Wednesday, February 22, 2017

Aluminum linked directly to early onset of Alzheimer’s disease

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Natural News

Aluminum is everywhere: it contaminates vaccines, it’s in a variety of medications, baby products, cosmetics, and it’s even in the food you eat. And like several other metals, it isn’t really all that great for the human brain (or the rest of the body).

Even the CDC’s Agency for Toxic Substances and Disease Registry (ATSDR) notes that aluminum can elicit negative effects in the musculoskeletal, neurological, and respiratory systems. This is especially worrisome because some research indicates that aluminum is capable of building up in bodily tissues, which would greatly increase its potential to cause harm. [RELATED: Keep up with the latest CDC headlines at CDC.news]
Research has suggested that there may be a link between aluminum exposure and Alzheimer’s disease for several years. That link, however, has always been somewhat murky. The evidence to support their claims has often been lacking. Recently, however, scientists have found a direct link between the metal and the onset of the neurological disorder.

Connecting the dots: aluminum and Alzheimer’s

According to scientists from Keele University, located in Staffordshire, aluminum actually plays a role in most — if not all– cases of Alzheimer’s. Professor Exley, a scientist from the university, has been studying this connection at length. In a recent article for The Hippocratic Post, Exley explained, “We already know that the aluminium content of brain tissue in late-onset or sporadic Alzheimer’s disease is significantly higher than is found in age-matched controls. So, individuals who develop Alzheimer’s disease in their late sixties and older also accumulate more aluminium in their brain tissue than individuals of the same age without the disease.”
Exley went on to say that even higher levels of aluminum have been found in individuals with certain forms of Alzheimer’s disease and notes that these high amounts of exposure are often attributed to the environment these people live in, or their workplace. “This means that Alzheimer’s disease has a much earlier age of onset, for example, fifties or early sixties, in individuals who have been exposed to unusually high levels of aluminium in their everyday lives,” contends Exley.

High aluminum content in Alzheimer’s patients

In 2016, Exley published his most revealing study yet in the Journal of Trace Elements in Medicine and Biology. This study is believed to be of exceptional value because it is the first to measure aluminum content in the brain tissue of individuals that have been diagnosed with familial Alzheimer’s disease.
Alzheimer’s is considered to be “familial” when two or more people in the same family are stricken by the condition.
Exley and his team found that people who had passed away with diagnosed familial Alzheimer’s disease had the highest concentrations of aluminum in their brain tissue that had ever been recorded.
“We now show that some of the highest levels of aluminium ever measured in human brain tissue are found in individuals who have died with a diagnosis of familial Alzheimer’s disease,” Exley wrote. He went on to note that the amount of aluminum found in the brain tissue of the individuals with familial Alzheimer’s disease were almost identical to those seen in individuals who died of aluminum-induced encephalopathy while undergoing renal dialysis. [RELATED: Learn more about toxic metals and other damaging compounds at Toxins.news]
Exley and his team concluded that their research indicates that the genetic predisposition for Alzheimer’s disease is likely tied to the accumulation of aluminum in brain tissue. The researchers note that aging is a risk factor for Alzheimer’s and that the human brain tends to accumulate more aluminum as we get older. Because of aluminum’s neurotoxic effects, its accumulation in brain is going to exacerbate or contribute to any ongoing disease or toxicity.
Sources:

Sunday, February 19, 2017

Solving the Puzzle of Alzheimer’s Disease

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Summary: A new study reports a compound by the name of AC253 may inhibit amyloid beta.

