Super Sea Veg, Fish Oil and Preventing Alzheimers
U.S. sets 2025 as target for Alzheimer’s solution
Goals include effective treatment, ways to delay disease
by Lauran Neergaard – Jan. 17, 2012 11:54 PM
Associated Press
WASHINGTON – Effective treatments for Alzheimer’s by 2025? That’s the target the government is eyeing as it develops a national strategy to tackle what could become the defining disease of a rapidly aging population. Already families approach the advisory committee “reminding us of the enormity of our task,” said Dr. Ron Petersen, an Alzheimer’s specialist at the Mayo Clinic who chairs the panel. The plan still is being written, with the advisory panel’s input. But a draft of its goals sets 2025 as a target date to have effective treatments and ways to delay the illness.
An estimated 5.4 million Americans have Alzheimer’s or similar dementias.
And the disease is growing steadily as the population ages. By 2050, 13 million to 16 million Americans are projected to have Alzheimer’s, costing $1 trillion in medical expenditures.
Today’s treatments only temporarily ease some dementia symptoms, and work to find better treatments has been frustratingly slow. Scientists now know that Alzheimer’s is brewing for years before symptoms appear, and they’re hunting for ways to stall the disease.
Fishing for answers to Alzheimer’s
By Kathleen Fackelmann, USA TODAY
Experts predict Alzheimer’s will quadruple by mid century rising from 4.5 million cases to 16 million cases by 2050
Shannon Adkins eats fish — lots of fish — for the most powerful of reasons: She’s determined to avoid her mother’s fate.
Adkins is only 32. But her mother, Suzie Smith, was diagnosed with Alzheimer’s disease at age 52. Five years later, Smith can’t feed or dress herself.
Could something as simple as eating fish save Adkins from a disease that is progressively destroying her mother’s mind? Well, there’s fresh evidence that fish — often dubbed “brain food” — also may be something far more potent: brain-saving food. People who frequently eat fish may protect themselves from Alzheimer’s, according to separate scientific studies by top researchers at Tufts University in Boston, Rush University in Chicago and the University of California-Los Angeles.
Fish is fast becoming to Alzheimer’s candidates what an aspirin-a-day regimen is to many heart patients. This movement toward fish already has started to change the way some Americans live their daily lives. It’s changing the way many Americans shop and eat. (The purported health benefits of fish have helped push seafood consumption to record levels, going from 15.6 pounds consumed per person in 2002 to more than 16.3 pounds consumed in 2003.) And it has empowered people such as Adkins to help themselves not by visiting the clinic or hospital, but the fish aisle of the local grocery store.
Increasingly, the experts now also say that a healthful diet, one that includes fish, might help delay or even prevent the dreaded disease that killed such American icons as former president Ronald Reagan, boxer Sugar Ray Robinson and actress Rita Hayworth. This disease also unhinges the lives of everyday Americans, like those of Adkins and her mother.
Adkins first realized that something was seriously wrong with her mom in 1997, when Smith, who was driving on a multilane highway, suddenly took her hands off the wheel. Adkins, who was sitting in the passenger seat, had to steer the car to safety.
From Dr. Stefan Kraan, PhD, Marine Botany. FarmaSea’s Scientific Advisor and Partner.
Neurite outgrowth promoting activity of marine algae from Japan against rat adrenal medulla pheochromocytoma cell line, PC12D
Yuto Kamei
Marine and Highland Bioscience Center, Saga University, 152-1 Shonan-cho, Karatsu, Saga, Japan (Author for correspondence)
Atsuko Sagara
Marine and Highland Bioscience Center, Saga University, 152-1 Shonan-cho, Karatsu, Saga, Japan
We screened for biological activity which induces neurite outgrowth in vitro from 300 species of marine algae for possible use as a treatment for the lack of neurotrophic factor which is considered to be a cause of Alzheimer’s disease.
In this study, we evaluated the neurite outgrowth promoting activity in a rat adrenal medulla pheochromocytoma cell line, PC12D, using a low level of NGF (nerve growth factor). Although most of the samples had no activity, a brown alga, Sargassum macrocarpum and a red alga, Jania adharens, exhibited neurite outgrowth promoting activity and induced neuron specific dendrites and axons from the surfaces of PC12D cells.
The active substance present in S. macrocarpum seemed to be lipid and heat stable with molecular weight of around 500 to 1000. These results suggest that marine algae may constitute a good source for development of promising novel agents with neurotrophic activity in brain nerve systems for future use in treatment of Alzheimer’s disease.
