Cinnamon beats Alzheimers

The miracle spice cinnamon is the scented bark of a tropical evergreen tree, native to India and Sri Lanka. Cinnamon comes from an evergreen tree in Southeast Asia and is cultivated widely in Vietnam, China, Burma, and Laos for its bark and the oil processed from the bark. Once upon a time in ancient Rome, cinnamon was worth more than silver.

Cinnamon is harvested from the inner bark of the tree branches after scraping off the corky outer layer and then drying the bark. As it dries, the bark curls up into quills which are then cut into sticks to be ground into the spice form. Full of calcium and fiber, cinnamon is one of the oldest known spices, it is mentioned in the Bible and was used in ancient Egypt as medicine, beverage flavoring and an embalming agent.

According to traditional Chinese medicine, cinnamon helps improve the body's "fire."

Cinnamon - Not just a spice!

Professor Daniel Fung, an expert in food science at Kansas State University, says cinnamon contains a compound that has the ability to kill bacteria. "If cinnamon can knock out E.coli 0157:H7, one of the most virulent food-borne microorganisms that exists today, it will certainly have antimicrobial effects on other common food-borne bacteria such as Salmonella and Campylobacter."

Now researchers from Tel Aviv University found that extracts from cinnamon bark inhibit the toxic amyloid polypeptide oligomers and fibrils that have been found in Alzheimer's Disease (AD) brain plaque formations. In animal models of Alzheimer's, cinnamon reduced s-amyloid plaques associated with the pathology of AD. Reduction of these proteins can improve mental cognition. In one model, cinnamon extract resolved AD associate reduced longevity, helped recover locomotion defects and completely abolished tetrameric species of plaque in the brain.

Other benefits of cinnamon are: anti-microbial actions, blood sugar balancing, improving colon health, boosting brain function. Cinnamaldehyde in cinnamon has been well researched for its effects on blood platelets which help the blood clot to stop bleeding. Platelets can also cause strokes if they clump together too much. Cinnamon has been shown to help prevent this deadly clumping. Cinnamon will stop vomiting and relieve feelings of nausea. Cinnamon also helps slow tumor growth while inhibiting inflammatory markers connected to cellular proliferation.

In a recent study, people reduced their blood sugar levels by as much as 29 percent with cinnamon in just 40 days. That's with NO drugs, NO diet changes - just plain old cinnamon!

Study volunteers who took a cinnamon extract showed significant decreases in fasting blood glucose and increases in lean muscle mass compared with the placebo group. Pre and post study analysis of the extract group revealed a statistically significant decrease in body fat and blood pressure.

Research found that cinnamon can have favorable effects on brain function. Participants in a study chewed cinnamon gum or even just smelled the sweet spice. Cognitive tests revealed that subjects who used cinnamon had better memory functions and could process information more quickly.

What kind and how much

Which is best: Ceylon cinnamon, Saigon cinnamon, cinnamomum zeylanicum or regular grocery store variety cinnamon? Interestingly, the grocery store variety known as cinnamomum cassia works the best in most research studies and clinical trials.

Drink cinnamon in tea or sprinkle a little cinnamon on your toast, cereal, oatmeal, or sliced apples. It not only tastes good, it lowers your blood sugar!

Taking two 500 mg capsules of cinnamon a day will help good cholesterol levels and taking two capsules with each meal can make a big difference in blood sugar and insulin levels for diabetics.

Alzheimer’s Aggression

Alzheimer’s aggression most often flares up during the later stages of Alzheimer’s disease. The person may become easily agitated, angry, and abusive - often for no apparent reason. The person may curse, hurl insults, and scream. Though verbal assaults are more common than physical assaults, a person with Alzheimer’s disease may throw things or resist care by pushing and hitting.

Why Does Alzheimer’s Aggression Occur? - No one knows for sure why Alzheimer’s patients become aggressive. Aggression may be a symptom of Alzheimer’s disease itself. It may also be a reaction to actions of others or to the environment around the person with Alzheimer’s disease.

