Monday, December 5, 2011

RIM writes off value of tablet inventory

NEW YORK (AP) ? Research In Motion Ltd., the struggling maker of the BlackBerry phones, is writing off much of its inventory of PlayBook tablets, since it has to sell them at a deep discount.

The Canadian company on Friday said it's taking a pre-tax charge of $485 million in the just-ended quarter to account for the declining value of the tablets. The model originally priced at $500 now costs $200.

A year ago, co-CEO Jim Balsillie said pent-up interest in the PlayBook was "really overwhelming." Companies are looking for an equivalent of the iPad of corporate use, he said.

In March, Balsillie said "The launch of the PlayBook may well be the most significant development for RIM since the launch of the of the first BlackBerry device back in 1999."

But when the tablet went on sale in April, reviewers puzzled over the lack of email software, saying the device seemed half-baked. RIM now promises updated software in February.

RIM said it shipped 150,000 PlayBooks to stores and distributors in the fiscal third quarter, which ended Nov. 26. "Sell-through," or the number actually bought by users, was slightly higher, reflecting sales of tablets shipped earlier. It shipped 500,000 in the first quarter and 200,000 in the second.

RIM also said it sold 14.1 million BlackBerrys in the third quarter, slightly better than analysts expected. It then expects sales to fall slightly in the current quarter, roughly in line with analysts' expectations.

The company provided preliminary revenue and profit figures for the third quarter that were lower than it previously projected, but not a surprise to analysts.

RIM said it expects earnings at the "low to mid point" of the $1.20 to $1.40 per share it previously forecast. Analysts polled by FactSet have on average been expecting $1.18 per share.

The company expects revenue slightly the below the $5.3 billion to $5.6 billion in its previous forecast. Analysts had been expecting $5.27 billion, on average.

RIM shares fell $1.76, or 9.5 percent, to $16.82 in morning trading Friday. The stock hit a seven-year low of $15.98 last month.

The PlayBook charge comes as analysts have started to conclude that RIM's management has no chance of really righting the ship. They've started to value the company not on its future prospects, but on how much it would be worth if acquired, broken up, or simply run down while keeping BlackBerry service going.

The company is also taking a charge of $50 million for an embarrassing October outage of email and Web services that lasted days for millions of overseas BlackBerry users. It briefly spread to the U.S. and Canada before the company was able to contain the damage.

RIM reports fiscal third-quarter earnings on Dec. 15.

Associated Press

Source: http://hosted2.ap.org/APDEFAULT/495d344a0d10421e9baa8ee77029cfbd/Article_2011-12-02-Research%20In%20Motion-Tablet/id-bbdd23d28d4f46e8a8144d8726644f02

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Carlos Mencia Attempts Comeback On Comedy Central With New Style

Tomorrow night, Comedy Central will broadcast Carlos Mencia's new one-hour special, "New Territory." And everyone is asking, ?Has he stopped stealing jokes?"

It's impossible to talk about Carlos Mencia without mentioning "joke theft." Last year, Marc Maron confronted Mencia on the allegations on his podcast "WTF." Maron also sat down with Mencia's fellow comedians, Willie Barcena and Steve Trevino, in a separate podcast. And then he got Mencia to sit down for a follow-up discussion where Mencia said, "I was defeated... I don't know what to say. That was the beginning of the realization that, like it or not, I'm complicit in this."

Mencia was accused of stealing material from Bill Cosby, George Lopez and Ari Shaffir.

He isn't the first comic accused of stealing jokes and he certainly won't be the last.

The 44-year-old comic said he has been through a lot of personal changes. He described it as an "evolution as a human being" that is now incorporated into his new special. That's why the special is called "New Territory." He feels like he's "in new territory." Mencia said changing his style of delivering comedy was "really, really hard."

HuffPost LatinoVoices chatted with Mencia about his new special, his losing 70 pounds and living down his "joke stealer" rep.

Why was it so difficult to change your comedy style?
Imagine being successful at how you write and all of a sudden you have to come up with a new writing style because you realize what you were doing didn't really reflect you. What happened was, I would go on stage and tell a joke and it didn't work. Or it didn't work as well as I wanted to and I immediately wanted to go back to my old style of being you know, more aggressive and screaming or whatever, but I had to tell myself, ?No, you have to trust it. You have to go with it.?

What was therapy like for you? What did you have to ask yourself?
I know what I'm not, but what am I? And, at that point, I realized that I needed to go seek professional help to answer this question because I obviously have no clue as to who I am.

Why did you decide to lose weight?
The weight loss came about because a buddy of mine who was diagnosed with diabetes because of his obesity told me that I was fat. And, I started laughing and he was like, no seriously, you're fat. And I said, ?Oh wow, really.? People say, Congratulations to me but this is nothing to be congratulated on, anybody can do this. It's not hard.

