Alzheimer disease

The benefits of pool

2011-11-28T04:53:00.000-08:00

The benefits of pool

Billiards ... It is difficult to find another such game anywhere so to diversify would appear physical and mental capacities player.

In a game of billiards people constantly moving. During one party player can wind up in total around the table, two - three miles, and even more. In fact, playing in the pool - this is long (from one hour up to ...) useful walk without leaving the premises.

Known is the fact that even in pre-revolutionary times many inactive and apathetic doctors advised patients to play billiards, snooker for them was a great way to support reasonable physical condition.

On top, the game of billiards improves eye, sharpens the player coordinate his movements.

In humans who plays billiards, eyes are rests and restores his sight. The game of billiards triggers active ocular muscles, this phenomenon has some similarity with movement exercises for the eyes, which favorably affect the visual acuity. All of that while playing your eyes have to constantly keep track of the same balls at different distances, among other things, the position of the balls are constantly changing ... Note that most of the professional pool players, even in middle age have excellent vision.

Billiards helps to become more balanced, it teaches players to be patient and cold reason, in other words helping people to acquire a number of qualities he needed in everyday life.

Billiards produces in human the will to win, but at the same time learn to accept defeat with dignity, do not despair and do not lose faith in yourself.

We must not forget that the game of billiards is also a great holiday. Starting to play pool in a few minutes to remove the accumulated stress. Playing human almost completely forget about the daily minutiae and the whole is immersed in the exciting action.

Play Pool and Be Healthy!

Some diets may help prevent Alzheimer's disease

2011-11-28T04:00:00.000-08:00

Some diets may help prevent Alzheimer's disease, others may increase the risk and according to some studies antioxidant vitamins may be ineffective in the treatment of diseases associated with clouding of the mind.
Some diets that aim to strengthen the heart muscle, also increase the risk of getting Alzheimer's disease ..

Scientists from Columbia University have shown that the use of antioxidants completely ineffective in preventing the disease, tend to think that vitamins do not work on older people, because they are less susceptible to their action, and action is of short duration. This was stated by Dr. Jose Lachsinger Columbia University.

Another study on the effect of fat on the heart and the brain was conducted by Dr. Martha Clare Morris of Chicago Medical Center, Presbyterian St. Luke's. The study involved 815 volunteers aged 65 and older. All were interviewed about diet and eating habits. The subsequent four years later tests showed that in 131 of the test developed Alzheimer's disease.

People who used the saturated fats in large amounts (products of animal origin such as meat, butter) doubled the risk of Alzheimer's disease compared with those who almost never ate food with saturated fats. This risk is particularly increased in those who ate more than 25 grams of saturated fat daily. For comparison, one tablespoon of butter - 7 grams. Those who ate less than 25 grams have a smaller but still significant risk of developing Alzheimer's disease.

Patients who consumed 14.5 grams of polyunsaturated fat daily (polyunsaturated fats found in vegetables, fish and nuts) reduced the risk by 70%, compared with those who ate little of these fats.

Dr. Morris believes that the Diet is the regular consumation of toast with margarine with polyunsaturated fats, peanut butter, nuts and canola salad dressing. The discovery of researchers is that they proved that the products that increase the risk of cardiovascular disease, also increase the risk of Alzheimer's disease.

Study about the effect of antioxidants was carried out in New York. 980 patients aged over 75 also interviewed about their food parcels during the first year of a four-year study.
After research on Alzheimer's disease diagnosed 242 patients. The subjects consumed a variety of foods rich in antioxidants, such as oranges, corn oil margarine on, and carrots. Some take vitamin supplements, but the absence or lack of antioxidants in the diet had no relation to the development of the risk of Alzheimer's disease.

Antioxidants block the effect of oxygen molecules called free radicals that damage cells. But their action does not preclude the possibility of Alzheimer's disease.