Understand the Triggers of Alzheimer’s Aggression - Alzheimer’s aggression can flare up without warning. There may not be an obvious cause. However, often there are triggers that caregivers can look for. By knowing the triggers, you may be able to lower the frustration level of the person with Alzheimer’s disease. This can reduce the number of aggressive outbursts. Here are some common triggers of Alzheimer’s aggression:

Discomfort caused by lack of sleep, side effects from medication, or pain that the person is not able to describe
The surrounding environment, such as loud noises, busyness around the person, or clutter
Confusion caused by being asked too many questions at once, trying to understand complex instructions, or feeling the stress of caregivers

Tips to Reduce Alzheimer’s Aggression - Once you understand the triggers for Alzheimer’s aggression, you can take steps to prevent it. Try these suggestions:

• Anticipate situations in which the person with Alzheimer’s may be uncomfortable, overstimulated, or confused.
• Avoid asking too many questions at once, giving overly complicated instructions, and speaking negatively. That way, you are less likely to confuse and agitate the person you are caring for.
• Limit the amount of loud noises, frenetic movement, and clutter.
• Don’t contradict. Those with Alzheimer’s disease see a different reality than you do. Rather than challenge that reality, sit and listen. Ask questions about it.
• Focus on the past. Alzheimer’s affects short-term memory. It’s often easier and less stressful for someone with Alzheimer’s disease to recall and talk about distant memories than it is for them to remember what they watched on TV the night before.
• Use memory cues. As the disease progresses, remembering to do and how to do everyday tasks like brushing your teeth or getting dressed becomes more difficult. Reminder notes placed in key locations can help prevent frustration.

Caregiver Stress and Alzheimer’s Aggression - It’s not easy to care for a person with Alzheimer’s disease. The burden of round-the-clock care takes an emotional toll. Add to it the frustration and sadness of watching a loved one deteriorate. It’s not surprising that caregivers may feel isolated and depressed. Left unrelieved, these feelings can lead to abusive behavior toward the person with Alzheimer’s disease, from insults to physical injury.

If you are a caregiver, do yourself and the person you care for a favor. Seek help for yourself if you notice signs of depression, anxiety, sleeplessness, exhaustion, or irritability. Taking care of yourself will help you take better care of others.

Mechanism of Alzheimer's Therapy

Gammagard™ IVIg is a therapy that has been investigated for treatment of Alzheimer's. Despite small clinical studies that have reported efficacy of the approach, the mechanism of action is poorly understood.
The UK researchers set out to investigate the mechanism by which the treatment may act in the brain to lower amyloid deposition (amyloid deposits being a key pathology in Alzheimer's).

To conduct their investigation, researchers introduced IVIg directly into the brains of mice which carry a human gene causing them to develop amyloid plaques. They found that IVIg lowers amyloid deposits in the brains of the mice over the course of seven days. Their data suggest that the modulation of inflammation in the brain by IVIg is a key event that leads to the reduction in amyloid deposition.

The scientists hypothesize that the IVIg acts as an immune modulator, and this immune modulation is responsible for the reductions in amyloid pathology.

The data suggests that modulating the immune response in the brain may help ameliorate the Alzheimer's pathology. Researchers are currently investigating other ways to produce the same modulation of the immune response because the access of IVIg to the brain when administered peripherally is very limited.

Promising Alzheimer's 'Drug' Halts Memory Loss

A new class of experimental drug-like small molecules is showing great promise in targeting a brain enzyme to prevent early memory loss in Alzheimer's disease, according to Northwestern Medicine® research.
Developed in the laboratory of D. Martin Watterson, the molecules halted memory loss and fixed damaged communication among brain cells in a mouse model of Alzheimer's.
"This is the starting point for the development of a new class of drugs," said Watterson, lead author of a paper on the study and the John G. Searle Professor of Molecular Biology and Biochemistry at Northwestern University Feinberg School of Medicine. "It's possible someday this class of drugs could be given early on to people to arrest certain aspects of Alzheimer's."
Changes in the brain start to occur ten to 15 years before serious memory problems become apparent in Alzheimer's.
"This class of drugs could be beneficial when the nerve cells are just beginning to become impaired," said Linda Van Eldik, a senior author of the paper and director of the University of Kentucky Sanders-Brown Center on Aging.