Source: University of Alberta.
UAlberta scientist seeks to neutralize ‘rogue’ protein believed to be a key player in the development of Alzheimer’s.
Every day tens of thousands of Canadians unwillingly find themselves becoming shadows of their former selves. They grasp onto moments of clarity–fleeting windows of time–before slipping away again into confusion; robbed of memories, talents and their very personalities.
Alzheimer’s is a heart-wrenching disease that directly affects half a million Canadians. There is no cure, let alone treatment to stop progression of the disease. While current answers are few, research at the University of Alberta is spearheading the discovery of new potential therapies for the future.
A study published in the journal Alzheimer’s and Dementia: Translational Research and Clinical Intervention examines if a compound called AC253 can inhibit a “rogue” protein called amyloid. The protein is found in large numbers in the brains of Alzheimer’s patients and is suspected to be a key player in the development of the disease.
“The way I look at it, it’s hard to ignore the biggest player on the stage, which is the amyloid protein. Whatever treatment you develop, it’s got to address that player,” says Jack Jhamandas, Professor of Neurology in the Faculty of Medicine & Dentistry at the University of Alberta and senior author of the study. “In our previous work we have shown that there are certain drug compounds that can protect nerve cells from amyloid toxicity. One of these is a compound we call AC253. It sounds like an Air Canada flight. I hope this one is on time and takes us to our destination!”
The team, comprised of postdoctoral fellows and research associates Rania Soudy, Aarti Patel and Wen Fu, tested AC253 on mice bred by David Westaway (a University of Alberta collaborator) to develop Alzheimer’s. Mice were treated with a continuous infusion of AC253 for five months, beginning at three months of age before development of the disease.
“We found at eight months, when these mice typically have a lot of amyloid in the brain and have a lot of difficulty in memory and learning tasks, that they actually improved their memory and learning,” says Jhamandas, also a member of the U of A’s Neuroscience and Mental Health Institute.
As part of the study, the team of local and international researchers also developed and tested a more efficient method of getting the compound into the brain. Given an injection three times a week for 10 weeks of AC253 with a slightly modified structure, they again found there was an improvement in memory and learning performance. In addition, the researchers noted there was a lower amount of amyloid in the brains of mice treated with the compound compared to mice that did not get the drug, and that they exhibited reduced inflammation of the brain.
A diagram of an alzhiemer's brain.
The team is now planning additional studies to examine optimal dosage and methods of further improving the compound to increase its effectiveness in the brain. Much more work is needed before the research can move to human trials. Image is for illustrative purposes only.
The team is now planning additional studies to examine optimal dosage and methods of further improving the compound to increase its effectiveness in the brain. Much more work is needed before the research can move to human trials.
Despite the long path still ahead, Jhamandas believes the findings offer both hope and a new way forward to unlock the Alzheimer’s enigma.
“Alzheimer’s is a complex disease. Not for a moment do I believe that the solution is going to be a simple one, but maybe it will be a combination of solutions.”
“We can’t build nursing homes and care facilities fast enough because of an aging population. And that tsunami, the silver tsunami, is coming if not already here,” adds Jhamandas. “At a human level, if you can keep someone home instead of institutionalized, even for a year, what does it mean to them? It means the world to them and their families.”
ABOUT THIS ALZHEIMER’S DISEASE RESEARCH ARTICLE
Funding: Funding provided by Canadian Institutes of Health Research, Alberta Innovates, Alberta Prion Research Institute, Alzheimer Society of Alberta, University Hospital Foundation.
Source: Ross Neitz – University of Alberta 
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Cyclic AC253, a novel amylin receptor antagonist, improves cognitive deficits in a mouse model of Alzheimer’s disease” by Rania Soudy1, Aarti Patel, Wen Fu, Kamaljit Kaur, David MacTavish, David Westaway, Rachel Davey, Jeffrey Zajac, and Jack Jhamandas in Alzheimer’s and Dementia. Published online December 9 2016 doi:10.1016/j.trci.2016.11.005
CITE THIS NEUROSCIENCENEWS.COM ARTICLE
University of Alberta “Solving the Puzzle of Alzheimer’s Disease.” NeuroscienceNews. NeuroscienceNews, 16 February 2017.
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Abstract
Cyclic AC253, a novel amylin receptor antagonist, improves cognitive deficits in a mouse model of Alzheimer’s disease
Introduction
Amylin receptor serves as a portal for the expression of deleterious effects of amyloid β-protein (Aβ), a key pathologic hallmark of Alzheimer’s disease. Previously, we showed that AC253, an amylin receptor antagonist, is neuroprotective against Aβ toxicity in vitro and abrogates Aβ-induced impairment of hippocampal long-term potentiation.
Methods
Amyloid precursor protein–overexpressing TgCRND8 mice received intracerebroventricularly AC253 for 5 months. New cyclized peptide cAC253 was synthesized and administered intraperitoneally three times a week for 10 weeks in the same mouse model. Cognitive functions were monitored, and pathologic changes were quantified biochemically and immunohistochemically.
Results
AC253, when administered intracerebroventricularly, improves spatial memory and learning, increases synaptic integrity, reduces microglial activation without discernible adverse effects in TgCRND8 mice. cAC253 demonstrates superior brain permeability, better proteolytic stability, and enhanced binding affinity to brain amylin receptors after a single intraperitoneal injection. Furthermore, cAC253 administered intraperitoneally also demonstrates improvement in spatial memory in TgCRND8 mice.
Discussion
Amylin receptor is a therapeutic target for Alzheimer’s disease and represents a disease-modifying therapy for this condition.
“Cyclic AC253, a novel amylin receptor antagonist, improves cognitive deficits in a mouse model of Alzheimer’s disease” by Rania Soudy1, Aarti Patel, Wen Fu, Kamaljit Kaur, David MacTavish, David Westaway, Rachel Davey, Jeffrey Zajac, and Jack Jhamandas in Alzheimer’s and Dementia. Published online December 9 2016 doi:10.1016/j.trci.2016.11.005
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Thursday, February 16, 2017

