New drug may stop the progression of Alzheimer's disease

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Medical News Today

According to findings in a study published in PLoS One, a new drug candidate may be the first drug that is capable of halting the devastating mental decline of Alzheimer's disease. Researchers administered the drug, known as J147, to mice with Alzheimer's disease and observed an associated improvement in memory and prevention in brain damage. The new drug was developed by scientists at the Salk Institute for Biological Studies, led by David Schubert, and could be trialled as a treatment for Alzheimer's disease in humans in the near future.

David Schubert, head of Salk's Cellular Neurobiology Laboratory, explained:

"J147 enhances memory in both normal and Alzheimer's mice and also protects the brain from the loss of synaptic connections. No drugs on the market for Alzheimer's have both of these properties."


The researchers say that even though the new compound's efficacy and safety in humans has not yet been established, the results indicate that the drug could become a potential treatment in people with Alzheimer's. 



 According to figures of the National Institutes of Health, a staggering 5.4 million Americans suffer from Alzheimer's. The Alzheimer's Association estimates that by 2050 more than 16 million will be affected by the disease, resulting in annual medical costs of over $1 trillion. 


Alzheimer's causes a steady, irreversible decline in brain function. Affected individuals experience a progressive loss of memory and ability to think clearly, which subsequently leads to the person being unable to perform simple tasks, such as eating and talking, and ultimately ends in death.

Alzheimer's is associated with aging, with a typical onset in individuals aged 60 years or above, although a small percentage of families carry a genetic risk for earlier onset. Amongst the top ten causes of mortality, Alzheimer's is the only disease that cannot be prevented, cured or reduced to progress slowly.

Onset of Alzheimer's seems to be influenced by a complex mixture of genetics, lifestyle factors and environment, although scientists still remain unclear what causes the disease. Until now, drugs developed for the treatment of Alzheimer's, such as Aricept, Razadyne and Exelon have only produced short periods of memory improvements, yet do not halt the overall progression of the disease.

Schubert and his team set out to find a new type of drug, but instead of following the current trend of the pharmaceutical industry, they decided to take a different approach. The pharmaceutical industry seems to focus exclusively on the biological pathways involved in the formation of amyloid plaques, the dense deposits of protein, which characterize the disease, but according to Schubert, until now, all amyloid-based drugs have failed in clinical trials.

Instead, they developed methods in which they used living neurons grown in laboratory dishes to assess the probability of whether or not new synthetic compounds prove effective in protecting the brain cells against several pathologies connected with brain aging. Based on the test results from each chemical iteration of the lead compound, a test originally designed for treating stroke and traumatic brain injuries, Schubert and his team managed to alter its chemical structure to produce a much more potent Alzheimer's drug. 



Marguerite Prior, a research associate in Schubert's lab, who led the project together with Qi Chen, a former Salk postdoctoral researcher, explained:

"Alzheimer's is a complex disease, but most drug development in the pharmaceutical world has focused on a single aspect of the disease - the amyloid pathway. In contrast, by testing these compounds in living cell cultures, we can determine what they do against a range of age-related problems and select the best candidate that addresses multiple aspects of the disease, not just one."




 The researchers subsequently tested their promising J147 compound as an oral medication in mice. In collaboration with Amanda Roberts, a professor of molecular neurosciences at The Scripps Research Institute, they performed a series of behavioral tests, which demonstrated that the drug improved memory in normal rodents. 


They subsequently demonstrated that J147 prevented cognitive decline in animals with Alzheimer's and also proved that mice and rats treated with the drug produced more of a protein called brain-derived neurotrophic factor (BDNF). BDNF is a molecule involved in memory formation and protects neurons from toxic insults. It also helps in the growths of new neurons and connects with other brain cells.

According to the researchers, based on the compounds broad ability to protect nerve cells, J147 may also be effective in the treatment of other neurological disorders, including Parkinson's and Huntingdon's disease as well as amyotrophic lateral sclerosis (ALS), and stroke.

