming only after the other. David R. Borchelt, a professor of neuroscience, and Guilian Xu, an assistant research scientist at the UF College of Medicine, have used a mouse model to find a potential explanation for how the first type of brain lesion may trigger the second. They report their findings in the current issue of the journal Human Molecular Genetics. "Understanding how this sequence of events works is thought to be critical and could lead to new therapeutic approaches," said Borchelt, director of the SantaFe HealthCare Alzheimer's Disease Research Center at UF and the McKnight Brain Institute. The lesion that appears first is an amyloid plaque, an incorrectly folded protein structure that forms when a small peptide called the amyloid-beta peptide clumps together. However, scientists have known that amyloid alone does not produce Alzheimer's disease, and all patients with symptoms have a second type of brain lesion called a neurofibrillary tangle. This second lesion appears later in the disease, and as more of these lesions develop, patient symptoms get worse. Finding an explanation for the sequential appearance of these lesions has challenged scientists, but understanding how the amyloid plaques trigger the tangles could help scientists devise ways to slow disease progression. The explanation lies at the heart of how cells function. All cells produce proteins, the molecular workhorses of the cell. Proteins have specific, three-dimensional shapes critical to proper function. This is so important that large amounts of cell energy go into making correctly folded proteins and eliminating incorrectly folded ones. The study by the Borchelt laboratory provides evidence that the abnormal accumulation of the amyloid peptide in the brain that produces the plaque lesions also interferes with brain cells' ability to keep proteins correctly folded. "This deficiency in cell function could set the stage for allowing the formation of the neurofibrillary tangles that seem to be the key pathology to symptoms," Borchelt said. These tangles form when a protein called tau loses its normal shape and folds into a shape that allows it to bind to other tau proteins. This becomes a runaway process that fills the cell with abnormally shaped tau clumps that produce the tangles. In recent years, pharmaceutical and biotech companies have begun to look for drugs that could stimulate better protein folding in brain cells. The study by Xu suggests that these companies may be on the right track. Borchelt cautions that more work is needed to fully understand how amyloid pathology is linked to the tangle pathology, but this recent study offers a new avenue of investigation that could lead to a clearer picture. Journal reference: Human Molecular Genetics 

Study: Enzyme Linked to Obesity May Contribute to Alzheimer's

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CoronadoPatch

 

Brain damage caused by Alzheimer's disease could be the result of over-activation of an enzyme linked to obesity and insulin production, the Scripps Research Institute reported.
When scientists blocked the enzyme, AMP-activated protein kinase (AMPK), in mice, neurons were protected from the loss of synapses (neuron-to-neuron connection points) that are typical of the early phase of Alzheimer's disease, according to the study.
"These findings open up many new avenues of investigation, including the possibility of developing therapies that target the upstream mechanisms leading to AMPK over-activation in the brain," said professor Franck Polleux, who led the study.
His team's report appears in this week's edition of the journal Neuron.
Alzheimer's disease, a fatal neurodegenerative disorder that afflicts more than 25 million people worldwide, has no cure or disease-delaying therapy.
The reseachers said its been known for years that patients in the early stages of Alzheimer's diseases lose synapses in areas of the brain that involve memory, but didn't know how. Recent studies have shown that AMPK might lead to tangles of the protein tau that are seen in the brains of patients.
The enzyme is also tied to regulation of insulin synthesis and secretion in pancreatic cells, and modulation of hypothalamic functions, according to themedicalbiochemistrypage.org.
Polleux said the discovery not only could impact potential Alzheimer's treatments, but also suggests a need for further safety studies on an existing drug, metformin, a popular treatment for Type 2 Diabetes. He said metformin causes AMPK over-activation.
The scientists also are studying what else the over-activation of the AMPK enzyme causes, and how it might contribute to the progression of Alzheimer's disease over the long term.
— City News Service

Gene May Double Risk of Alzheimer's in Blacks

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By Amy Norton
HealthDay Reporter
 -- A particular variant of a cholesterol-related gene may double the risk of Alzheimer's disease in older blacks, a new study suggests.