Alzheimer’s May Be Linked to Defective Brain Cells Spreading Disease

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NEUROSCIENCE NEWS



Summary: Findings may help researchers better understand how diseases can spread through the brain.
Source: Rutgers.
Rutgers study finds toxic proteins doing harm to neighboring neurons.
Rutgers scientists say neurodegenerative diseases like Alzheimer’s and Parkinson’s may be linked to defective brain cells disposing toxic proteins that make neighboring cells sick.
In a study published in Nature, Monica Driscoll, distinguished professor of molecular biology and biochemistry, School of Arts and Sciences, and her team, found that while healthy neurons should be able to sort out and rid brain cells of toxic proteins and damaged cell structures without causing problems, laboratory findings indicate that it does not always occur.
These findings, Driscoll said, could have major implications for neurological disease in humans and possibly be the way that disease can spread in the brain.
“Normally the process of throwing out this trash would be a good thing,” said Driscoll. “But we think with neurodegenerative diseases like Alzheimer’s and Parkinson’s there might be a mismanagement of this very important process that is supposed to protect neurons but, instead, is doing harm to neighbor cells.”
Driscoll said scientists have understood how the process of eliminating toxic cellular substances works internally within the cell, comparing it to a garbage disposal getting rid of waste, but they did not know how cells released the garbage externally.
“What we found out could be compared to a person collecting trash and putting it outside for garbage day,” said Driscoll. “They actively select and sort the trash from the good stuff, but if it’s not picked up, the garbage can cause real problems.”
Working with the transparent roundworm, known as the C. elegans, which are similar in molecular form, function and genetics to those of humans, Driscoll and her team discovered that the worms – which have a lifespan of about three weeks — had an external garbage removal mechanism and were disposing these toxic proteins outside the cell as well.
Iliya Melentijevic, a graduate student in Driscoll’s laboratory and the lead author of the study, realized what was occurring when he observed a bright blob forming outside of the cell in some of the worms.
“In most cases, you couldn’t see it for long but in a small number of instances, it was like a cloud that accumulated outside the neuron and just stayed there,” said Melentijevic, who spent three nights in the lab taking photos of the process viewed through a microscope every 15 minutes.
Research using roundworms has provided scientists with important information on aging, which would be difficult to conduct in people and other organisms that have long life spans.
In the newly published study, the Rutgers team found that roundworms engineered to produce human disease proteins associated with Huntington’s disease and Alzheimer’s, threw out more trash consisting of these neurodegenerative toxic materials. While neighboring cells degraded some of the material, more distant cells scavenged other portions of the diseased proteins.
“These finding are significant,” said Driscoll. The work in the little worm may open the door to much needed approaches to addressing neurodegeneration and diseases like Alzheimer’s and Parkinson’s.”