The research was supported through funding by the Fritz B. Burns Foundation, the National Institutes of Health, the Bundy Foundation and the Alzheimer's Association.

Written by Petra Rattue

View drug information on ARICEPT; Exelon.

Copyright: Medical News Today

The life of the brain: The promise of restoration (part 3)

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thestar.com

Kenneth Kidd
Feature Writer
DALLAS-And if there's a research community that could use a dose of very good news, it's the Alzheimer's crowd.

Roughly 500,000 Canadians over the age of 65, about one in 11, now suffer from dementia, more than half of those as a result of Alzheimer's disease.

By 2038, the number of people with dementia is projected to more than double as the huge baby boom generation moves squarely into its sunset years. (In Canada, the oldest baby boomers turn 63 this year, while those at the absolute peak of the boom are turning 49 and 50.)

Put another way, within a generation, roughly one in three Canadian households will have an extended family member suffering from dementia.

Progressive and ultimately fatal, Alzheimer's can be as emotionally draining for family members as it is confusing and debilitating for those afflicted with the disease.

The other dispiriting fact is how research into Alzheimer's is so far adhering to the old undergraduate mantra: the more we discover, the more we realize how much we don't know.

First described in 1906 by a German psychiatrist Alois Alzheimer, the disease kills off neurons and the connections between them, resulting in the familiar loss of memory and language skills.

As Alzheimer's moves to other parts of the brain, confusion, mood swings, irritability and social withdrawal often ensue.

Two proteins, beta amyloid and tau, have so far been identified as the leading culprits in bringing about the death of cells. Both proteins occur naturally in healthy brains — even if the precise role of beta amyloid is uncertain — but something happens to tilt the balance.

Enzymes normally help clear away excess beta amyloid. In the brains of Alzheimer's patients, however, beta amyloid molecules start sticking together to form toxic clumps and, eventually, larger agglomerations called plaques.

Tau is a bit trickier in that it normally performs some essential tasks, such as maintaining what amounts to the transport system that ferries needed chemicals between the body of the cell and its nerve endings.

With Alzheimer's, the tau instead starts to pile up in thread-like tangles, effectively choking the cell to death.

Many researchers believe beta amyloid also plays a role in developing these tangles, that it has a sort of cascading effect.

But with Alzheimer's, things can get...more next time on dementia views about The life of the brain: The promise of restoration

The life of the brain: The promise of restoration (part 2)

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thestar.com

Kenneth Kidd
Feature Writer
DALLAS—Until the 1960s, the received wisdom was that once you became an adult, you had your full complement of brain cells. Hence your mother's stern warnings about protecting the only brain cells you'd ever have.

We've since learned that all mammals, including humans, give birth to new brain cells throughout their lifespan. But not all of those cells survive to become fully fledged neurons.

Somewhere along their journey to getting wired into the brain, they essentially commit suicide, a process called apoptosis, or programmed cell death.

For the most part, this is just the natural state of affairs. Biology isn't always efficient, discarding much of what it builds. Human embryos, for instance, wouldn't develop fingers if the cells between their digits didn't go through apoptosis.

The trouble is, as we age, the rate of programmed cell death in the brain increases. More and more of those new cells simply don't make it through the 30-day process of becoming fully connected neurons.

In effect, our brains lose some of their ability to repair themselves.

This, however, wasn't what Pieper was seeing in Room K3.406.

The relative multitude of new neurons that he eventually detected were the product of mice whose brains had been treated with a chemical compound dubbed P7C3 or, in subsequent tests, a derivative of P7C3 that proved even more effective.

The drug wasn't making the mice produce more cells, but it was somehow protecting more of those cells from apoptosis.

“Instead of 70 or 80 per cent dying along the route, only 40 or 50 per cent are dying,” says Steven McKnight, another University of Texas biochemist who worked on the study, published last month in the journal Cell.

This could have profound implications in treating what for many is the most terrifying brain disease associated with old age: Alzheimer's.

