Alzheimer's may originate in a form similar to that of infectious prion diseases

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The brain damage that characterizes Alzheimer's disease may originate in a form similar to that of infectious prion diseases such as bovine spongiform encephalopathy (mad cow) and Creutzfeldt-Jakob, according to newly published research by The University of Texas Health Science Center at Houston (UTHealth).

"Our findings open the possibility that some of the sporadic Alzheimer's cases may arise from an infectious process, which occurs with other neurological diseases such as mad cow and its human form, Creutzfeldt-Jakob disease," said Claudio Soto, Ph.D., professor of neurology at The University of Texas Medical School at Houston, part of UTHealth. "The underlying mechanism of Alzheimer's disease is very similar to the prion diseases. It involves a normal protein that becomes misshapen and is able to spread by transforming good proteins to bad ones. The bad proteins accumulate in the brain, forming plaque deposits that are believed to kill neuron cells in Alzheimer's."

The results showing a potentially infectious spreading of Alzheimer's disease in animal models were published in the Oct. 4, 2011 online issue of Molecular Psychiatry, part of the Nature Publishing Group. The research was funded by The George P. and Cynthia W. Mitchell Center for Research in Alzheimer's Disease and Related Brain Disorders at UTHealth.

Alzheimer's disease is a form of progressive dementia that affects memory, thinking and behavior. Of the estimated 5.5 million cases of Alzheimer's in the United States, 90 percent are sporadic. The plaques caused by misshapen aggregates of beta amyloid protein, along with twisted fibers of the protein tau, are the two major hallmarks associated with the disease. Alzheimer's is the sixth leading cause of death in the United States, according to the Alzheimer's Association.

Researchers injected the brain tissue of a confirmed Alzheimer's patient into mice and compared the results to those from injected tissue of a control without the disease. None of the mice injected with the control showed signs of Alzheimer's, whereas all of those injected with Alzheimer's brain extracts developed plaques and other brain alterations typical of the disease.

"We took a normal mouse model that spontaneously does not develop any brain damage and injected a small amount of Alzheimer's human brain tissue into the animal's brain," said Soto, who is director of the Mitchell Center. "The mouse developed Alzheimer's over time and it spread to other portions of the brain. We are currently working on whether disease transmission can happen in real life under more natural routes of exposure."

Source: University of Texas Health Science Center at Houston

Blood Test Predicts Course of Alzheimer's

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By Crystal Phend, Senior Staff Writer, MedPage Today

Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planne

Plasma levels of sphingolipid compounds can predict progression of Alzheimer's disease, a small, early, observational study showed.

Higher ratios of sphingomyelins to ceramide and of dihydrosphingomyelin to dihydroceramides predicted significantly slower clinical progression, Michelle M. Mielke, PhD, of Johns Hopkins University, and colleagues found. Mielke is now at Mayo Clinic in Rochester, Minn.

If validated, sphingolipids could be "a sensitive, and easily accessible, biomarker" for Alzheimer's progression, they reported online in the Journal of Alzheimer's Disease.

That would be a big advantage for families and caregivers and also may help in development of better treatments for Alzheimer's, the group suggested.

Sphingolipids play a critical role in cellular signaling as major components of cell membranes, particularly in the central nervous system, where the proper balance of different species of these fats is essential for normal function of neurons.

The researchers correlated sphingolipid levels measured in 120 patients with probable Alzheimer's disease, predominantly of mild to moderate severity, at a single center. They were followed for progression over 2.3 years on average.

Higher levels of the various sphingolipids didn't predict more severe dementia at baseline, but they did predict rate of decline.

Higher dihydroceramides predicted significantly greater decline on the Mini-Mental State Exam (MMSE, P=0.050 as a continuous variable), while ceramides showed a similar but nonsignificant trend.

On the other hand, plasma sphingomyelins at higher levels predicted less progression on the MMSE (1.15 points difference for highest versus lowest tertile, P=0.006).

The same was true for dihydrosphingomyelin, with the top tertile progressing by 0.84 fewer points than those in the bottom tertile (P=0.046).

But the strongest predictors were ratios of metabolically-linked pairs of these lipids.

Ceramides are both a precursor for sphingomyelins and can be formed by their catabolism, and the same is true for the dihydro form of both.

The ratio of sphingomyelins to ceramides was associated with 1.19-points less decline on the MMSE (P=0.004) and 2.42-points less worsening on the Alzheimer's Disease Assessment Scale-Cognitive Subscale for the top versus bottom tertile (P=0.016).