Monday, February 13, 2017

Is Alzheimers a type of diabetes

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Alzheimer's and Dementia Weekly


MEMORY PROBLEMS are an early sign of Alzheimer's. New research directly links these problems to sugar (glucose) deprivation in brain cells. In diabetes, a well-known Alzheimer's risk factor, sugar is blocked from entering cells. How likely does this make the Alzheimer's-sugar-diabetes triangle? 



(Philadelphia, PA) - One of the earliest signs of Alzheimer's disease is a decline in glucose levels in the brain. It appears in the early stages of mild cognitive impairment -- before symptoms of memory problems begin to surface. Whether it is a cause or consequence of neurological dysfunction has been unclear, but new research at the Lewis Katz School of Medicine at Temple University now shows unequivocally that glucose deprivation in the brain triggers the onset of cognitive decline, memory impairment in particular. 

As diabetes is a condition in which glucose cannot enter the cell, this research gives good reason to suggest that Alzheimer's is caused by a pathway similar or related to a type of diabetes. This possibility is strengthened by the fact that insulin resistance in type 2 diabetes is a known risk factor for dementia. 

"In recent years, advances in imaging techniques, especially positron emission tomography (PET), have allowed researchers to look for subtle changes in the brains of patients with different degrees of cognitive impairment," explained Domenico Praticò, MD, Professor in the Center for Translational Medicine at the Lewis Katz School of Medicine at Temple University (LKSOM). "One of the changes that has been consistently reported is a decrease in glucose availability in the hippocampus." 

The hippocampus plays a key role in processing and storing memories. It and other regions of the brain, however, rely exclusively on glucose for fuel -- without glucose, neurons starve and eventually die. 

The new study, published online January 31 in the journal Translational Psychiatry, is the first to directly link memory impairment to glucose deprivation in the brain specifically through a mechanism involving the accumulation of a protein known as phosphorylated tau. 

Friday, February 10, 2017

Dementia: Free hearing aid offer

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Here is a www.hear.comgreat offer

To exercise your brain, you need to hear well and hear often. The Signia Silks delivers crystal clear sounds, even in noisy settings. The SpeechMaster technology focuses on the speaker while reducing background noise. Do you visit many places throughout the week? Local coffee shop, library, restaurant?  No problem. The Signia Silk automatically adjusts to make sure you have the best listening experience in every location. By transmitting clearer sounds more often, the Signia Silk makes listening a joy.
After an audiology exam with a Partner Provider, you may try the hearing aids for 45 days. If you are not completely satisified, you will receive 100% of your money back. Sign up for a free consultation with one of our hearing experts to determine if the Signia Silk is right for you! 

Sunday, February 5, 2017

Determine Early Stages Of Alzheimer's Disease Through Testing The Eyes And Nose Function

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scienceworldreport.com

Eye Test



Two studies suggested that older adults with a decreasing ability to identify odors may already started to have a decline in cognitive functions. According to CNN, other studies probed on different types of eye tests to help them determine the disease. These were all presented during the Alzheimer's Association International Conference 2016 Tuesday in Toronto.
As many may have already known, Alzheimer's is the most common type of dementia which causes a person to have problems with memory, thinking and behavior.
It looks like "the eyes and the nose are a window to the brain," observed CBS News medical contributor Dr. David Agus.
One of the studies revealed that the thinning of the retinal nerve fiber layer in the eye could happen to those who performed poorly in the testing of cognitive skills like memory, reasoning and reaction time.
Agus, who appeared on "CBS This Morning," said the finding makes sense. "If you look in the eye, the retinal nerve that comes out of the brain, if it gets narrower, that's an indicator of the onset of Alzheimer's."
Meanwhile, aside from MRI scan that measured the thickness of the brain area where Alzheimer's typically first develops, the entorhinal cortex, one of the studies used the smell test on 397 adults in Manhattan. These men were 80 years old, on average, and didn't have dementia. The study involved 40 scratch-and-sniff surfaces scented with a range of familiar scents including turpentine, lemon, licorice, bubble gum and even "eau de skunk."
It was found that fifty of these people (12.6 percent) had dementia four years after undergoing the initial smell test, while nearly 20 percent showed signs of cognitive decline.
Basically, Agus said that if a person can name 35 out of the 40 scents, then that person has a lower chance of developing Alzheimer's. However, if you got less than 35 scents correct, you may have already started the process of developing the disease condition, US News reported.
Researchers cleared out that it is not the sensitivity of the nose that diminishes; it is the cognitive impairment that's developing. The brain is not very capable of identifying what those smells are.
"Our research showed that odor identification impairment, and to a lesser degree, entorhinal cortical thickness, were predictors of the transition to dementia," study author Seonjoo Lee, assistant professor of clinical biostatistics (in psychiatry) at Columbia University Medical Center, said in a statement. "These findings support odor identification as an early predictor, and suggest that impairment in odor identification may precede thinning in the entorhinal cortex in the early clinical stage of Alzheimer's disease

