Thursday, December 24, 2009

“Delaying Aging Process Best Guard Against Alzheimer’s Disease - Senior Journal” plus 4 more

“Delaying Aging Process Best Guard Against Alzheimer’s Disease - Senior Journal” plus 4 more


Delaying Aging Process Best Guard Against Alzheimer’s Disease - Senior Journal

Posted: 24 Dec 2009 08:27 AM PST

Alzheimer's, Dementia & Mental Health

Delaying Aging Process Best Guard Against Alzheimers Disease

Looking at the way we age may have more impact on treatment, prevention of AD than studying basic biology of the disease

Dec. 24, 2009 Aging, something most senior citizens try to resist, is the single greatest risk factor for Alzheimer's disease. In a study released this month, researchers at the Salk Institute for Biological Studies found that simply slowing the aging process in mice prone to develop Alzheimer's disease prevented their brains from turning into a neuronal wasteland.

"Our study opens up a whole new avenue of looking at the disease," says the study's leader, Howard Hughes Medical Investigator Andrew Dillin, Ph.D., a professor in the Salk Molecular and Cell Biology Laboratory.

"Going forward, looking at the way we age may actually have more impact on the treatment and prevention of Alzheimer's disease than studying the basic biology of the disease itself."

 

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Their finding, published in the Dec. 11, 2009 issue of the journal Cell, is the latest clue in the Salk scientists' ongoing quest to shed light on the question of whether Alzheimer's disease onset late in life is a disastrous consequence of the aging process itself or whether the beta amyloid aggregates that cause the disease simply take a long time to form.

Age is the major risk factor for the development of Alzheimer's disease. Beyond age 65, the number of people with the disease doubles every five years. Centenarians, however, seem to escape most common age-related diseases, including the ravages of Alzheimer's disease.

"In this study, we went directly to the root cause of Alzheimer's disease and asked whether we could influence the onset of the disease by modulating the aging process," says first author Ehud Cohen, Ph.D., formerly a postdoctoral researcher in Dillin's lab and now an assistant professor at the Hebrew UniversityHadassah Medical School in Jerusalem, Israel.

To answer this intriguing question, he slowed the aging process in a mouse model for Alzheimer's by lowering the activity of the IGF-1 signaling pathway. "This highly conserved pathway plays a crucial role in the regulation of lifespan and youthfulness across many species, including worms, flies, and mice and is linked to extreme longevity in humans," he explains. As a result, mice with reduced IGF-1 signaling live up to 35 percent longer than normal mice.

Cohen then employed a battery of behavioral tests to find out whether it was simply the passage of time or aging per se that determined the onset of the disease. Chronologically old but biologically young animals appeared nearly normal long after age-matched, normal-aging Alzheimer's mice exhibited severe impairments in their ability to find a submerged platform in the Morris water maze or stay atop a revolving Rota Rod.

"These behavioral differences between normal and long-lived mice were apparent at nine months of age, but the big surprise came when we took a closer look at the plaques in their brains," says Cohen.

One of the telltale signs of Alzheimer's disease is the buildup of toxic clumps of beta amyloid plaques in the brain. Beta amyloid production probably occurs in all brains, but healthy cells clear away excess amounts. Brains of people with Alzheimer's disease, on the other hand, are unable to control beta amyloid accumulation. The same is true for Alzheimer's mouse models, which are genetically engineered to overproduce beta amyloid.

Although long-lived mice didn't show any of the cognitive or behavioral impairments typical of Alzheimer's disease till very late in life, their brains were riddled with highly compacted plaques.

"Although before it was thought that plaques are the causative agents of Alzheimer's disease, our results clearly support the emerging theme that they have a protective function," says Cohen. "As mice age, they become less efficient at stowing away toxic beta amyloid fibrils in tightly packed aggregates."

An earlier study by Cohen, Dillin, and colleagues, in which they had used roundworms to study the effects of the aging process on protein aggregation, had indicated that high molecular weight aggregates of beta amyloid might actually be less toxic than smaller beta amyloid fibrils. "But worms don't have brains as we do, and it wasn't clear whether these results would be relevant for mammals," he says.

And what about those lucid centenarians? "Interestingly, three studies found that some very long-lived humans carry mutations in components of the IGF-1 signal pathwaythe same pathway that we perturbed to increase the lifespan of the mice in our study," says Dillin.

"The reporting of this work is a celebration for the entire field of aging researchers, as it validates the long-held hypothesis that genetic and pharmacologic changes to create a healthy lifespan, or 'healthspan,' can greatly reduce the onset of some of the most devastating diseases that afflict mankind," he adds.

Notes:

The work was funded in part by the National Institutes of Health and the McKnight Endowment for Neuroscience.

Researchers who also contributed to the work include Johan F. Paulsson, Deguo Du and Jeffery W. Kelly at the Skaggs Institute of Chemical Biology, The Scripps Research Institute, Pablo Blinder in the Department of Physics at the University of California, San Diego, Tal Burstyn-Cohen in the Molecular Neurobiology Laboratory at the Salk Institute, Anthony Adame, Hang M. Pham and Eliezer Masliah in the Department of Neurosciences at University of California, San Diego, and Gabriela Estepa in the Molecular and Cell Biology Laboratory at the Salk Institute.