And if there's a research community that could...more next time on dementia views about The life of the brain: The promise of restoration

The life of the brain: The promise of restoration

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Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Here are more interesting dementia brain boosting activities





Get your subscription to Activity Director Today's e magazine" />

Thestar.com

Kenneth Kidd
Feature Writer
DALLAS—Dr. Andrew Pieper isn't sure how many hours he spent in room K3.406, a windowless space not much bigger than a broom closet, except that it all amounted to “quite a lot of time.”

This, it turns out, translates into many visits per week over the course of three years, enough to peer through a microscope at roughly 27,000 very thin sections of the brains of lab mice.

Or, to be precise, the so-called dentate gyrus in the hippocampus region of their brains.

The hippocampus is associated with memory, and the dentate gyrus is one part of the brain that generates new neurons, or nerve cells — the little building blocks that get wired into the mind's complicated circuitry.

Pieper, a biochemist at the University of Texas Southwestern Medical Center, had the “very tedious” task of detecting those new neurons, employing a series of antibodies to help amplify their telltale signal.

He found a great many nascent neurons, and this is very good news.

Until the 1960s, the received wisdom was more next time on dementia views about The life of the brain: The promise of restoration

Strategies to Protect New Brain Cells Against Alzheimer's Disease

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ScienceDaily — Stimulating the growth of new neurons to replace those lost in Alzheimer's disease (AD) is an intriguing therapeutic possibility. But will the factors that cause AD allow the new neurons to thrive and function normally? Scientists at the Gladstone Institute of Neurological Disease (GIND) have discovered that two main causes of AD amyloid-beta (Aβ) peptides and apolipoprotein E4 (apoE4) impair the growth of new neurons born in adult brains.

What is more, they have identified drug treatments that can normalize the development of these cells even in the presence of Aβ or apoE4. The findings are described in two separate papers published in the current issue of Cell Stem Cell.

Although it had long been assumed that neurons cannot be renewed, it is now well established that new neurons are generated throughout the lives of mammals. One brain region in which new neurons are born in adults, the hippocampus, is involved in learning and memory and affected severely by Alzheimer's disease.

GIND investigator Li Gan, PhD, and her collaborators studied the development of neurons born in the hippocampus of adult mice genetically engineered to produce high levels of human Aβ in the brain. Surprisingly, Aβ initially accelerated the development of newborn neurons but then profoundly impaired their maturation at later stages of development.

"Interestingly," Dr. Gan said, "we were able to....read all of Strategies to Protect New Brain Cells Against Alzheimer's Disease

Protein linked to Alzheimer's disease doesn't act alone

EurekAlert

Karen Mallet


GUMC researchers find APP needs to work with 'Reelin' protein to maintain healthy communication between brain neurons

Washington, DC – A team of U.S. investigators led by neuroscientists at Georgetown University Medical Center (GUMC) are steadily uncovering the role that amyloid precursor protein (APP) - the protein implicated in development of Alzheimer's disease - plays in normal brain function. In the June 10 issue of the Journal of Neuroscience, they discovered that APP interacts with another protein known as Reelin to promote development of abundant connections between brain neurons.

Reelin, named for mice that "reel" around when they don't have the protein, has been thought to be involved in stimulating growth of neuronal dendrites – the branching projections that transmit signals to other neurons. It also has been implicated in some brain disorders, but up until now, little was known about how Reelin interacts with APP.

Researchers say that showing that APP and Reelin work together doesn't have immediate implications for therapeutic treatment of Alzheimer's disease in humans, but they say the work helps provide the background necessary to understand finally why a brain veers toward the progressive memory loss seen in this devastating disease, which impacts 5.3 million people yearly in the U.S..

"In the last 20 years we have made tremendous progress in understanding how APP can become toxic. But I think the flip side is equally interesting: Why does APP even exist in the brain? We are only now just beginning to figure that out," says the study's senior author, G. William Rebeck, PhD, associate professor in the Department of Neuroscience at GUMC.

What has long been known is that mutations in the gene that produces..........read the whole article

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