The novel drug-like molecule, called MW108, reduces the activity of an enzyme that is over-activated during Alzheimer's and is considered a contributor to brain inflammation and impaired neuron function. Strong communication between neurons in the brain is an essential process for memory formation.
"I'm not aware of any other drug that has this effect on the central nervous system," Watterson said.
"These exciting results provide new hope for developing drugs against an important molecular target in the brain," said Roderick Corriveau, program director at the National Institute of Neurological Disorders and Stroke, which helped support the research. "They also provide a promising strategy for identifying small molecule drugs designed to treat Alzheimer's disease and other neurological disorders."
Watterson and his collaborators have a new National Institutes of Health (NIH) award to further refine the compound so it is metabolically stable and safe for use in humans and develop it to the point of starting a phase 1 clinical trial.
In a key memory experiment in the study, mice brains were injected with beta-amyloid, whose increase is one hallmark of Alzheimer's in humans. One group of mice was then administered MW108 and another group was administered a placebo.
Next, each group of mice was taught environmental cues to learn how to swim through a water maze to find a resting platform. Then the mice were placed in a different arm of the maze and tested on their ability to remember the location of the platform based on the environmental cues.
The mice administered MW108 found the resting platform in the water maze as quickly as a control group of mice. The mice given the placebo made more mistakes and took longer to find the platform. They also had difficulty learning the location of the resting platform during the teaching phase.
"The results show the compound prevented the cognitive impairment," Van Eldik said..

Steroids might slow Alzheimer’s disease progression

Anti-inflammatory drugs for treatment and prevention of Alzheimer’s disease have to date proved disappointing, including a large study of low-dose prednisone, but higher dose of anabolic steroids significantly reduced amyloid secretion in a small series of nondemented patients. In addition, there is a case report of a patient with amyloid angiopathy who had complete remission from two doses of dexamethasone, and very high dose steroids are already used for systemic amyloidosis. This paper presents the hypothesis that pulse-dosed intrathecal methylprednisolone or dexamethasone will produce detectable slowing of Alzheimer’s progression, additive to that obtained with cholinesterase inhibitors and memantine. 

A protocol based on treatment regimens for multiple sclerosis and central nervous system lupus is outlined, to serve as a basis for formulating clinical trials. Ultimately intrathecal corticosteroids might become part of a multi-agent regimen for Alzheimer’s disease and also have application for other neurodegenerative disorders.

Gene May Protect Against Alzheimer’s Disease

New research has identified a genetic mutation that may protect against both Alzheimer's disease and age-related declines in thinking and memory. And future drug treatments already in the pipeline may help prevent against both.

Amyloid protein plaques in the brain are seen in people with Alzheimer's disease. A gene for amyloid-beta precursor protein (APP) plays a key role in the formation of these plaques. Researchers from Reykjavik, Iceland, found that a mutation in this gene may help protect against Alzheimer's disease and age-related mental decline.

This mutation is rare, but, when present, confers about a 40% reduction in amyloid plaque-forming proteins. What's more, study participants between 80 to 100 years old without Alzheimer's disease who carry this mutation have better mental function than those without the mutation, the study shows.

Alzheimer's disease affects memory and thinking. Symptoms usually develop slowly and worsen with time. One in eight older Americans has Alzheimer's disease, making it the most common type of dementia in the U.S., according to the Alzheimer's Association.

New Chemical Approach to Treat Alzheimer's

Scientists developed a new chemical approach to help harness the natural ability of complex sugars to treat Alzheimer's disease.

The team used a new chemical method to produce a library of sugars, called heparan sulphates, which are known to control the formation of the proteins in the brain that cause memory loss.

Heparan sulphates are found in nearly every cell of the body, and are similar to the natural blood-thinning drug, heparin. Now scientists have discovered how to produce them chemically in the lab, and found that some of these sugars can inhibit an enzyme that creates small proteins in the brain.

These proteins, called amyloid, disrupt the normal function of cells leading to the progressive memory loss that is characteristic of Alzheimer's disease.

There are more than 800,000 people in the UK, and 50,000 in New Zealand living with dementia. Over half of these have Alzheimer's disease, the most common cause of dementia. The cost of these diseases to the UK economy stands at £23 billion, more than the cost of cancer and heart disease combined. Current treatments for dementia can help with symptoms, but there are no drugs available that can slow or stop the underlying disease.