Means of preventing Alzheimer's disease

2011-11-09T03:55:00.000-08:00

A group of scientists from the University of Minnesota Medical School, "Mount Sinai" (USA) discovered that isolated from grape seed polyphenols are capable of lowering the content in the brain of a substance called "beta-peptide amilodny Aβ». Its toxic effects on brain cells is the reason of memory loss in Alzheimer's disease.

Now the researchers plan to find a biomarker that will enable patients to determine a high probability of developing Alzheimer's disease. This would allow for early prevention of severe illness, even when the symptoms are absent or mild.

7 possible signs of Alzheimer's disease

2011-11-09T03:40:00.000-08:00

Human...
-Specifies the same questions over and over again.
- Repeats the same story word for word, again and again.
- Forget how to cook, to fix anything, or those activities that were previously carried out easily and regularly.
- Loses the ability to pay bills.
- Disoriented in familiar surroundings or arranges household items not in their places.
- Neglects taking a bath or constantly wears the same clothes one and insists that he washed his clothes, or even clean.
- Shifts to someone else, such as a spouse, the responsibilities to make decisions or answer questions despite the fact that before doing this myself.

What are the different types of vascular dementia?

2011-09-28T05:26:00.000-07:00

There are two main types of vascular dementia: one caused by stroke and one caused by small vessel disease. A third type is a mixture of the two. There are many other types of vascular dementia.
Stroke-related dementia

Stroke is the term used to describe permanent brain damage caused by an interruption in the supply of blood to specific parts of the brain. The symptoms that a person experiences as a result of a stroke depend on which area of the brain has been damaged. If the area in question is responsible for movement of a limb, paralysis might occur. If it is responsible for speech, the person might have problems communicating. Equally, damage to particular areas in the brain can cause the symptoms of dementia.

When vascular dementia is caused by a single stroke, it is sometimes called single-infarct dementia. Vascular dementia can also be caused by a series of small strokes. These can be so tiny that the person might not notice any symptoms, or the symptoms may be only temporary. This is called multi-infarct dementia.

Always consult a doctor if you experience any sudden symptoms, such as slurred speech, weakness on one side of the body, or blurred vision - even if they are only temporary. These episodes may be caused by temporary interruptions in the blood supply within the brain, known as transient ischaemic attacks. If left untreated, they can lead to permanent damage.
Small vessel disease-related dementia

This type of dementia, also known as sub-cortical vascular dementia or, in a severe form, Binswanger's disease, is caused by damage to tiny blood vessels that lie deep in the brain. The symptoms develop more gradually and are often accompanied by walking problems.
Vascular dementia and Alzheimer's disease (mixed dementia)

A diagnosis of mixed dementia means that Alzheimer's disease, as well as stroke or small vessel disease, may have caused damage to the brain.

What is vascular dementia?

2011-09-27T05:28:00.000-07:00

Vascular dementia is the second most common form of dementia after Alzheimer's disease. This factsheet will help you to understand vascular dementia by explaining the causes, symptoms and treatments available.

What do we mean by 'vascular dementia'?

The term 'dementia' is used to describe the symptoms that occur when the brain is damaged by specific diseases. These diseases include Alzheimer's disease and vascular dementia. Someone with dementia may have difficulties remembering, solving problems or concentrating. Vascular dementia is a type of dementia caused by problems in the supply of blood to the brain.
How does it develop?

To be healthy and function properly, the brain cells need a good supply of blood. The blood is delivered through a network of blood vessels called the vascular system. If the vascular system within the brain becomes damaged and blood cannot reach the brain cells, the cells will eventually die. This can lead to the onset of vascular dementia.

What causes damage to the vascular system in the brain?

There are a number of conditions that can cause or increase damage to the vascular system. These include high blood pressure, heart problems, high cholesterol and diabetes. This means it is important that these conditions are identified and treated at the earliest opportunity.
What are the symptoms?

Vascular dementia affects different people in different ways and the speed of the progression varies from person to person. Some symptoms may be similar to those of other types of dementia.