Do people treat you differently now that you lost so much weight?
They look at me with reverence in a way that they never did before. Like with this level of respect that I never got before. And, believe it or not, in a weird way, a level of sympathy as well. I was never one of those fat victim people. I always have to address how much weight I lost and people always realize then how fat I was.

Your real name is Ned Arnel, why did you change your name?
The owner of the Comedy Store suggested it. She said to me, "You can't be an angry Mexican named Ned." I told her I wasn't Mexican and she replied, "Everyone is going to think you are Mexican. It's the way it is. Don't fight it." And, I remember thinking, ?Well, I have an uncle named Carlos.? She said, ?Carlos Mencia, that's melodious.? And, that was it.

Are you happy with your decision?
In retrospect, I believe that I am the first person who has a name that was pretty white and changed it to an ethnic name like ?Carlos.? I actually did the opposite of what a lot of people did in my industry. But this was someone that could help me get my career going so, fuck yea, I'll change my name.

How do you feel about George Lopez getting fired from TBS?
Here's what I know about the business I am in. It's all based on money. It's all based on ratings.
I wish there were more like him on TV. We don't have that chance to fail because it becomes a Latino thing as opposed to a ?Carlos thing? or a "George thing" or a time slot thing or a network thing. It becomes, "Latinos are not going to be successful in television." And, that's just bullshit.

How much has your reputation as a "joke stealer" affected you?
I had to ask myself, "Okay, why are they hating on me? What am I doing to facilitate this or to bring this on? Where is my part in all of this?" And, that's what became important. It became something to look at within myself.

Do you think you are ever going to live the reputation down?
I think that a lot of people don't understand it. If that reputation was real, I never would have gotten work at comedy clubs in the first place. They would've told me, "We can't have you here doing that stuff."

How have you changed?
My whole thing is, waking up everyday and thinking in the positive and not the negative. Listen, there are three people I know in the world, that professed love, harmony and peace: Ganghi, Jesus Christ and Martin Luther King. I don't even put myself in those guys shoes. But what I do realize is, if those guys have haters, it's just the way things are. You gotta move on. When I was younger, I was angry. I was boisterous and loud. I was on top of the mountain, screaming at everybody, "Look at me!" Now I'm more of a Taoist.

How has the audience embraced you?
I've never gotten a response that I'm getting today. I've never gotten the laughs that I'm getting today. Never gotten the respect that I'm getting from audiences. It's a different vibe, a different feel, and definitely a different type of special.

You talk a lot about America, why do you love it so much?
When I hear people say, ?America sucks!? I just want to slap them in the face and say, "Shut up!" You don't know what suck is. You don't know what poor is. You know what poor in America is? I'm poor and live in the projects. You know what poor in Honduras is, that man died because of malnutrition.

Why does the set background of your new show say, "Department of Immigration?"
Part of those pieces of Americana in the background is me telling the audience that this guy's perspective is that of an immigrant.

You joke about the SB1070 law, but how do you feel about it?
Illegal immigration is not a problem in this country. The reason we have illegal immigration is because we give them jobs. We don't need any other law. Don't employ them, they won't come. That law is not necessary. It's that simple.

Do you ever regret anything you said on stage?
I've never said anything to be mean. The only things I wish I can take back, but not really, is how I dealt with the hecklers because it came off as so real but it wasn't. I wish I could go back and say, you know I'm kidding right? This isn't real. With stand-up, it's different. People believe that is exactly who you are and that might be 1 percent of your personality blown up for comedic purposes but people don't look at it that way because what we do we do so well that it comes off as that is exactly how we are.

What can we expect from the new and improved Carlos Mencia?
I have been writing screenplays, a couple of TV show ideas, a book and a one man show.
I plan to get back on that horse. You know, get out there again. I want the world to engage with Carlos Mencia again.

On Tuesday, Dec. 6, An Extended And Uncensored Version Of "Carlos Mencia: New Territory" DVD Will Be Released By Comedy Central Home Entertainment And Paramount Home Entertainment.

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Source: http://www.huffingtonpost.com/2011/12/03/carlos-mencia-comeback_n_1127370.html

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Sunday, December 4, 2011

No. 3 Okla St makes BCS case in 44-10 win over OU (AP)

STILLWATER, Okla. ? A dominating performance made Oklahoma State a conference champion for the first time in decades. Now, the Cowboys want a shot at an even bigger title.

Joseph Randle ran for 151 yards and two touchdowns, Richetti Jones returned a fumble for a score and No. 3 Oklahoma State throttled No. 13 Oklahoma 44-10 Saturday night to win the Big 12 championship and make its case to play for the BCS national title.

The Cowboys (11-1, 8-1 Big 12) snapped an eight-game losing streak in the Bedlam rivalry and won their first outright conference title since 1948 in the three-team Missouri Valley.