The ratio of dihydrosphingomyelins to dihydroceramides correlated with a decline of 1.35 fewer points on the MMSE and an increase of 3.18 fewer points on the cognitive scale (both P=0.001).

"Together, these results suggest a shift in the metabolic pathways from ceramide to sphingomyelins over the course of Alzheimer's disease," such that the ratios may be useful predictors of clinical progression in later stages of the disease, Mielke's group suggested in the paper.

Total cholesterol and triglycerides didn't predict progression of Alzheimer's disease.

The researchers also looked at correlation of all the factors with functional decline measured on the Clinical Dementia Rating-Sum of Boxes but found no significant predictors.

They cautioned that the lipid levels measured at baseline weren't taken while fasting, which may have affected levels of some plasma sphingolipids.

But controlling for body mass index, diabetes and cardiovascular disease status, as well as other factors in the individuals in whom they were known didn't appear to impact the results.

The study was funded by a grant from George P. Mitchell and the late Cynthia W. Mitchell and by the National Institute of Aging.

The researchers reported having no conflicts of interest to disclose.



Primary source: Journal of Alzheimer's Disease
Source reference:
Mielke MM, et al "Plasma sphingomyelins are associated with cognitive progression in Alzheimer's disease" J Alzheimers Dis 2011; DOI: 10.3233/JAD-2011-110405.

Study: Apparent cause of accelerated formation of amyloid beta in Alzheimer's disease

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Cell Press

In their study, first author Dr. Markus P. Kummer and colleagues discovered that amyloid beta(AΒ) is a novel nitric oxide(NO) target. They observed nitrated AΒ in Alzheimer's disease(AD) and AD mouse models and found that this modification accelerated the deposition of human AΒ. Importantly, reduction of nitric oxide synthase(NOS2) reduced AΒ deposition and memory deficits in a mouse model of AD. Further, nitrated AΒ induced the formation of amyloid plaques when injected into the brains of mice with genetic mutations associated with AD.

"Taken together, our results identify a novel modification of AΒ, tyrosine nitration, and propose a causative link between the AΒ cascade, activation of NOS2, and the subsequent increase in its reaction product nitric oxide during AD," concludes Dr. Heneka. "We think that nitrated AΒ may serve as marker of early AΒ plaque formation. More importantly, it may be a promising target for an AD therapy, and that application of specific inhibitors of NOS2 may therefore open a new therapeutic avenue in AD."

Could taking vitamin C help those with dementia

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Times of India

Taking vitamin C might help patients with Alzheimer's disease, a study has suggested.

According to Lund University researchers, treatment with vitamin C can dissolve the toxic protein aggregates that build up in the brain in Alzheimer's disease.

The brains of people with Alzheimer's disease contain lumps of so-called amyloid plaques, which consist of misfolded protein aggregates. They cause nerve cell death in the brain and the first nerves to be attacked are the ones in the brain's memory centre.

"When we treated brain tissue from mice suffering from Alzheimer's disease with vitamin C, we could see that the toxic protein aggregates were dissolved. Our results show a previously unknown model for how vitamin C affects the amyloid plaques", said Katrin Mani, reader in Molecular Medicine at Lund University.

"Another interesting finding is that the useful vitamin C does not need to come from fresh fruit. In our experiments, we show that the vitamin C can also be absorbed in larger quantities in the form of dehydroascorbic acid from juice that has been kept overnight in a refrigerator, for example," added Mani.

There is at present no treatment that cures Alzheimer's disease, but the research is aimed at treatments and methods to delay and alleviate the progression of the disease by addressing the symptoms.

"The notion that vitamin C can have a positive effect on Alzheimer's disease is controversial, but our results open up new opportunities for research into Alzheimer's and the possibilities offered by vitamin C", said Mani.

The findings have been published in the Journal of Biological Chemistry .

Cognitive, Not Bio, Markers Predictive of Cognitive Decline

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Doctors Lounge

Cognitive markers are more effective predictors of conversion from mild cognitive impairment to Alzheimer's disease than biomarkers, according to a study published in the September issue of the Archives of General Psychiatry.


(HealthDay News) -- Cognitive markers are more effective predictors of conversion from mild cognitive impairment to Alzheimer's disease than biomarkers, according to a study published in the September issue of the Archives of General Psychiatry.