However, people with vascular dementia may particularly experience:

* problems concentrating and communicating
* depression accompanying the dementia
* symptoms of stroke, such as physical weakness or paralysis
* memory problems (although this may not be the first symptom)
* a 'stepped' progression, with symptoms remaining at a constant level and then suddenly deteriorating
* epileptic seizures
* periods of acute confusion.

Other symptoms associated with vascular dementia may include:

* visual mistakes and misperception
* walking about and getting lost
* changes in behaviour
* restlessness
* problems with continence.

Types of Dementia

2011-09-26T06:36:00.001-07:00

There are many different types of dementia although some are far more common than others. They are often named according to the condition that has caused the dementia. Some of the more common types are outlined below.

Alzheimer's disease
vascular dementia
dementia with Lewy bodies (DLB)
fronto-temporal dementia (including Pick's disease)
Korsakoff's syndrome
Creutzfeldt-Jakob disease (CJD)
HIV-related cognitive impairment
Mild cognitive impairment

Dementia

2011-09-26T04:37:00.000-07:00

Dementia is a term used to describe various different brain disorders that have in common a loss of brain function that is usually progressive and eventually severe. There are many types of dementia. The most common are Alzheimer's disease, vascular dementia and dementia with Lewy bodies.

The term 'dementia' is used to describe the symptoms that occur when the brain is affected by specific diseases and conditions.

Symptoms of dementia include
-loss of memory
-confusion and problems with speech and understanding.

Vitamin B may lower Alzheimer's risk

2011-09-19T05:38:00.000-07:00

Daily consumption of B- vitamins and folic acid may considerably slow the onset of memory loss in older people and even prevent Alzheimer's disease.

A study of 266 people aged 70 and older showed that large doses of B6, B12 and folic acid reduced the overall senile shrinkage of brains by 30 percent.

Participants were suffering mild cognitive impairment (MCI), a condition which is an intermediate stage between the expected cognitive decline of normal aging and the more pronounced decline of dementia. It involves problems with memory, language, thinking and judgment and increases the risk of developing dementia and Alzheimer's disease.

According to the results published in the International Journal of Geriatric Psychiatry, and PLoS One, brain scans of those who took the prescribed supplements showed that the vitamin pills reduced brain atrophy by 30 percent on average.

Taking the vitamins was even more effective on patients with high levels of an amino acid called homocysteine and reduced brain atrophy among them by 50 percent.

"High homocysteine is a known risk factor for cognitive decline in the elderly and Alzheimer's disease and also for other kinds of dementia like vascular dementia," said lead researcher Celeste de Jager. "It can be damaging to the endothelial lining of the blood cells. It also binds to receptors in the brain that are on the neurons and it seems to contribute the atrophy that's associated with Alzheimer's."

Taking B vitamins and folic acid is known to control the levels of homocysteine, which increases in old age, added the scientist who works with Oxford University.

The new findings "definitively" showed that the vitamins were a good way of preventing mental decline, the study concluded.

"A lot of the time brain changes start in your 40s and 50s before you get clinical symptoms," de Jager told the British Science Festival. "I would think that in middle age people should start thinking about their vitamin levels."

Researchers, however, warned people not to take vitamins without consulting their doctors because supplements can cause some harmful impact on other conditions such as cancer.

Asked if she would take the vitamins as a precaution, Dr de Jager said: "I would ask the doctor to check my B12 and my folic acid levels for starters. "I take supplements when I'm feeling a bit low, I don't take one every day but I would certainly have multi-vitamins and B vitamins in my cupboard."

Alzheimer's drug guidelines

2011-09-19T05:36:00.000-07:00

What are the drugs involved?

The three drugs which look likely to be available to patients with "mild" Alzheimer's are Aricept (donepezil), Reminyl (galantamine) and Exelon (rivastigmine).

In addition, NICE says a fourth drug, Ebixa, should be prescribed to patients with more advanced Alzheimer's.

How do they work?

One theory of the origins of Alzheimer's disease in some patients is damage to the "cholinergic" system in the brain, which leads to a shortage of a neurotransmitter called acetylcholine which has been linked to memory function in Alzheimer's.