The gene -- known as ABCA7 -- is also linked to Alzheimer's among whites, but it appears much more important in blacks' risk of the memory-robbing disease, the researchers said.
Still, although a doubling in risk may sound large, the researchers stressed that it's actually a modest increase. Older adults' risk of Alzheimer's is thought to depend on many factors -- not only an array of different genes, but also environmental influences.
"How much does this increase your risk? It's modest," said Dr. Robert Nussbaum, a professor of medicine at the University of California, San Francisco, who was not involved in the study.
But the findings are important because they add to the understanding of the complex underpinnings of Alzheimer's, said Nussbaum, who wrote an editorial published with the study in the April 10 issue of the Journal of the American Medical Association.
The results come from what is believed to be the most extensive search yet for Alzheimer's-linked genes in older blacks.
Most of what is known about Alzheimer's genes has come from data on white adults, because until now there hadn't been a study sample of blacks that was large enough for a gene study, said study lead researcher Dr. Christiane Reitz, an assistant professor of neurology at Columbia University Medical Center in New York City.
Researchers have known for years that whites with a particular variant in the ApoE gene -- called ApoE4 -- have a higher risk of Alzheimer's than whites who carry other variants of the gene.
About 25 percent to 30 percent of the population is thought to carry the Alzheimer's-linked E4 variant.
In the new study, ApoE4 also was linked to an increased Alzheimer's risk among nearly 6,000 blacks aged 60 and older. But the ABCA7 gene was equally important. People with a particular variant of the gene had twice the risk of Alzheimer's as those who carried other variants.
The higher-risk variant was seen in 7 percent of the study participants, Reitz said.
As for what it all means, she said, it's too early to tell.
"This finding needs to be replicated, and we need to learn more about the biological mechanisms," Reitz said.
Like ApoE, the ABCA7 gene is involved in cholesterol metabolism, Reitz said. High cholesterol, heart disease and stroke are considered risk factors for Alzheimer's, and black Americans have higher rates of those cardiovascular problems than whites.
But it's not clear if cardiovascular disease explains why the genes are linked to Alzheimer's -- or why ABCA7 is more important in blacks' risk.
"It's all up in the air," editorial author Nussbaum said. "Gene studies like this are good for finding connections between genes and [disease], but they can't tell us what the mechanisms are."
He said his "gut feeling" is that ApoE and ABCA7 are linked to Alzheimer's independent of their effects on cholesterol and heart disease.
Research has shown that ABCA7 also is involved in transporting amyloid precursor proteins, which help feed the "plaques" that build up in the brains of people with Alzheimer's. That is another potential reason that the gene is linked to Alzheimer's, Reitz said.
But, Nussbaum said, much more research is needed to understand the biology of Alzheimer's. For example, he said, after years of study, researchers are still divided over whether the amyloid plaques in the brains of people with Alzheimer's actually cause the disease.
Reitz said it's too early for people to seek testing for which ABCA7 variant they carry.
You would not be able to run to your doctors' office for such a test anyway -- although there are private companies that offer ApoE testing, Nussbaum said. But that testing is controversial, he said. Many people believe that since there is no known way to prevent Alzheimer's, knowing you have a higher-risk gene will do little good, but potentially create a lot of distress.
On top of that, Reitz said, it is thought that there are probably many gene variants that each increase Alzheimer's risk by a small amount. No single gene variant is the whole story.
Ultimately, Nussbaum said, the hope is that gene studies will help reveal the underlying biological causes of Alzheimer's, and new treatments or preventive measures can be developed.
"The personal, emotional and financial cost of Alzheimer's is huge," Nussbaum said. "It should be a national priority to gain a better understanding of the disease."
It is estimated that about 5 million older Americans have Alzheimer's, and a recent study projected that without any strides in prevention, that number will triple by 2050.
"If we could figure out ways to delay Alzheimer's by even five years, that would have a big impact," Nussbaum said.
The study was funded by grants from the U.S. government, the Alzheimer's Association and drug maker GlaxoSmithKline. Nussbaum has financial ties to Complete Genomics, a company that does gene sequencing for researchers.
More information
Learn more about Alzheimer's genes from the U.S. National Library of Medicine.
Copyright © 2012 HealthDay. All rights reserved.