Jesus J. Gomar, Ph.D., from the Benito Menni Complex Assistencial en Salut Mental in Barcelona, Spain, and colleagues investigated the discriminative utility of different classes of biomarkers and cognitive markers by assessing their ability to predict conversion from mild cognitive impairment to Alzheimer's disease. The Alzheimer's Disease Neuroimaging Initiative (ADNI) database was analyzed to study 116 patients with mild cognitive impairment who converted to Alzheimer's disease, and 204 patients who did not convert within a two-year study period. The predictive utility of 25 variables from all classes of markers, biomarkers, and risk factors were determined by logistic regression models and effect size analyses.

The investigators found that, in logistic regression models, which included variables from all classes of markers, two measures of delayed verbal memory and middle temporal lobe cortical thickness predicted conversion within a two-year period. Effect size analyses revealed that biomarkers had modest change scores for two years, but change in an everyday functional activities measure was substantially larger. Approximately 50 percent of the predictive variance in conversion from mild cognitive impairment to Alzheimer's disease was attributed to decline in scores on the Functional Assessment Questionnaire and Trail Making Test, part B.

"We demonstrated that cognitive markers were consistently significant and generally stronger predictors than biomarkers," the authors write.

Two authors disclosed financial ties with the pharmaceutical industry. One of the study authors receives royalties for use of a cognitive test battery in clinical trials. The ADNI database used in the study was funded by the pharmaceutical industry.

Osteoarthritis accelerates and exacerbates Alzheimer's disease pathology in mice

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Journal of Neuroinflammation

tephanos Kyrkanides, Ross H Tallents, Jen-nie H Miller, Mallory E Olschowka, Renee Johnson, Meixiang Yang, John A Olschowka, Sabine M Brouxhon and M. KERRY O'Banion

Abstract (provisional)
Background
The purpose of this study was to investigate whether localized peripheral inflammation, such as osteoarthritis, contributes to neuroinflammation and neurodegenerative disease in vivo.

Method
S We employed the inducible Col1-IL1betaXAT mouse model of osteoarthritis, in which induction of osteoarthritis in the knees and temporomandibular joints resulted in astrocyte and microglial activation in the brain, accompanied by upregulation of inflammation-related gene expression. The biological significance of the link between peripheral and brain inflammation was explored in the APP/PS1 mouse model of Alzheimer's disease (AD) whereby osteoarthritis resulted in neuroinflammation as well as exacerbation and acceleration of AD pathology.

Results
Induction of osteoarthritis exacerbated and accelerated the development of neuroinflammation, as assessed by glial cell activation and quantification of inflammation-related mRNAs, as well as Abeta pathology, assessed by the number and size of amyloid plaques, in the APP/PS1; Col1-IL1betaXAT compound transgenic mouse.

Conclusion
This work supports a model by which peripheral inflammation triggers the development of neuroinflammation and subsequently the induction of AD pathology. Better understanding of the link between peripheral localized inflammation, whether in the form of osteoarthritis, atherosclerosis or other conditions, and brain inflammation, may prove critical to our understanding of the pathophysiology of disorders such as Alzheimer's, Parkinson's and other neurodegenerative diseases.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.

Antiviral drugs could slow Alzheimer's disease

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University of Manchester

Antiviral drugs used to target the herpes virus could be effective at slowing the progression of Alzheimer’s disease (AD), a new study shows.

The University of Manchester scientists have previously shown that the herpes simplex virus type 1 (HSV1) is a risk factor for Alzheimer’s when it is present in the brains of people who have a specific genetic risk to the disease.

AD is an incurable neurodegenerative condition affecting about 18 million people worldwide. The causes of the disease or of the abnormal protein structures seen in AD brains – amyloid plaques and neurofibrillary tangles – are completely unknown.

The Manchester team has established that the herpes virus causes accumulation of two key AD proteins – β-amyloid (Aβ) and abnormally phosphorylated tau (P-tau) – known to be the main components of plaques and tangles respectively. Both proteins are thought by many scientists to be involved in the development of the disease.

“We have found that the viral DNA in AD brains is very specifically located within amyloid plaques,” said Professor Ruth Itzhaki, who led the team in the University’s Faculty of Life Sciences. “This, together with the production of amyloid that the virus induces, suggests that HSV1 is a cause of toxic amyloid products and of plaques.

“Our results suggest that HSV1, together with the host genetic factor, is a major risk for AD, and that antiviral agents might be used for treating patients to slow disease progression.”

Currently available antiviral agents act by targeting replication of HSV1 DNA, and so the researchers considered that they might be successful in treating AD only if the accumulation of β-amyloid and P-tau accumulation caused by the virus occurs at or after the stage at which viral DNA replication occurs.