Oklahoma State's defense, badmouthed much of the season while giving up big yardage but leading the nation in takeaways, forced the Sooners into five turnovers ? four of them by quarterback Landry Jones.

Fans started chanting "L-S-U!" midway through the fourth quarter with the victory well in hand, then stormed the field and tore down the goal posts when it was over.

While the top-ranked Tigers won the SEC championship Saturday to lock up a spot in the BCS title game, No. 2 Alabama sat at home idle after finishing second in its division. Oklahoma State, meanwhile, proved itself the best team in its state and its conference. But it's up to the voters, who had the Cowboys fifth in the coaches' poll and Harris poll, to decide whether Oklahoma State will play for the highest stakes.

Coach Mike Gundy proclaimed earlier this week that he considered the Crimson Tide to be the second-best team in the nation "right now" ? maybe because that's what he thought his team needed to hear that to get fired up and prove him wrong.

"Last week, I said Alabama should be there," Gundy said on the field after the game. "There's no question Oklahoma State should be No. 2 right now. No question."

For most of the 107 years of the Bedlam rivalry, the Sooners had the better team and more on the line.

But each of the past two years, Oklahoma came in with a lower ranking and still found a way to derail a couple of the best teams in Oklahoma State history ? first dashing any hopes of a BCS at-large berth two years ago and then taking away the Cowboys' shot at the Big 12 championship last season.

With all that history on their side, the Sooners came out looking to intimidate.

After coming onto the field, players ran into the west end zone for a pregame prayer and then lingered after it was over ? right outside the gate where the Cowboys were getting ready to run out. Coaches, game officials and security officers made them get out of the way.

The Sooners couldn't back up the pregame bluster, though.

Brandon Weeden's 53-yard pass to Tracy Moore set up Jeremy Smith's 9-yard touchdown run, and the Cowboys defense ? which entered the game ranked 107th out of 120 teams in the nation ? never needed any more than that.

Brodrick Brown outfought Jaz Reynolds to pick off Landry Jones' pass in the end zone and prevent an Oklahoma score, and Alex Elkins stripped the ball from the quarterback on a sack to set up a TD for the Cowboys.

Jamie Blatnick picked up the fumble and returned it 59 yards to the 1-yard line, and Randle scored on the next play to make it 17-0. Randle added a 2-yard run after Sam Proctor's holding penalty on a kickoff return backed the Sooners up, and they went three-and-out ? punting it back to Oklahoma State on a shortened field.

Richetti Jones made it 34-3 after Landry Jones reached back to pass the ball and fumbled it onto the turf, with the OSU defender bobbling it and then finally controlling it for a 5-yard return.

The Sooners got their only points on Michael Hunnicutt's 48-yard field goal at the end of the first half and Blake Bell's 28-yard TD scamper with 2:25 left in the game.

Gundy thinks there's more to the Cowboys than the nation's second-highest scoring offense, and he wants a chance to prove it against LSU and its second-ranked defense.

"We'd love to have that challenge. I think our defense is better than what other people say," Gundy said.

It ended up as Oklahoma's most lopsided defeat since losing the 2005 Orange Bowl against Southern California, and the second-biggest margin of victory for the Pokes in the series ? behind only a 47-0 shutout in 1945.

Oklahoma State's case to play against LSU in New Orleans next month will be hurt by a double-overtime loss 15 days earlier at Iowa State, which finished its season 6-6. It'll bolstered by five wins against teams in the BCS Top 25, compared to two for Alabama.

And, of course, the Cowboys will have the momentum from not only winning a conference title but doing it in dominating fashion against a team that was ranked No. 1 earlier this season.

Source: http://us.rd.yahoo.com/dailynews/rss/topstories/*http%3A//news.yahoo.com/s/ap/20111204/ap_on_sp_co_ga_su/fbc_t25_oklahoma_oklahoma_st

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[OOC] Skyrim: Brotherhood

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Saturday, December 3, 2011

Justin Bieber Tweets Encouragement To 'X Factor' Contestant

'Keep your head up,' Bieber wrote to eliminated teen Drew Ryniewicz.
By Gil Kaufman


Justin Bieber
Photo: Jeffrey Ufberg/ Getty Images

There was just no consoling weepy 15-year-old "X Factor" contestant Drew Ryniewicz on Thursday night when she was sent home in an double elimination episode. The quirky teen with the fluttery, dramatic voice was in tears for most of the episode and when her time came even usually unflappable mentor Simon Cowell seemed choked up with emotion.

But avowed Belieber Ryniewicz got some serious consolation less than an hour after her run on the show ended when none other than idol add link: Justin Bieber Tweeted out a message of support to the Chino Valley, Arizona high schooler.