Keywords
Alzheimer’s disease, nerve growth factor, neurite outgrowth, promoting activity, PC12D cells, marine algae, Sargassum macrocarpum
Report: 35 million-plus worldwide have dementia
September 21st, 2009 By LAURAN NEERGAARD , AP Medical Writer
(AP) — More than 35 million people around the world are living with Alzheimer’s disease or other types of dementia, says the most in-depth attempt yet to assess the brain-destroying illness – and it’s an ominous forecast as the population grays.
The new count is about 10 percent higher than what scientists had predicted just a few years ago, because earlier research underestimated Alzheimer’s growing impact in developing countries.
Barring a medical breakthrough, the World Alzheimer Report projects dementia will nearly double every 20 years. By 2050, it will affect a staggering 115.4 million people, the report concludes.
“We are facing an emergency,” said Dr. Daisy Acosta, who heads Alzheimer’s Disease International, which released the report Monday.
The U.S. and other developed countries long have been bracing for Alzheimer’s to skyrocket. But the report aims to raise awareness of the threat in poorer countries, where finally people are living long enough to face what is mostly a disease of the 65-and-older population.
While age is the biggest driver of Alzheimer’s, some of the same factors that trigger heart disease – obesity, high cholesterol, diabetes – seem to increase the risk of dementia, too. Those are problems also on the rise in many developing countries.
In poorer countries, “dementia is a hidden issue,” Acosta said, and that’s complicating efforts to improve earlier diagnosis. “You’re not supposed to talk about it.”
For example, the report notes that in India, such terms such as “tired brain” or “weak brain” are used for Alzheimer’s symptoms amid widespread belief that dementia is a normal part of aging – when it’s not.
That mistake isn’t confined to the developing world. Even in Britain, the report found, just over half of the families caring for someone with dementia believed the same thing.
The new study updates global figures last reported in 2005, when British researchers estimated that more than 24 million people were living with dementia. Using that forecast, scientists had expected about 31 million people would be struggling with dementia by 2010.
Mitochondria and brain function/aging
By Benjamin V. Treadwell, Ph.D.
Where did I place the car keys? Deterioration in mental function with age occurs throughout the animal kingdom, but the degree of deterioration varies. There are some smart old mice as well as some smart old people. Why do some have a sharper decline in mental function than others?
A recent study suggests some potential answers. Post-mortem examination of the brains of elderly persons with a neurodegenerative condition, as compared to the brains of elderly persons with no such condition, demonstrated a significant increase in mutations in mitochondrial genes. Mutations in the region involved in switching the gene on and off were two-thirds more common in diseased brains than their normal counterparts.
Alzheimer’s brains harbor somatic mtDNA control-region mutations that suppress mitochondrial transcription and replication
Pinar E. Coskun *, M. Flint Beal and Douglas C. Wallace *,
*Center for Molecular and Mitochondrial Medicine and Genetics, University of California, Irvine, CA 92697-3940; andDepartment of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY 10021
Contributed by Douglas C. Wallace, May 24, 2004
Defects in mitochondrial oxidative phosphorylation have frequentlybeen associated with Alzheimer’s disease (AD), and both inheritedand somatic mtDNA mutations have been reported in certain ADcases. To determine whether mtDNA mutations contribute moregenerally to the etiology of AD, we have investigated the sequenceof the mtDNA control region (CR) from AD brains for possibledisease-causing mutations. Sixty-five percent of the AD brainsharbored the T414G mutation, whereas this mutation was absentfrom all controls. Moreover, cloning and sequencing of the mtDNACR from patient and control brains revealed that all AD brainshad an average 63% increase in heteroplasmic mtDNA CR mutationsand that AD brains from patients 80 years and older had a 130%increase in heteroplasmic CR mutations. In addition, these mutationspreferentially altered known mtDNA regulatory elements. CertainAD brains harbored the disease-specific CR mutations T414C andT477C, and several AD brains between 74 and 83 years of ageharbored the CR mutations T477C, T146C, and T195C, at levelsup to 70–80% heteroplasmy. AD patient brains also hadan average 50% reduction in the mtDNA L-strand ND6 transcriptand in the mtDNA/nuclear DNA ratio. Because reduced ND6 mRNAand mtDNA copy numbers would reduce brain oxidative phosphorylation,these CR mutations could account for some of the mitochondrialdefects observed in AD.
Abbreviations: AD, Alzheimer’s disease; APP, A precursor protein;CR, control region; CSB, conserved sequence block; mtPTP, mitochondrialpermeability transition pore; mtTFA, mitochondrial transcriptionfactor A; np, nucleotide pair; OXPHOS, oxidative phosphorylation;PL and PH, L- and H-strand promoters; PNA, protein nucleic acid;ROS, reactive oxygen species.