“If these proteins are produced independently of HSV1 replication, antivirals might not be effective,” said Professor Itzhaki. “We investigated this and found that treatment of HSV1-infected cells with acyclovir, the most commonly used antiviral agent, and also with two other antivirals, did indeed decrease the accumulation of β-amyloid and P-tau, as well as decreasing HSV1 replication as we would expect.

“This is the first study investigating antiviral effects on AD-like changes and we conclude that since antiviral agents reduce greatly β-amyloid and P-tau levels in HSV1-infected cells, they would be suitable for treating Alzheimer’s disease. The great advantage over current AD therapies is that acyclovir would target only the virus, not the host cell or normal uninfected cells. Further, these agents are very safe and are relatively inexpensive.

“Also, by targeting a cause of Alzheimer’s disease, other viral damage, besides β-amyloid and P-tau, which might be involved in the disease’s pathogenesis, would also be inhibited.

“The next stage of our research – subject to funding – will focus on finding the most suitable antiviral agent – or combination of two agents that operate via different mechanisms – for use as treatment. We then need to investigate the way in which the virus and the genetic risk factor interact to cause the disease, as that might lead to further novel treatments.

“Eventually, we hope to begin clinical trials in humans but this is still some way off yet and again will require new funding.”

The study, carried out with Dr Matthew Wozniak and other colleagues in the Faculty of Life Sciences, is published in the Public Library of Science (PLoS) One journal

Gantenerumab: New Alzheimer's drug shows early promise

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USA Today

The new study, which appears online Oct. 10 in the Archives of Neurology, is among the first to show the effects of an anti-amyloid drug in humans with Alzheimer's disease, but experts caution that while promising, more research is needed before this drug can be deemed safe or effective.
And, in what may turn out to be an equally important caveat, experts also say that it's by no means certain that reducing levels of amyloid plaque would stave off memory loss and the other mental declines associated with the disease because the role of the plaque in Alzheimer's isn't fully understood.
Alzheimer's disease is the most common form of dementia. Symptoms including serious memory loss, confusion and mood changes develop gradually and worsen with time. Recently, many strides have been made in diagnosing Alzheimer's disease earlier, but doctors have been stymied by a lack of effective treatments to stop or slow the course of the disease.
It's long been known that a protein fragment called beta-amyloid builds up in the spaces between nerve cells in the brains of people with Alzheimer's disease. The new drug, gantenerumab, targets these amyloid proteins by priming the body's immune system to recognize them as invaders.
Of 16 people with mild-to-moderate Alzheimer's disease, those who received two to seven infusions of the experimental drug every four weeks showed marked reductions in the amount of plaque in their brains via imaging tests that were conducted several months after their treatments.
By contrast, amyloid load increased among people who were randomized to receive the placebo. The new drug was given at either 60 or 200 milligrams (mg) doses. The higher dose yielded greater reductions in amyloid levels, the study showed. People who were given the 60 mg doses saw a nearly 16 percent reduction in the amount of amyloid, and those given the 200 mg doses saw a 36 percent reduction. The new study was conducted and funded by the drug's manufacturer, F. Hoffmann-LaRoche Ltd., in Basel, Switzerland.
The big question is whether or not reducing amyloid levels has any effect on the symptoms or progression of Alzheimer's disease, said Dr. Patrick Lyden, chief of neurology at Cedars-Sinai Medical Center in Los Angeles. "There is a growing concern that amyloid is a guilty bystander, but not the actual culprit in the brains of people with Alzheimer's disease, and taking away the bystander may not help the patient," he said.
There are approximately one dozen therapies, including vaccines, for Alzheimer's disease that are currently in the pipeline, Lyden noted. "They are all extremely exciting and promising in animals," he said. "This is the first one to show a preliminary result in people, but we have a huge way to go to make sure it is safe and improves symptoms."
Many in the Alzheimer's research community are awaiting these drugs with bated breath, but "none are ready for prime time," he said.
The leading theory of Alzheimer's disease is that an imbalance in the production or clearance of the amyloid plaque in the brain initiates a cascade of events that lead to dementia, explained Dr. Neelum Aggarwal, an associate professor of neurological sciences at Rush Alzheimer's Disease Research Center at Rush University Medical Center in Chicago.
"Accumulation of the plaques cause a variety of cellular responses: inflammation, neuronal death, and thus any potential treatment that can alter these processes would be beneficial," she said. The hope is that gantenerumab or other drugs like it will not only prevent amyloid from accumulating in the brain, but also slow down the cognitive impairment that occurs in people with Alzheimer's disease, she added.
That said, these experimental drugs carry the potential for serious side effects, including causing the immune system to go haywire. "The main issue that remains for this type of drug development is managing the immune response," Aggarwal said. Other side effects include a potentially fatal fluid build-up in certain areas of the brain. "This is problematic in that use of these treatments may carry a very high risk for neurologic complications, thus necessitating heightened monitoring, and diminishing its applicability as a treatment for a larger patient population such as the Alzheimer's disease population," she said.
If any of these drugs make it through the pipeline, it also needs to be determined who will get them, including whether the drugs will be given to prevent Alzheimer's in patients at high-risk of the disease or to treat it once it's started.
The need for a drug to delay the onset or slow progression of Alzheimer's disease can't be underestimated, Aggrawal said. In the United States alone, there are 5.4 million people with Alzheimer's disease, and the numbers are expected to increase to 13 million by 2050, when approximately three of every five people over the age of 85 will have Alzheimer's disease, she said.