All of the three drugs work by inhibiting an enzyme which breaks down acetylcholine - hopefully boosting levels of the brain chemical.

What benefits have been seen?

The drugs do not cure Alzheimer's. There is no proof that the drugs can alter the course of the disease or extend life. However, there is evidence that they can lessen symptoms such as memory loss and confusion in patients with "mild" Alzheimer's. This in turn can improve quality of life, and allow patients to live more independently for longer. One analysis conducted by NICE suggests that they could delay the need for someone to go into full-time care by over six weeks.

However, they do not work for everyone. It is estimated that between 40% and 70% of patients achieve some kind of benefit, and side effects can include dizziness, insomnia and nausea.

Why have the guideline changes been proposed?

NICE says that the publication of further clinical studies into the drugs in the five years since they were last appraised show more clearly the benefits to patients with "mild" Alzheimer's.

Campaigners had argued that the "economic model" used to calculate whether the drugs offered economic "value for money", did not accurately reflect the hidden economic costs of extra care outside hospital.

NICE says this time around it considered new evidence on the possible cost savings of treating early Alzheimer's patients.

How much more will it cost the NHS?

This is not entirely clear yet. The cost of the drugs themselves is roughly £1,000 per year, per patient, but the benefits of the treatment do not continue forever, and the exact number of patients who will benefit has yet to be determined. NICE calculates that more than 380,000 have Alzheimer's, approximately half of these being in the "mild to moderate" group.

The Alzheimer's Society believes the number is higher, but with an estimated 62,000 people developing Alzheimer's each year, it is likely that hundreds of thousands of people could potentially be eligible over the next few years.

However, NICE says it is confident that the extra cost of caring for these patients outweighs the cost of the drugs themselves.

Coffee protects brain from Alzheimer's

2011-09-16T05:48:00.000-07:00

For years we’ve been told that was bad for us. It’s unhealthy and addictive, doctors warned. But as vindication for all who stuck by their energizing elixir, a new study shows that coffee may actually be good for our brains. In fact, it may help keep Alzheimer disease away.

The study, which was published early online in the Journal of Alzheimer’s Disease, was in mice whose DNA had been tweaked to contain a human Alzheimer’s gene. Just like humans with familial Alzheimer’s, these mice become increasingly forgetful as they age.

Amazingly, the equivalent of four to five cups of caffeinated coffee every few days led to much improved memories in the Alzheimer’s mice, says study co-author Gary Arendash, a scientist at the Florida Alzheimer’s Disease Research Center in Tampa.

Earlier research by Arendash and his colleagues showed that caffee could at least partially block the production of beta amyloid, the sticky protein that clogs the brains of Alzheimer’s patients. They also found that a substance called granulocyte-colony stimulating factor, or GCSF, sparked the production of new axons, the communication cables that link nerve cells together, as well as new nerve cells themselves.

What’s really interesting is that caffeinated coffee and decaffeinated coffee -help us to keep away Alzheimer disease.

For the new study, Arendash and his colleagues “treated” healthy mice and Alzheimer’s mice with either caffeinated or decaffeinated coffee. Then the researchers ran a test to see if either beverage led to better memories.

The test they used mimics one that is given to humans to diagnose Alzheimer’s. In that test, people are given a bag of objects to look through (we’ll call that Bag A). And then they’re shown another bag of objects (Bag B). Later on, they’re asked to remember what was in Bag A.

Studies have shown that people with Alzheimer’s have a tough time remembering what was in Bag A because the distraction of looking through the objects from Bag B gets in the way of storing the contents of A in their long term memories. That’s generally not a problem for people with healthy brains.

The two part mouse test involved water mazes. The mice has to find -- and remember -- the location of a submerged platform in a tub of water that is deep enough that they need to swim till they find the platform.

After they find the platform in one tub, they’re moved to another tub where they have to find yet another platform. Mice with Alzheimer’s generally have a tough time remembering the location of the first platform when they’re placed in the original tub. But in Arendash’s study, Alzheimer’s mice that got caffeinated coffee and decaffeinated coffee had memories that were just as good as those of normal mice.