Thursday, February 2, 2017

Morning Mix Could this computer game delay Alzheimer’s symptoms? New study suggests it could.

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A new analysis of previous research data announced at the Alzheimer’s Association International Conference this week tentatively suggests that this kind of game could decrease the risk of symptoms of dementia by almost half, compared to not having any brain training at all. The study presented is under peer review and hasn’t yet been published. (Studies can change dramatically from the conference setting to the pages of a journal, reminds PLOS blogger Hilda Bastian, so the findings should be considered preliminary for now.)
The game is called a speed-of-processing task. It’s one of three types of cognitive training that 2,800 people took part in during the Advanced Cognitive Training for Independent and Vital Elderly (ACTIVE) study, a randomized longitudinal study funded by NIH. The participants averaged 74 years old when the trial began. Scientists tracked them for 10 years, hoping to find out how cognitive training could impact the functioning of healthy older adults.
The participants were split into four groups. One played the speed-of-processing games, and two other groups took a memory or reasoning class. The last group did nothing, and served as a control. The memory classes taught tricks for memorization, like mnemonic devices or “methods of loci,” which is a tool to remember a series of objects by visualizing each one in a different physical location. The reasoning course taught logic and pattern recognition, and trained people how to choose the next letter in a series, based on the order of the ones that precede it.
The most recent ACTIVE paper was published in 2014 and concluded that the different cognitive training could in fact help a little with certain basic tasks, like driving or balancing a checkbook, as people got older.
Monday in Toronto, a research team led by Jerri Edwards at the University of South Florida announced that they had used the wealth of data from the ACTIVE study to ask a different and more provocative question: Could cognitive training delay the onset of dementia or cognitive decline related to Alzheimer’s?
Their findings showed that the group that completed 10 to 14 hours— that’s total, over 10 years — of the speed-of-processing games were 48 percent less likely to have developed Alzheimer’s or other forms of dementia, compared to those who received no brain training at all. These participants did 10 hours of game play in the first year of the study, and then were randomly selected to receive booster sessions up to four more hours throughout the rest of the trial.
“We believe this is the first time a cognitive training intervention has been shown to protect against cognitive impairment or dementia in a large, randomized, controlled trial,” Edwards said, in a news release.
The result caused a stir of cautious curiosity at its presentation, said one attendee, Penny Dacks, a neuroscientist and the director of aging and Alzheimer’s prevention at the Alzheimer’s Drug Discovery Foundation. It raises some meaty questions: Why did speed-of-processing show the strongest correlation and not, for example, the memory classes? And could it really be possible that only 10 to 14 hours had such a large effect, years later?
“I think it’s really exciting,” Dacks said in an interview with The Washington Post. “For one thing, it shows us that not all cognitive training is equal. This is not going get us all the way, but if it could help even a fraction of the population, I think that it should be applauded. And certainly pursued with more research.”
While the study is a secondary analysis of past data, the researchers claim it could be the first hint that a brain training game could alter the onset of dementia.“That’s a spectacular finding,” Susanne Jaeggi, the director of the Working Memory and Plasticity Laboratory at the University of California, Irvine told Dan Hurley in a New Yorker article. “We didn’t have any evidence that computerized training had any preventive effects on dementia. You could argue that this study provides evidence that it is possible.”


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