Afib increases risk of dementia (part 2)

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Group Health

Dr. Dublin's study, which ran from 1994 to 2008, followed 3,045 people. The researchers relied on Group Health's advanced electronic data systems to determine whether participants had atrial fibrillation. The cognitive function of all study participants was evaluated every two years with tests and interviews as part of ACT. Patients whose ACT tests indicated possible dementia had additional tests including physical, neurological, and psychological exams, and many also had brain scans. A panel of experts determined the correct diagnosis for patients with cognitive problems.

Atrial fibrillation affects 3 million Americans. Dr. Dublin says that some ways it might increase dementia risk are:


•weakening the heart's pumping ability, leading to less oxygen going to the brain;


•increasing the chance of tiny blood clots going to the brain, causing small, clinically undetected strokes;


•a combination of these plus other factors that contribute to dementia such as inflammation.

Dr. Dublin said an important next step is studying whether any treatments for atrial fibrillation reduce the risk of developing dementia. The researchers also hope their results reach primary care providers, who are often the main doctors caring for people with atrial fibrillation, dementia, or both.

"Right now, we think we are protecting our patients' brains as long as they don't have a stroke, but tiny insults over time can add up," said Dr. Dublin, who is a primary care physician at Group Health. "This paper is a wakeup call, telling us that we need to learn more about how to protect brain function, while continuing to give patients with atrial fibrillation the best possible care."


Source: Group Health Research Institute

Lack of key protein linked to Alzheimer's

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Catholic Online (www.catholic.org)

Alzheimer's patients have lower levels of ubiquilin-1 in their brains, a study finds.

Scientists have found that Alzheimer's disease patients have reduced levels of a critical protein. The protein, ubiquilin-1, is found in nearly all tissues and is used by the body to mark damaged or unnecessary proteins for destruction. Reduced ubiquilin-1 means that other damaged proteins persist in the brain and contribute to the formation of cells that are associated with Alzheimer's.

LOS ANGELES, CA (Catholic Online) - The study observed for the first time, much lower than normal ubiquilin-1 levels in the entire set of 20 brains that were examined.


The lower levels means that other proteins, amyloid precursor proteins, which have been linked to Alzheimer's, are able to persist in the brains of patients instead of being properly regulated.

The information helps scientists to better understand the cause of Alzheimer's disease and may suggest new avenues for research and treatment.

Alzheimer's disease is a specific form of dementia that worsens over time and notoriously affects memory, thought, and behavior. It is also the most common form of dementia. Most patients are diagnosed as they grow older and find problems with language, decision-making and judgment.
Many simply attribute these symptoms to aging, but experts stress that such symptoms are not a normal part of the process. The rate of diagnosis of Alzheimer's is increasing, so scientists are anxious to learn more about the disease.

The link between ubiquilin-1 and Alzheimer's is new information for researchers.

The study was conducted by researchers at the University of Texas Medical branch at Galveston and published in the journal of Biological Chemistry.

Vegetarianism: Does it lower the risk of developing Alzheimer's disease

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Celestial Healing
There are many mental illnesses and disease that are related to the consumption of meat. Take Alzheimer for example. According to the American Alzheimer Association, between 6 and 8% of the population over 60 has Alzheimer's disease, and the rate has been increasing steadily. Several scientific literatures have affirmed that Alzheimer correlates with the consumption of meat and dairy. A review of studies published in Preventive Magazine two years ago sheds important light on a central risk factor in Alzheimers -- high levels of a blood substance called homocysteine.