Lest you dismiss this study because it’s just in rodents, Arendash says he’s got new data in humans. That data is still being analyzed, he says, but so far it looks like caffeinated and decaffeinated coffee has the same impact in people as it does in mice.

Insulin spray slows Alzheimer's disease

2011-09-16T05:39:00.000-07:00

Using a nasal insulin spray twice a day may slow and even reverse the symptoms of memory loss in patients with early Alzheimer's disease.

During a four months study, researchers tested the effectiveness of using insulin spray for people without diabetes who had been diagnosed with mild memory problems related to Alzheimer's disease or with amnestic mild cognitive impairment (aMCI).

Participants were divided into three groups either receiving 20 milligrams of insulin twice a day, 40 mg twice a day or a saline solution as a placebo.

Findings showed those who received 20 mg of insulin improved performance on a memory test after two months. Improvements persisted after four months and were still observable some time after the insulin treatment stopped.

Patients on higher doses of insulin had no change in their memory status, while those who got the placebo showed a decline.

The differences between those on insulin and those on the placebo were "small in absolute terms" but they were robust enough, authors wrote in the Archives of Neurology.

"Our results suggest that the administration of intranasal insulin may have a therapeutic benefit for adults with aMCI or Alzheimer's disease," wrote Suzanne Craft of the Veterans Affairs Puget Sound Health Care System and the University of Washington School of Medicine.

"The results of our pilot trial demonstrate that the administration of intranasal insulin stabilized or improved cognition, function and cerebral glucose metabolism for adults with aMCI or AD [Alzheimer's disease]," the researcher added.

According to the report, "these results provide an impetus for future clinical trials of intranasal insulin therapy and for further mechanistic studies of insulin's role in the pathogenesis of AD."

Alzheimer's disease and Health

2011-08-02T04:58:00.000-07:00

Alzheimer's disease (AD) - a primary degenerative disease of the brain - is characterized by progressive memory loss and other cognitive functions, as well as behavioral and other disabilities. According to the experts of the World Health Organization, asthma is the most common cause of dementia in elderly and senile age. Prevalence increases with age. In the group of persons over 65 years, the number of patients doubles every 5 years. In a changing demographic situation with the projected aging of the population worldwide problem of asthma is of particular relevance and socio-economic importance. In developed countries, asthma is considered as a future major public health problem. This is due to steadily increasing number of people at risk of developing the disease, and duration of disease and severe disability of patients requiring in some cases life-long hospitalization in special hospitals and orphanages. This disease creates a huge financial difficulties, and great social and psychological problems for the family and society. For example, in U.S. spending on management of patients with dementia in 2009 amounted to 144 billion dollars.

Global prevalence of dementia in the world (with a predominant proportion of BA), according to 2006 is 26.55 million persons. In the U.S., asthma affects 5.3 million people. A lot of people have reduced levels of cognitive function (eg, the syndrome of mild cognitive decline), which eventually may reach the level of dementia, thus increasing the number of sick people. By 2030 it is expected that 7.7 million Americans age 65 and older will suffer with asthma. According to statistical projections, the number of patients with asthma in the United States will steadily progress and may reach 11-16 million by 2050, a similar upward trend in the U.S. registers of patients with asthma and other industrialized countries, as well as in countries where there is a rapid increase in the older segment of the age in the population. According to current data, the global prevalence of asthma and other dementias will increase dramatically the next 40 years. Stunning data concerning forecasting prevalence of dementia worldwide, listed in records in 2009 and 2010, the International Association on the BA (ADI). Thus, the global prevalence of dementia in 2010 would be more than 35 million cases and nearly doubling every 20 years to 65.7 million in 2030 and 115.4 million in 2050, particularly the sharp increase of patients will occur in middle-and low-income countries.