"@drewryniewicz keep your head up," Bieber wrote to the fan who showed off her bedroom shrine to the Canadian pop star during her audition episode. "I lost my first competition too. This is just the beginning for u. Never say never. Best wishes." Though the departure from the show hurt — fellow teen rapper Astro was also sent packing — Ryniewicz tried to keep an upbeat attitude, following up Bieber's Tweet with her own message of hope. "Hey thank you for your love!," . "I'll miss the xfactor but have a lot more in stor for you all! Upbeat? Yes."

Because she's a teenage girl who auditioned for the show with an impassioned take on Bieber's "Baby," Drew couldn't help bragging a short time later, "Justin Bieber follows me now!" Good sport that she is, Drew also gave props to the remaining girls on Team Simon, Melanie Amaro and Rachel Crow, while accepting some positive vibes from Astro, remaining contestant Marcus Canty and former "American Idol" contestant Casey Abrams.

One of Cowell's favorites, Ryniewicz was done in by her piano-driven, seated take on Michael Jackson's "Billie Jean," which the show's other judges dinged for being too sleepy. While Cowell said that criticism was "absolute nonsense," fiercely defending his decision to have her sing another ballad — though Drew seemed to have wanted otherwise — on Thursday night he made a startling admission. "The reason Drew is in this position tonight is my fault," said Cowell, typically adverse to any second-guessing or display of weakness. "I take total responsibility. I genuinely believe you deserve a second chance. I'm begging these two [judges] to give her another chance."

But, alas, Cowell's fellow judges cast their votes against Drew and Cowell seemed ready to storm off the set, getting up from his chair with an angry look and taking the stage to console his charge while staring daggers at his fellow panelists and angrily ignoring host Steve Jones' requests for comment.

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Source: http://www.mtv.com/news/articles/1675267/x-factor-drew-justin-bieber.jhtml

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'Arsenic life' debate still buzzes after a year

Henry Bortman / 2010

Other scientists are analyzing the controversial strain of bacteria that biologist Felisa Wolfe-Simon and her colleagues found in California's Mono Lake.

By Alan Boyle

It's been one year since researchers shook up the scientific world by claiming they bred bacteria that used arsenic in place of phosphorus, and the controversy is still simmering: The lead researcher and her critics say they're taking a closer look at the microbe at the center of the "weird life" claims.

After hitting the highs and the lows of academic acclaim, Felisa Wolfe-Simon has left her original research group and joined up with Lawrence Berkeley National Laboratory in California to continue her research into the bacterium known as GFAJ-1, which gets its name from the acronym for "Give Felisa a Job." (No joke!)

"There is so much work to do we're focusing on that and look forward to communicating our efforts in the coming months," Wolfe-Simon told me in an email this week.

Meanwhile, Wolfe-Simon's highest-profile critic, University of British Columbia microbiologist Rosie Redfield, took on the task of replicating the GFAJ-1 experiment. "I'm doing this even though I agree with all the other researchers who said this result is almost certainly wrong," Redfield told me. "Scientifically, it's really kind of a waste of time to try to replicate this yourself. But there's always the possibility that you could be wrong. And more than that, there was just a general sense that, you know, somebody should try."


Redfield has sent purified DNA samples to collaborators at Princeton University for mass spectrometry analysis ? to see whether any arsenic was really taken up into the molecular structure. "We just got the DNA from Rosie Redfield," one of those collaborators, Leonid Kruglyak, told me this week. A graduate student in Kruglyak's lab, Marshall Louis Reaves, is currently working out the protocols for analyzing the DNA.

"We want to be able to fragment the DNA and run the fragments on the mass spectrometer," Krugylak said. "Those fragments should look quite different in the mass spectrometer if there is arsenate."

Just today,?another team of?researchers, led by Simon Silver of the University of?Illinois at Chicago,?announced that they have sequenced GFAJ-1's genome and will be analyzing it for new clues in the case.

Argonne National Laboratory's Jack Gilbert, a member of the team, characterized himself as a "100 percent skeptic" about the findings announced a year ago, but?said that the gene sequence?was still worth having. He and his colleagues have already found some interesting genetic twists, even if there's no evidence?of arsenic in the DNA. "It's interesting to have this information to determine what the mechanism might be if other evidence shows this to be true," he explained.

Gilbert said it was mere coincidence that the genome sequence was published online exactly one year after Wolfe-Simon and her colleagues kicked off the controversy. "I hadn't even considered that today was the anniversary," he told me.

Why all the fuss?
The case of GFAJ-1 is significant on more than one level.

If the central claim of the original paper holds true, that means the machinery of life can be tinkered with to replace one seemingly essential chemical ? phosphorus?? with?a different?chemical that's seemingly inimical to life. One of Wolfe-Simon's original collaborators, Arizona State University astrobiologist Paul Davies, has long maintained that "weird life," built on a different biochemical platform, could exist right under our noses and we wouldn't know it.