Homocysteine is an amino acid. Amino acids are the building blocks of proteins. The only source of homocysteine for use in our bodies is that which the liver forms after the ingestion of another amino acid. Methionine is found in protein foods. Animal protein contains two to three times the amount of methionine as does plant protein. Homocysteine levels can be lowered very effectively by avoiding meat and dairy consumption. In fact, a recent study performed at Harvard Medical School showed that subjects who adopted a vegan diet had their homocysteine levels drop between 13% and 20% in just one week.

A 1993 study found that subjects, who ate meat, including poultry and fish, were more than twice as likely to become demented as their vegetarian counterparts. [Neuroepidemiology, 12:28-36, 1993]

Depression, anxiety, and schizophrenia can be connected to meat consumption. The amount of tryptophan (An amino acid necessary for normal growth in infants and for nitrogen balance in adults.) in the foods that are eaten has only a small influence upon the amount of tryptophan that enters the brain. The most important factor determining the total amount of tryptophan that does enter the brain is the concentration of other large-molecule amino acids concurrently present in the blood. Large-molecule amino acids, among them tryptophan, compete with each other to enter "gates" between the circulating blood stream and the relatively confined brain fluids. A high-protein meal (full of meats, dairy foods, and eggs) provides many other amino acids that compete with tryptophan for entry into the brain; the end result is less tryptophan passing into the brain and a decrease in the synthesis of serotonin (a phenolic amine neurotransmitter that is a powerful vasoconstrictor and is found especially in the brain, blood serum, and gastric mucosa of mammals). Conversely, a low-protein, carbohydrate-rich diet (full of starches, vegetables, and fruits) results in the highest levels of serotonin in the brain, because fewer large-molecule amino acids are competing with tryptophan to enter the brain. For most this means less hyperactivity, anxiety, depression, and insomnia-provided they eat a vegetarian diet.

In some people anxiety, depression, and fatigue are caused by allergic reactions to foods. The most common causes of food allergies are dairy products, followed by eggs. These reactions are often subtle and difficult to recognize until the offending food has been eliminated, either by accident or by intention, and then, later, when the body is challenged with the suspect food, a recognizably adverse reaction occurs.
A serious psychological disease caused by foods in some people is schizophrenia. In hospital-based studies, some patients have been identified who react with dramatic behavioral changes to milk products and animal products. Some people with schizophrenia have actually been cured of their disease by changing their diet, (eliminating meat and dairy) and including more natural foods like fruits, vegetables, and whole grains.

I recall an Herbalist saying, “Tell me what a person eats and I shall tell you what sort of person he or she is and what type of character and behavior they hold.” No doubt, there are other factors also that determine a person's personality and behavior, but food also has a great effect on one's mind. Experience tells me that one's diet is closely connected with one's thoughts and conduct. So anyone who wishes to purify their thoughts and to elevate their character must partake in a vegetarian diet. If we eat live food, we will be helping our mind and emotions to remain in a state of peace and self-control. Pure food enables one to feel light and fresh and the mind opens out to the pure life and beauty of the world. The mind becomes undisciplined, wild, agitated or fickle when the diet is exciting, intoxicating or inebriating (intoxicant), the character constantly declines and the result is tension, depression, sorrow and disquiet.
Finally, the subject of meat consumption linked to brain disease has firmly come to the front of my research with the issue of “mad cow” disease. While scientist debate whether it is due to a mysterious prion or a virus, health-conscious advocates and nutritionist are using the scandal to point out numerous disadvantages of the typical animal-based Western diet as well as the corrupt manner in which the meat-producing industry is manufacturing its products. Specifically, it is imagined that ‘mad cow’ disease results from contaminated animal feed which has been fortified with ground up intestines, brains, spinal cords, bones, and other parts from cows, chickens and sheep – in effect turning herbivores into cannibalistic carnivores. Four with “mad cow” disease (also known as bovine spongiform encephalopathy – BSE), which is being linked to a correspondingly similar brain disorder in humans known as Creutzfeldt-Jakob disease, the symptoms are attributed to microscopic holes in the brain. So how did cows get mad cow disease, known by its medical name as "bovine spongiform encephalopathy," or "BSE"? For several decades, cattle feed had included a cheap protein supplement made from the carcasses of other animals, including sheep and cows. BSE probably arose when sheep infected with scrapie or cows with BSE were turned into feed. The feed then infected other cows that ate it, and when those animals died, they were fed back to more cows, creating a rapidly escalating epidemic. It was a kind of cattle cannibalism. And for two years after BSE was known, infected cattle were still allowed into England's food supply, raising fears that people might get BSE. To assess that risk, the British government called upon the scientific community. The scientific community noticed several behaviors, which has been related to the effects of people who ate beef from cows with “mad cows” disease. Some of those behaviors were hallucination, disorderly conduct, hyperactivity rudeness, agitation, and neglectfulness. With all this information, I see why Oprah stated to millions of Americans that she will never eat another hamburger again.