As already noted, asthma is the leading cause of dementia in the elderly. Life expectancy as a risk factor for asthma is estimated 1:4-1:2. More than 14% of people over 65 suffer from asthma, and prevalence increased by at least 40% in people older than 80 years. The prevalence of asthma is higher among persons older than 60 years. Some forms of familial Alzheimer's disease with early onset disease may have been even in the third decade. However, these cases are sub groupings of less than 10% of all familial cases of Alzheimer's disease. More than 90% of cases of asthma are sporadic and occur in individuals older than 60 years.

Of interest are data from studies that examine groups of people aged 90-99 years, and century-old and older. Based on an analysis of the data suggested that the risk of disease may increase in persons over 90 years. In this case, age can be regarded as an absolute risk factor for the disease, but more research is needed.

According Plassman et al., The risk of developing asthma is significantly higher in women than in men, mainly due to higher average life expectancy of women compared with men.

Alzheimer's Drugs Decision Based On Flawed Calculations

2009-01-26T07:45:00.000-08:00

Thousands of people with early stage Alzheimer's are being denied access to the only drugs for the disease due to fundamental flaws in the way their cost effectiveness has been calculated.

There has been widespread condemnation of the National Institute for Health and Clinical Excellence's (NICE) decision to restrict Alzheimer's drugs that cost just £2.50 a day on the NHS.

Following a ruling by the Court of Appeal in May 2008, NICE was ordered to release the health economic model used to make the decision to key stakeholders. Alzheimer's Society has reviewed the calculations and submitted a detailed analysis to NICE. The charity has today appealed for NICE to review its decision on Alzheimer's drugs.

Neil Hunt, Chief Executive of Alzheimer's Society, says,
'We have always argued that the way NICE calculated the cost effectiveness of Alzheimer's drugs was fundamentally flawed. Now that we have examined NICE's calculations first hand and taken expert advice, Alzheimer's Society remains convinced that denying people with Alzheimer's effective drugs makes no sense.

NICE must urgently review its decision. One in three people over 65 will die with dementia; the current state of dementia care and treatment in the UK is a national scandal.' Alzheimer's Society cannot release its full response to NICE due to NICE's confidentiality rules. However, previously the charity has highlighted the following concerns about the way cost effectiveness is calculated:

- NICE assumes everyone who starts treatment continues on it. In reality, only those who benefit from drugs would stay on them.
- NICE has drastically underestimated the cost savings to the State of people receiving treatment and remaining active in the community (rather than cared for in homes or hospitals)
- NICE does not take into account the full benefit drug treatment can have on a carer's quality of life.

In October 2008, the House of Lords denied NICE the right to appeal the high court decision which ordered it to release a copy of the executable model.

- Since May 2006 three Alzheimer's drugs have been denied to people in the early stages of the disease on the NHS.

- On 1 May 2008 the Court of Appeal found in favor of Eisai/Pfizer ruling NICE should have allowed public access to the health economic model that it used to make its decision.

- On 17 June 2008 NICE sought permission from the House of Lords to appeal the Court of Appeal decision.

- 1 in 3 people over the age of 65 will die with dementia.

- 700,000 people in the UK have a form of dementia, more than half have Alzheimer's disease. In less than 20 years nearly a million people will be living with dementia. This will soar to 1.7 million people by 2051.

- Dementia is not a natural part of aging; it is caused by diseases of the brain and robs people of their lives.

- Alzheimer's Society champions the rights of people living with dementia and those who care for them. Alzheimer's Society works in England, Wales and Northern Ireland.

Lower Risk Of Dementia And Alzheimer's Linked To Midlife Coffee Drinking

2009-01-26T07:42:00.000-08:00

Researchers in Finland and Sweden who followed over 1,400 middle-aged people over twenty years, found that those who drank three to five cups of coffee a day in their midlife years were less likely to develop dementia or Alzheimer's disease in old age compared with those who drank either no coffee at all or very little.

The findings came from the Finnish Cardiovascular Risk Factors, Aging and Dementia (CAIDE) Study, conducted by researchers at the University of Kuopio, Finland and the Karolinska Institutet, Stockholm, Sweden, and the National Public Health Institute, Helsinki, Finland. It is published in the January 2009 issue of the Journal of Alzheimer's Disease, currently in press, although abstracts can be viewed online.