About the Salk Institute for Biological Studies:

The Salk Institute for Biological Studies is one of the world's preeminent basic research institutions, where internationally renowned faculty probe fundamental life science questions in a unique, collaborative, and creative environment. Focused both on discovery and on mentoring future generations of researchers, Salk scientists make groundbreaking contributions to our understanding of cancer, aging, Alzheimer's, diabetes, and cardiovascular disorders by studying neuroscience, genetics, cell and plant biology, and related disciplines.

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Dr. Louis Velotti Jr. - Standard Speaker

Posted: 24 Dec 2009 05:35 AM PST

Dec. 23, 2009

Dr. Louis Velotti Jr., 84, of West Hazleton passed away Wednesday at Hazleton General Hospital.

Born in 1925, in Uniontown, he was the son of the late Louis and Mary (Marsilio) Velotti Sr. and was a member of Queen of Heaven Church at Our Lady of Grace Parish, Hazleton.

Dr. Velotti was a native of Bridgeport, Conn.

He was a graduate of Franklin & Marshall University, receiving a Bachelor of Science degree in biology; he received a Master of Science degree from the University of Miami in parasitology and marine biology; and received a Doctorate of Optometry from the Philadelphia College of Optometric Medicine.

Dr. Velotti practiced optometry in Hazleton since 1955.

He was also a member of the Army Calvary division.

Preceding him in death, in addition to his parents, was his brother, Charles Velotti.

Surviving are his wife, the former Catherine Marino, who would have been married 56 years on Dec. 26; son, Dr. Thomas Velotti, and his wife, Kwan, Elkton, Md.; brother, Emil Velotti, and his wife, Gloria, Lewisburg; and nieces and nephews.

His funeral will be held Monday at 9 a.m. from Joseph A. Moran Funeral Home Inc., 229 W. 12th St., Hazleton.

A Mass of Christian Burial will be celebrated at 9:30 a.m. in Queen of Heaven Church at Our Lady of Grace Parish.

Burial will be in Calvary Cemetery, Drums.

Friends may call at the funeral home on Monday from 8:30 a.m. until the time of service.

Condolences may be sent through www.moranfuneral home.com.

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Post a Comment - Coloradoan

Posted: 24 Dec 2009 05:35 AM PST

Julie McQueen has been promoted to regional therapeutic massage clinic director at IBMC.

McQueen graduated from CSU with a Bachelor of Science in biology and has a diploma in therapeutic massage from IBMC.

To submit items for On the Agenda or Business Applause, send mail to Pat Ferrier, 1300 Riverside Ave., Fort Collins, CO 80524, fax (970) 224-7899 or e-mail BusinessNews@ coloradoan.com.

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Edwin Krebs, Nobel winner, dead at 91 - United Press International

Posted: 24 Dec 2009 08:34 AM PST

SEATTLE, Dec. 24 (UPI) -- Dr. Edwin Krebs, a Nobel Prize winner in medicine, has died in Seattle of progressive heart failure, a colleague said.

Krebs, who died Monday at the age of 91, was awarded the Nobel in 1992 with Eddy Fischer, a friend and colleague at the University of Washington who had known Krebs for more than 60 years.

His death is "difficult to accept. But this is biology and there is nothing you can do about it," Fisher, 89, told The Seattle Times.

Fischer and Krebs won the Nobel for the development of anti-cancer drugs and for discovering a chemical reaction with phosphate that activates an enzyme in muscles.

Krebs, born in Lansing, Iowa, did his medical residency at Washington University in St. Louis and served as a Navy medical officer in World War II before taking a faculty position at the University of Washington School of Medicine in 1948.

He is survived by his wife, Deedy, 86, three children, five grandchildren and five great-grandchildren.

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Licking Heights whiz aces ACT science section - Newark Advocate

Posted: 24 Dec 2009 07:16 AM PST

PATASKALA -- Licking Heights senior Joey Samons now occupies pretty rarefied air, thanks to his skills in science.

Samons aced the science subsection of the most recent ACT college entrance exam, scoring a 36.

Only 3,599 out of 1.48 million students accomplished what Samons accomplished this year, according to Licking Heights guidance counselor Liz Hughes.

"It's pretty remarkable," she said.

For Samons, it came as a surprise. He went into the test hoping to post an overall score of 30 or better (The highest possible score is 36). A classmate scored a 29, and Samons said he wanted to best it.

"The only goal I really had was to get above a 30," he said.

Samons, who boasts a 3.9 GPA, did best his classmate. He scored a 32.

His skills in math and science -- two subsections on the test-- helped him. Samons excels at both subjects.

"I really like math and science," he said. "They are my two best subjects. I enjoy doing them, and I figure I'll enjoy doing it as a profession, too."

Samons found out he had an aptitude for both at a young age.

In elementary school, one of his math teachers gave out rewards -- ice cream topings -- for high scores.

By the end of the year, Samons had the largest sundae in his class.

Flash forward ten years, and Samons said he enjoys the puzzle-solving nature of science and math.

He takes AP biology and AP calculus at Licking Heights, and his love of the two subjects prompted him to enroll at Ohio State University, where he plans on studying engineering next year.

One of his two brothers already attends OSU, but he is studying theater, not science or math.

"He (Michael) was the one who was good at English and art," said Samons, smiling at the dichotomy.

Hughes thinks Samons will succeed at Ohio State, but not solely because of his science and math skills.

"He's an overall great kid," she said.

Chad Klimack can be reached at (740) 927-3738 or cklimack@nncogannett.com.

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