A vegetarian diet produces higher levels of behavior than a diet containing meat when all types of caloric intake are equal. Vegetarians were shown in one university study to score higher on examinations than meat eaters. Vegetarians also showed less frustration and lower levels of irascibility than meat eaters. (Bulletin of the Psychosomatic Society 10:35-36, July 1977)

Vegetarianism is a cause that addresses several key major social issues: ethics, the environment, and health – mental, spiritual and emotional as well as physical. As Albert Einstein wrote: "Nothing will benefit human health or increase the chances for survival of life on earth as the evolution to a vegetarian diet. It is my view that the vegetarian manner of living, by its purely physical effect on the human temperament, would most beneficially influence the lot of mankind."

The correlation between people who eat meat and violence

Managing mealtime tasks: told by persons with dementia

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Journal of Clinical Nursing
     Linda Johansson,, Lennart Christensson,, Birgitta Sidenvall

Aim.  To capture the self-description of managing mealtime tasks by persons with dementia.


Background.  There are several factors that negatively affect food intake in persons with dementia that may increase the risk of developing malnutrition. Difficulties in managing daily activities increase gradually and mealtime tasks like food shopping, cooking and eating often become troublesome. Still, little is known about how persons with dementia themselves experience this issue.

Design.  A qualitative study with an ethnographic approach.

Method.  Ten women and five men aged 69–86 with dementia were interviewed. Interviews were carried out in the informants’ own homes and a thematic analysis was performed.

Results.  The informants described that they wanted to be independent and that the memory loss was not affecting them to a great extent. Old habits and routines, as well as newly developed strategies, helped them manage mealtime tasks despite the disease. Informants were satisfied with their current situation, even though it sometimes meant that they had changed their way of managing mealtime tasks, for instance receiving meals-on-wheels.

Conclusions.  Persons with dementia seem to be able to manage mealtime tasks and these activities were based on old habits and routines. Independence was highly valued and managing mealtime tasks seems to be one way to appear independent.

Relevance to clinical practice.  It is important for caregivers to understand that persons with dementia might not express difficulties in managing mealtime tasks for fear of losing their independence. It is, therefore, important to create a trustful relationship even before problems arise to be able to support the persons when necessary

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Can veggie juice lower risk of Alzheimer's?

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Seattle Times
Health

By Joe Graedon and Teresa Graedon, Ph.D.

Syndicated columnists

Q: We have heard that people who drink fruit and vegetable juice have a significantly lower risk of Alzheimer's disease. Are veggie juices as good as fruit juices? What about wine?



A: In particular, a diet high in nonstarchy vegetables, fruits, nuts and berries seems to be somewhat protective (Journal of Nutrition, Sept. 1, 2009).

Tomatoes are rich in antioxidant compounds, and so are berries, tea, cocoa, pomegranates and wine.

New research suggests that moderate social drinking, particularly wine, also may reduce the likelihood of developing cognitive impairment or Alzheimer's disease (Neuropsychiatric Disease and Treatment online, Aug. 11, 2011).

Common Signs of Aging Traced to Tiny Brain Blockages

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Here is information on being the best caregiver you can be

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

By John Gever, Senior Editor, MedPage Today


Blocked blood vessels in the brain, often too small to be seen with current medical imaging technologies, may explain some of the common signs of aging such as diminished walking ability and hand tremors, researchers said.


Brain autopsy findings showed microscopic infarcts in 57 individuals out of 418 examined, the presence of which was significantly associated with gait abnormalities similar to those seen in Parkinson's disease, reported Aron S. Buchman, MD, of Rush University in Chicago, and colleagues.
Signs of arteriolosclerosis invisible with standard imaging were also significantly associated witparkinsonian gait, as were macroscopic infarcts that would be picked up with CT or MRI scans, the researchers indicated online in Stroke: Journal of the American Heart Association.

"We are not aware of previous studies demonstrating independent roles for microinfarcts and the severity of arteriolosclerosis in the development of parkinsonian gait," Buchman and colleagues wrote.

"Given that microinfarcts and severity of arteriolosclerosis are not discernible during life, these pathologies likely represent unrecognized common etiologies for parkinsonian gait in older persons and support clinical-imaging studies that suggest subclinical cerebrovascular disease abnormalities are associated with gait dysfunction in older persons."