Hunger may help combat Alzheimer’s

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The Dementia Caregiver's Little Book of Hope [KindleThe sensation of hunger itself may protect against Alzheimer’s disease, a new study on mice has suggested.

ANI

Interestingly, the results of this study suggest that mild hunger pangs, and related hormonal pathways, may be as important to the much-discussed value of “caloric restriction"

Caloric restriction is a regimen where an individual consumes fewer calories than average, but not so few that they become malnourished. Studies in many species have suggested that it could protect against neurodegenerative disorders and extend lifespans, but the effect has not been confirmed in human randomised clinical trials.
But researchers behind the new study argued that hormonal signals are the middlemen between an empty gut and the perception of hunger in the brain, and that manipulating them may effectively counter age-related cognitive decline in the same way as caloric restriction.

restriction” as actually eating less

Genetic markers may predict dementia

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Fox News

 

Scientists have identified early genetic markers that can potentially predict who is at an increased risk for developing Alzheimer’s, Medical Daily reported.
Currently, in order to determine if someone will develop Alzheimer’s disease, doctors use tests that analyze the amount of Tau protein buildup in the central nervous system. The more Tau in an individual’s system, the more likely he or she will progress towards dementia.
However, there was no system to help determine who will start expressing this protein years ahead of time – until now.
Researchers from Washington University School of Medicine in St. Louis have identified genetic mutations that can influence the accumulation of Tau proteins, according to Medical Daily. This discovery could potentially lead to an early genetic test, which could help reveal those who are most at risk for Alzheimer’s – leading to earlier, more effective treatments.
"We have identified several genes that influence the levels of soluble tau in the cerebrospinal fluid,” senior author Dr. Alison Goate, of WU School of Medicine, told Medical Daily, “and we show that one of these genes also influences risk for Alzheimer's disease, rate of cognitive decline in Alzheimer's disease, and density of tangle pathology in the brain."
After performing a genetic analysis on 1,269 patients, Goate and her team identified genetic mutations in a previously implicated region, found in the gene TREM2, as putting people at risk for Alzheimer’s. A receptor gene, TREM2 can actually influence the development of another similar gene TREML2.
According to the researchers, the two genes – while similar – acted oppositely in association with the Tau protein levels. The first was associated with risk for Alzheimer’s and the other was protective against the disease.
Goate said the team would continue to perform more studies to determine the full effects of the gene mutations on nervous systems in the brain.
The research was published in the journal Neuron.

 

2013 Alzheimer's facts and figures

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CEDAR FALLS

alz.org

Every 68 seconds, someone in the U.S. develops Alzheimer's disease. The Alzheimer's Association just released its 2013 Facts and Figures Report, which is a compilation of national and state information on the disease.

The latest information reveals one in three seniors dies with Alzheimer's or a form of dementia. Iowa has the third highest Alzheimer's death rate in the country. Since 2000, Iowa has experienced an 84 percent increase in Alzheimer's deaths.
"It's more than memory loss. Alzheimer's disease actually kills and that's something difficult to wrap your head around," said Jessica Simon with the East Central Iowa Chapter of the Alzheimer's Association.
Simon said Alzheimer's disease will continue to become more prevalent in our state because of an aging population.
"Age is the greatest risk factor for Alzheimer's or dementia so as our population continues to age, we continue to see a large population over 65, the prevalence in Iowa will continue to grow," said Simon.
Right now, 69,000 Iowans are living with Alzheimer's. Last year, 15.4 million caregivers provided more then 17 point 5 billion hours of unpaid care. In 2013, Alzheimer's is estimated to cost the nation $203 billion.
"It's something everybody needs to be concerned about. Not just older adults. Not just people already touched by Alzheimer's, you don't have to have a family history to be concerned about this. It's really something that will have an impact on government, families and our health in the future," said Jessica Simon.
Alzheimer's disease is the sixth leading cause of death in the U.S. and the only top ten leading cause of death that can't be prevented, cured or have it's progression slowed.
To see the full 2013 Alzheimer's Disease Facts and Figures Report, click here