The prospect of weird life on Earth would also argue in favor of widening the search for weird life on other worlds, perhaps as close as Mars or the Saturnian moon Titan. That's what led NASA to tout the research a year ago as having extraterrestrial implications. "The definition of life has just expanded,"?said Ed Weiler, an associate administrator at the?space agency. The news reports went even farther. Here's a typical headline: "NASA Discovers Alien Life in California."

Actually, what Wolfe-Simon and her colleagues did was to take an existing strain of salt-loving bacterla from California's Mono Lake, and try to breed it in the presence of high concentrations of arsenic. GFAJ-1 emerged as the best prospect: The research team said it seemed to?take hold in the high-arsenic environment, and they said their?molecular analysis suggested that arsenic-based compounds known as arsenates were incorporated in?the place of phosphates.

The bacteria in the arsenic-rich culture weren't aliens at all. But for many chemists and microbiologists, the research team's claims, published online by the journal Science on Dec. 2, 2010, were as hard to believe as reports of a UFO landing.

One chemist, Steven Benner of the Florida-based Foundation for Applied Molecular Evolution, said he bet Wolfe-Simon $100 that the arsenic wasn't taken up in the DNA. Benner said in an email this week that?the proposition was "still in limbo ... so the bet is not yet collected." (Wolfe-Simon told me she doesn't remember the bet.)

The skepticism over the reported results erupted almost immediately in a wave of blog postings and Twitter updates?from commentators and?scientists, including Redfield. As a result, the #arseniclife case quickly became a case study for instant peer review, mediated by the Internet. It also turned into a case study for open science, in which researchers share their results as they become available rather than holding them back until they're published in a journal.

Redfield emerged as a strong voice, for the skeptics as well as for the open-science movement. Her technical?criticisms focused on the way that the bacteria samples were handled. "The way they isolated their DNA was almost 'I can't believe they did this' badly done," she told me this week. Such criticism led Science's editors to hold back the on-paper publication of the research for months, until eight sets of technical comments could be collected from Redfield and other observers and vetted through peer review. Wolfe-Simon and her colleagues were also given space to respond to the technical comments.

"That was pretty unprecedented," said Ginger Pinholster, director of the Office of Public Programs at the American Association for the Advancement of Science, which publishes the journal Science.

The next steps
Since then, the?focus has shifted from the headlines to the labs. A Popular Science profile of Wolfe-Simon created a bit of a stir a couple of months ago: She was quoted as saying that she was "basically evicted" from her research group and worried that "it's quite possible that my career is over."

But during this week's email exchange, Wolfe-Simon told me that?the "Popular Science article quotes were not what I said," and that?"what matters now is what these organisms are telling us about biology, and that is my focus." Here are some reflections on the one-year anniversary from one of her emails to me:

"What a busy year it has been!

"With the generous support of NASA, we are able now to dive deep and explore this scientific discovery. After such a discovery comes the time-intensive process of rigorous testing. We aim to unravel the mechanisms behind how this microbe accomplishes the ability to flourish and grow despite uptake and utilization of arsenic. This systematic rigorous testing is critical and needed to build upon an initial discovery of this type.

"To this end, I have joined the Lawrence Berkeley National Laboratory in collaboration with Dr. John Tainer and his group there. LBNL provides the diverse intellectual and material resources of a major national laboratory, affording us the opportunity to pursue our efforts to test multiple aspects and implications of the work efficiently and stringently. LBNL synergistically complements the generous financial support from NASA.

"Currently, we have made significant headway in optimizing the growth conditions of GFAJ-1 and preparing samples for a wide range of analyses, including biomolecule crystallization and metabolite characterization. There is so much work to do we're focusing on that and look forward to communicating our efforts in the coming months. ...

"I maintain my serious commitment to science and the process of data-driven research. I look forward to speaking with you some time in the not too distant future after we make additional scientific progress."

Other researchers are delving into the mysteries of GFAJ-1 as well, even though they don't?think the claims about arseno-DNA and other "weird life" wonders will hold up. "I don't have any money for this," Redfield told me. "This is just a side project in what would be my spare time, if professors have any spare time."

Redfield says the projects she gets paid for are more likely to be scientifically productive,?but they're not?as interesting to the general public. "This struck me as an opportunity to do science openly in a circumstance where people would be actually interested in what I'm doing, and what the results were," she said.

Now the fruits of her GFAJ-1 labors are in the hands of Kruglyak and his colleagues. If the arsenic in the samples has really been incorporated in the DNA, rather than merely representing sample contamination, traditional genetic sequencing techniques would not work. "They could give all sorts of unpredictable results," Kruglyak said. That's why mass spectrometry has to come into play.

Kruglyak can't predict how long it will take to get the answers. "It always takes longer than whatever I would say," he told me. "I would hope it's weeks, not months."