The participants of the study included survivors from other research programs, such as the North Karelia Project and the FINMONICA study in 1972, 1977, 1982 and 1987. After the midlife examination, the average follow up was 21 years, and a total of 1,409 participants, aged between 65 and 79 years, completed the project and undertook the end of follow up re-examination in 1998, when 61 of them were diagnosed with dementia, including 48 with Alzheimer's Disease (AD).

At the midlife examination, participants filled in questionnaires that asked them, among other things, how much coffee and tea they drank, and how often.

For this study, the researchers categorized coffee consumption into three bands: low (0-2 cups a day), moderate (3 to 5 cups) and high (over 5 cups a day). Tea drinking was categorized only into two bands: tea drinking and no tea drinking.

Lead researcher Miia Kivipelto, who is an associate professor at the University of Kuopio, Finland and the Karolinska Institutet, Sweden, explained why they did the study:

"We aimed to study the association between coffee and tea consumption at midlife and dementia/AD risk in late-life, because the long-term impact of caffeine on the central nervous system was still unknown, and as the pathologic processes leading to Alzheimer's disease may start decades before the clinical manifestation of the disease."

The results showed that:

* Those who drank coffee in midlife had a lower risk of developing dememtia and AD later in life than those who drank little or no coffee.

* The lowest risk (65 per cent lower risk) was among those who drank moderate amounts of coffee in midlife (3 to 5 cups a day).

* Removing the effect of potential confounders did not change the figures significantly.

* Tea drinking was relatively uncommon and no links were found between this and dementia/AD.

Kivipelto said:

"Given the large amount of coffee consumption globally, the results might have important implications for the prevention of or delaying the onset of dementia/AD. "

The researchers said the findings need to be confirmed by other studies, but nevertheless they highlight the possibility that diet can change a person's risk of late-life dementia or AD.

If, following confirmation of these findings by further research, scientists also discover the mechanisms by which coffee protects against dementia and AD, then it may also be possible to develop new therapies for these conditions, said Kivipelto.

Promising Hormone Treatment For Alzheimer's Disease And Stroke

2009-01-22T07:37:00.000-08:00

Saint Louis University researchers have identified a novel way of getting a potential treatment for Alzheimer's disease and stroke into the brain where it can do its work.

"We found a unique approach for delivering drugs to the brain," says William A. Banks, M.D., professor of geriatrics and pharmacological and physiological science at Saint Louis University. "We're turning off the guardian that's keeping the drugs out of the brain."

The brain is protected by the blood-brain barrier (BBB), a gate-keeping system of cells that lets in nutrients and keeps out foreign substances. The blood-brain barrier passes no judgment on which foreign substances are trying to get into the brain to treat diseases and which are trying to do harm, so it blocks them without discrimination.

"The problem in treating a lot of diseases of the central nervous system - such as Alzheimer's disease, HIV and stroke - is that we can't get drugs past the blood-brain barrier and into the brain," says Banks, who also is a staff physician at Veterans Affairs Medical Center in St. Louis.

"Our new research shows a way of getting a promising treatment for these types of devastating diseases to where they need to be to work."

The therapy - known as PACAP - is a hormone produced by the body that is a general neuro-protectant.
PACAP stands for pituitary adenylate cyclase-activating polypeptide. "It is a general protector of the brain against many types of insult and injury," Banks says.

He compares a specific guarding mechanism in the BBB - efflux pumps - to bouncers at exclusive nightclubs. While they welcome those on the approved guest list, they look for trouble-makers trying to crash the party, refuse to let them in and evict them if they do get in.

The scientists isolated the particular gatekeeper than evicts PACAP. Then they designed an anti sense, a specific molecule that turned off the impediment.

"We went after the guard and essentially told him to go on break for a while so PACAP could get into the brain," Banks says.

They used mouse models of Alzheimer's disease and stroke to test what would happen if PACAP could get into the brain.