The researchers added that more aggressive prevention and treatment strategies for vascular risk factors "might decrease the burden of mild age-related parkinsonian signs."

Such symptoms, which include rigidity and sluggish movements as well as tremors and gait problems -- are common in the elderly, affecting up to half of noninstitutionalized people 85 and older, according to Buchman and colleagues.

They pointed out that, although these symptoms are shared with Parkinson's disease (hence the "parkinsonian" rubric), most individuals showing them do not have the disease, as Lewy bodies and nigral degeneration, its neurological hallmarks, are absent.

On the other hand, cerebrovascular defects are common in older people and are known to produce parkinsonian symptoms, the researchers indicated.

To explore the connection, they reviewed autopsy findings from 418 deceased participants in the Rush Religous Orders Study, a prospective study that began in 1993 involving some 1,100 older nuns, brothers, and priests who underwent annual physical and psychological exams.

Those included in the current analysis had no signs of dementia at enrollment. At death, they averaged 88.5 years old and about 60% were women. Mean scores on the Mini-Mental State Examination at their last visit were 22.7, indicating significant cognitive impairment.

Microscopic infarcts were present without other abnormalities in 7.9%, and accompanied by arteriolosclerosis not detected in brain scans in 5.7%.

These small arteriolosclerosis lesions were seen alone in 14.8% of the autopsied brains, and relatively large infarcts were found in 36%.

At their yearly evaluations, study enrollees were assessed for Parkinsonian symptoms using a 26-item instrument derived from the Unified Parkinson's Disease Rating Scale. Each of the four major symptoms -- abnormal gait, bradykinesia, tremor, and rigidity -- were evaluated on 100-point scales. The average of these scores served as a global summary.

At death, the 418 individuals had had the following mean scores at their last evaluation:

•Gait: 41.5

•Rigidity: 11.7

•Bradykinesia: 21.4

•Tremor: 5.2

•Global summary: 18.6

Macroscopic infarcts were the most powerful predictors of these symptoms. Their presence was associated with increases of 0.359 points in the global score (P=0.013), 0.552 points on the gait scale (P=0.009), and 0.853 points on the rigidity scale (P<0.001).

Infarcts too small to be seen on imaging were associated with a 0.424-point increase in gait scores (P=0.047).

Arteriolosclerosis was a much smaller factor, although its association with gait scores (0.191 points, P<0.001) was statistically significant.

The location of infarcts within the brain appeared partly to determine their impact on parkinsonian signs. Multiple subcortical microinfarcts were more strongly associated with impaired gait (0.888 points, P=0.004) than cortical microinfarcts, the researchers found.

Similarly, subcortical macroscopic infarcts were also apparently more damaging than those within the cortex.

"Together these data suggest that a substantial portion of older people have brain tissue damage and small vessel disease that are unlikely to be detected before death and suggest that cerebrovascular disease may be an even larger public health challenge than currently estimated," Buchman and colleagues wrote.

They cited some limitations to the study. Microinfarcts and small arteriolosclerosis lesions were counted only in certain brain regions, potentially underestimating the association with parkinsonian signs. Study participants did not undergo brain imaging, so it is possible that signs of the cerebrovascular defects could be discernible in some cases.

Finally, the cross-sectional study design precludes firm conclusions about the direction of causality.

"It is possible that the cerebrovascular pathologies do not play a causal role in the development of parkinsonian signs, but rather both cerebrovascular pathologies and parkinsonian signs might be caused by a third factor," Buchman and colleagues noted.

The analysis was supported by the National Institutes of Health and the Illinois Department of Public Health.

Study authors declared they had no relevant financial interests.

Primary source: Stroke

Source reference:

Buchman A, et al "Cerebrovascular disease pathology and parkinsonian signs in old age" Stroke 2011; DOI: 10.1161/STROKEAHA.111.623462.

Is Alzheimer|s preventable?

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

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

healthnewsreview.com


A study led by a San Francisco mental-health researcher found that more than half of all Alzheimer’s disease cases are caused by risk factors that could potentially be controlled, according to a UCSF news release.
Dr. Deborah Barnes, a researcher at the San Francisco VA Medical Center, analyzed data from studies involving hundreds of thousands of participants worldwide, and concluded that the biggest modifiable risk factors for contracting the disease are low education, smoking, physical inactivity, depression, mid-life hypertension, diabetes and mid-life obesity. Combined, those factors are associated with up to 54 percent of Alzheimer’s cases in the United States, Barnes concluded.

Barnes presented her findings at the 2011 Alzheimer’s Association International Conference in Paris on July 20.