Meanwhile,?Gilbert and his colleagues will continue studying GFAJ-1's genetic makeup. He told me "there's nothing spectacularly amazing" about the bacteria, which was not subjected to the high-arsenic treatment applied by Wolfe-Simon's team and by Redfield. But?Gilbert said the raw bacteria's genome has some intriguing twists nevertheless.

"What is quite interesting is that this has very few arsenic resistance genes, i.e., it does not have the typical suite of genes that?would make the cell resistant to arsenic?in the environment," he?told me in an email.?Further study of the genome may at last point to an explanation for GFAJ-1's affinity for arsenic ? but as of today, one year after the bacteria came onto the world scene, Gilbert can't predict what that explanation might be.

"We will prod and poke at this thing for another year, and see if there's anything more interesting," he said.


Connect with the Cosmic Log community by "liking" the log's Facebook page, following @b0yle on Twitter and adding the Cosmic Log page to your Google+ presence. You can also check out "The Case for Pluto," my book about the controversial dwarf planet and the search for new worlds.

Source: http://cosmiclog.msnbc.msn.com/_news/2011/12/02/9168255-arsenic-life-debate-still-percolates

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Friday, December 2, 2011

Deepak Chopra: Alzheimer's Disease: How to Face Fear With Knowledge (Part 2)

By Deepak Chopra, M.D., FACP and Rudolph Tanzi, Ph.D., The Joseph P and Rose F. Kennedy, Professor of Neurology, Harvard Medical School, Director of Genetics and Aging, Massachusetts General Hospital

In the first post we confronted the primary fact about Alzheimer's disease -- fear and terror -- which is a psychological reality, not a piece of scientific data. Our minds are the window to reality. Any form of mental illness is frightening to the patient because their grip on reality has become tenuous, if not delusional. The same disorder is frightening to onlookers because the fragile bond that links us -- our agreement that A is real but B is not -- is threatened and often broken beyond repair.


Visualization is courtesy of TheVisualMD.com

To lose someone you love to Alzheimer's feels worse than death to many families. Death is a decisive break, and afterwards the grieving process occupies its own domain.? The territory is painful, to the point that many grieving survivors would rather follow their loved ones into the unknown after death. But Alzheimer's is a gray, ambiguous land where your loved one gradually fades away, with many false returns and defeated hopes.?Death is considered a mercy compared to the tormented stranger who torments those who suffer through the disease with them.

I said in the first post that knowledge is our best weapon in fighting fear. At least we can stand on rational ground.? And knowledge is advancing in the diagnosis and treatment of Alzheimer's.? As painfully slow as progress may seem -- like the disease itself, there have been defeated hopes along the way -- let me summarize the current state of affairs.

In Alzheimer's disease, two abnormal buildups accumulate in the brain. One type of buildup is a sticky substance called beta-amyloid. It deposits in senile plaques, on brain blood vessels, and as smaller clumps in the synapses where it can disrupt communication between nerve cells impairing learning and memory. The other type is the neurofibrillary (nerve cell) tangles. These buildups disrupt the trafficking of proteins and neurotransmitters in nerve cells leading nerve cell death and neurodegeneration. Together, these abnormal buildups lead to Alzheimer's type dementia and are targets of drug discovery aimed at treating and preventing this devastating disease.

Testing for and diagnosing Alzheimer's involves psychological tests that assess cognition. Doctors can make a probable diagnosis of Alzheimer's, but the only time a definite diagnosis can be made is at autopsy, when the pathologist confirms the widespread presence of plaques and tangles throughout the brain.

More recently specific types of brain imaging, including those capable of visualizing senile plaques and other beta-amyloid deposits are being used to detect Alzheimer's changes in the brain. Biomarkers in the cerebrospinal fluid can also indicate the presence of plaques and tangles in the brain. The combination of brain imaging and biomarkers is dramatically enhancing our ability to diagnose Alzheimer's and even detect it before any cognitive symptoms appear.

During the course of Alzheimer's disease, several key proteins are deposited in the brain, including proteins called amyloid beta protein and tau protein. Amyloid beta protein (in senile plaques, blood vessel beta-amyloid, and small clumps of beta-amyloid in synapses) accumulates in the areas of the brain responsible for learning and for creating, retaining, and extracting memories. The plaques occupy more and more space over time, causing brain inflammation. The smaller clumps of amyloid beta protein known as oligomers interfere with normal communication between brain cells, disrupting the neural network of the brain.

Most of the scientists who study Alzheimer's believe that it's the excessive accumulation of amyloid beta protein that induces the protein called tau to form nerve cell tangles that eventually choke and kill nerve cells. Beta amyloid protein is certainly a part of Alzheimer's, but the presence of beta amyloid alone isn't sufficient to cause the disease. Beta amyloid must trigger tangle formation to create dementia. So far, the genes that have been shown to affect risk for Alzheimer's have in common that they increase the accumulation of beta-amyloid in the brain. More recently, the Cure Alzheimer's Fund Alzheimer's Genome Project has identified dozens of new Alzheimer's disease gene candidates, many of which likewise influence beta-amyloid levels in the brain.


What tests are used for Alzheimer's?

There is no single test for Alzheimer's. A physician examining someone who may have the disease will consider many factors and conduct a number of tests ?before making a diagnosis. The physician will probably ask questions about the person's medical history and conduct a physical exam. A neurological exam will probably be given as well. Some of these tests are done to rule out another medical disorder (for example, a vitamin deficiency) that may be causing Alzheimer-like symptoms.


Cognitive tests for Alzheimer's

A commonly used mental status test is the mini-mental state examination (MMSE). The MMSE is a brief test that only takes about 10 minutes to complete. In it, the health care professional asks a series of questions designed to test a range of everyday mental skills. These include:

  • Orientation. Up to 10 questions are asked to determine if the person knows where he or she is as well as the time of day, day of the week, month, season, and year.
  • Registration. The examiner names three objects and asks the person to repeat all three names.
  • Calculation and attention. The person is asked to make a series of calculations.
  • Recall. The person being tested is asked to recall the three objects named earlier.
  • Language. Testing is done for a series of skills, including naming, repetition, the ability to follow oral instructions, reading, and writing.
  • Visual perception. The person is asked to copy shapes.
  • The highest possible score for the MMSE is 30. Scores of 25 or more are considered normal. Scores between 10 and 19 indicate moderate dementia. People with mild Alzheimer's tend to score from 19 to 24. However, scores need to be interpreted individually to account for a person's age, education, and other factors. It's possible for someone to receive a high score and still have significant cognitive deficits.


    Imaging tests for Alzheimer's

    Neuroimaging (brain imaging) uses a variety of different techniques, including radiation and magnetic fields, to generate pictures of what's happening inside the brain. Some methods show microscopic physical structures; others capture the activity of individual cells. By taking pictures of brain activity, doctors can get some idea of how much amyloid plaques have encroached on healthy brain tissue. The images can highlight where nerve cells are becoming weaker and starting to deteriorate, possibly leading to loss of function.

  • CT scans generate visual "slices" of the brain. They are used to make sure the person with Alzheimer's symptoms doesn't have a tumor or hasn't had a stroke.
  • MRI scans can be used to check for tumors or strokes. They are also used to see if there is shrinkage in different areas of the brain where groups of nerve cells have died due to Alzheimer's. Functional MRI can check whether the correct brain regions are being activated when carrying out a certain mental task.
  • PET scans show where nerve cells and their synapses are most active. They allow doctors to see whether any areas of the brain are not functioning correctly.
  • CT+PET scans combine the brain structure information provided by the CT scan with the brain function data shown by the PET scan. In Alzheimer's, areas of nerve cell loss correspond with regions where the level of brain activity has decreased.
  • PIB+PET imaging uses a substance called Pittsburgh Compound B (PIB). PIB binds to amyloid protein and also glows when patients' brains are scanned with PET. Using PIB during a brain scan may alert doctors to the presence of senile plaques and blood vessel amyloid before symptoms of Alzheimer's appear. One in five elderly persons who don't have cognitive impairment or memory problems still show brain deposits of beta-amyloid similar to levels found in people who have Alzheimer's. However, in these infrequent cases, it is usually the lack of abundant tangles that most likely explains the absence of dementia despite abundant brain amyloid. This also tells us that excessive beta-amyloid is necessary to trigger Alzheimer's, but it is not sufficient - tangles are needed to cause neurodegeneration and dementia.

  • Detecting Alzheimer's early

    Researchers are trying to find ways to do something they have never been able to do before: diagnose Alzheimer's years before the first symptoms appear. By identifying those most at risk, we may learn which lifestyle changes or medications can slow down or even reverse the progression of the disease. It would also help recruit the most appropriate patients into clinical trials.

    Biomarkers are biochemical features that can be used to measure the progress of a disease. Researchers can now detect the most toxic form of amyloid beta protein, called A-beta 42, in the cerebrospinal fluid (the fluid that surrounds the brain and spinal cord). Levels of this protein go down as the disease progresses, presumably because as A-beta 42 is released in the brain, it becomes sequestered by the growing numbers of senile plaques and other beta-amyloid deposits. Another useful cerebrospinal biomarker for Alzheimer's is called phospho-tau. Phospho-tau makes up the tangles and is released by dying nerve cells. Recently, it has been found that phospho-tau can travel from nerve cell to nerve cell and spread tangle pathology.

    By combining tests for decreased levels of A-beta 42 and increased levels of phospho-tau, researchers have reported impressive accuracy in predicting which people with mild cognitive impairment will go on to develop Alzheimer's. By recording levels over time, doctors may be able to determine if the disease is getting worse or remaining stable. Someday, the same biomarkers might be used to predict which cognitively normal individuals are already on their way to Alzheimer's. This will help improve recruitment of the best subjects for clinical trials of new therapeutics for treating Alzheimer's disease.


    Early prediction: Genes

    In the less-common form of the disease, familial early-onset Alzheimer's (which occurs under the age of 65), inherited gene mutations are clearly implicated. The mutations occur in three genes (named APP, PSEN1, and PSEN2) and increase the accumulation of beta-amyloid in the brain.

    In the more common, late-onset form of Alzheimer's, genetic inheritance also plays a role by increasing susceptibility to the disease. Certain gene variants, like APOE4, affect the accumulation of beta-amyloid in the brain by influencing how it efficiently it is cleared out of the brain. More recently, the efforts of the Cure Alzheimer's Fund Alzheimer's Genome Project and other international consortia have confirmed a dozen new late-onset Alzheimer's gene candidates. ?Some seem to affect the buildup of beta amyloid, while others influence the brain's immune system and cholesterol metabolism.

    There is no cure for Alzheimer's disease, but there are many things people can do to possibly reduce and delay symptoms of memory loss.

  • Know your enemy. There are many useful resources about Alzheimer's disease. The Alzheimer's Association and Cure Alzheimer's Fund ?as well as the National Institute on Aging ?provide basic information on the latest understanding of the disease, as well as updates on the newest research in diagnosis and treatment.
  • See a doctor. It's natural for memory to slip as we age. But if you've noticed that you or a loved one have lost the ability to recall or even learn new things, then it's worth discussing the problem with a doctor. He or she can help determine whether these lapses are a part of normal aging, another medical condition, or possibly the first signs of mild cognitive impairment or Alzheimer's.

  • Cognitive reserve

    Why do some people have beta amyloid plaques and neurofibrillary tangles and yet show no signs of dementia? The theory of cognitive reserve holds that these people have compensated for the gradual decline in cognitive function caused by accumulating amyloid plaques and neurofibrillary tangles. They've done this by building up enough reserves of synapses and nerve cell networks to make up for the loss of cells to disease.

    Here's how cognitive reserve can be built up:

  • Social network. Having a rich social life and keeping in touch with family and friends can stimulate the brain and may slow down cognitive decline.
  • Intellectual Stimulation Staying intellectually active by seeking new educational experiences like public lectures and seminars, going to museums all help to maintain or even increase the brain's nerve cell network. Every new synapse you make when learning something new will reinforce the synapses you already have. This is because all of learning is based on making associations with what you have already learned in the past.

  • Manage weight and other health factors

    A long-term study of 1,500 adults found that those who were obese when they were middle-aged were twice as likely to develop dementia later in life. Those who also had high blood pressure and high cholesterol levels had six times the risk of dementia. Clearly, there are benefits to keeping weight and cholesterol at healthy levels and managing high blood pressure.


    Eat a brain-health diet

    Foods containing high levels of antioxidants may protect brain cells. These foods include dark-skinned fruits (like blueberries) and vegetables, cruciferous vegetables (like kale, Brussels sprouts, and spinach), fatty cold-water fish (or flaxseeds for vegetarians), and nuts (like walnuts). It must be kept in mind, however, that there is no one-to-one link between any of these foods and the prevention of a disorder as specific as Alzheimer's.? Another antioxidant, Vitamin E, has had some persuasive results in the aging process generally; it can't hurt o take a supplement, as no negative effects have been noticed from large doses of Vitamin E.


    Exercise

    Exercising regularly may be one of the best ways to forestall the symptoms of Alzheimer's. One study used MRI scans to compare the brains of adults who ranged in fitness from sedentary to very athletic. They found the most distinct differences in the brains were in the areas associated with learning and memory: exercise decreased the amount of brain tissue lost in these areas. In mouse models of Alzheimer's disease, exercise dramatically reduced brain pathology.

    Exercise:

    • Improves concentration and attention
    • Reduces gray matter loss
    • Promotes growth of new nerve cells
    • Strengthens the connections between nerve cells
    • Enhances blood flow to the brain by increasing the size and density of brain capillaries
    • Reduces beta-amyloid levels.


    Because society is aging in unprecedented numbers around the world, any piece of good news about Alzheimer's will land on the front pages and on evening news. Research continues to be intensive and widely funded. But a realist must face the hard truth: this remains a devastating disorder that invades the most complicated organ of the body, the human brain, which may indeed be the most complex creation in the cosmos. No simple preventive is known' no simple cure is likely. The best policy is to remain focused on wellness as a long-term lifestyle. For my part, I believe that the deeper we delve into consciousness and how it affects the body down to the genetic level, the clearer the whole picture of dementia will become.

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    Follow Deepak Chopra on Twitter: www.twitter.com/DeepakChopra

    Source: http://www.huffingtonpost.com/deepak-chopra/face-alzheimers-fear-knowledge_b_1117748.html

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