"We reversed the symptoms of the illnesses," Banks says. "The mice that had a version of Alzheimer's disease became smarter and in the stroke model, we reduced the amount of damage caused by the blockage of blood to the brain and improved brain recovery."

Simply turning off the gatekeeper that kept PACAP out of the brain allowed enough of the hormone that already is in the body to get inside the brain, where it effectively treated strokes. However, the mice that had a version of Alzheimer's disease needed both an extra dose of PACAP and the anti sense that turned off the gatekeeper to improve learning.

"These findings are significant for three reasons. We have found a therapy that reverses symptoms of Alzheimers's disease and stroke in a mouse model. We have isolated the particular roadblock that keeps the treatment from getting into the brain. And we have found a way to finesse that obstacle so the medicine can get into the brain to do its work," Banks says. "This could have implications in treating many diseases of the central nervous system."

The findings were published in the Nov. Early online issue of the Journal of Cerebral Blood Flow & Metabolism.

Alzheimer's Disease Could Be Prevented And Treated By Common Epilepsy Drug

2009-01-21T05:57:00.000-08:00

The team led by UBC Psychiatry Prof. Weihong Song, who is also the Jack Brown and Family Professor and Chair in Alzheimer's Disease at UBC, found that if Valproic Acid (VPA) is used as a treatment in early stages of AD memory deficit is reversed.

The study, published in the Journal of Experimental Medicine, reveals that VPA works by inhibiting the activity of an enzyme that produces a neurotoxic protein called beta Amyloid. In doing so, plaque formation is discontinued. Amyloid beta-proteins are the central component of neurotoxic plaques in AD.

"We found that if we used VPA in the early stage of Alzheimer's disease, in model mice, it reduced plaque formation and further prevented brain cell death and axon damage," says Song, who is a Canada Research Chair in Alzheimer's disease and Director of the Townsend Family Laboratories in UBC's Faculty of Medicine. "The drug also improved performance in memory tests."

The results will help inform the design of human clinical trials because researchers now understand the mechanisms and pathology of VPA in AD animal models.

"We are very excited about these results because we now know when VPA should be administered to be most effective and we now know how VPA is working to prevent AD," says Song, who is also a member of the Brain Research Centre at UBC and VCHRI. "A small human clinical trial is currently underway and we expect results to be available in the next year."

AD is a neurodegenerative disorder characterized by progressive cognitive deterioration and is the most common form of dementia. The Alzheimer Society of Canada estimates that AD affects close to 300,000 Canadians and accounts for two-thirds of all cases of dementia. By 2031, about 750,000 Canadians will suffer from AD and related dementias.

Approximately $5.5 billion per year is spent caring for persons with AD and related dementias in Canada. The Alzheimer's Association in the U.S. estimates there are approximately 500,000 Americans younger than 65 with Alzheimer's or other dementia.

Major funding for this research has been provided by the Canadian Institutes of Health Research, the Canadian Government agency for health research. CIHR's mission is to create new scientific knowledge and to catalyze its translation into improved health, more effective health services and products, and a strengthened Canadian health care system. Composed of 13 Institutes, CIHR provides leadership and support to more than 10,000 health researchers and trainees across Canada.

Additional funding has been provided by: the Michael Smith Foundation for Health Research, British Columbia's provincially mandated health research organization and through a donation from the Townsend Family as well as from a private donation from the Jack Brown and Family Alzheimer Foundation.

The UBC Faculty of Medicine provides innovative programs in the health and life sciences, teaching students at the undergraduate, graduate and postgraduate levels, and generates more than $200 million in research funding each year.

The Brain Research Centre comprises more than 200 investigators with multidisciplinary expertise in neuroscience research ranging from the test tube, to the bedside, to industrial spin-offs. The center is a partnership of UBC and VCHRI.

VCHRI is the research body of Vancouver Coastal Health Authority. In academic partnership with UBC, the institute advances health research and innovation across B.C., Canada, and beyond.

Possible Alzheimer's Disease Marker Discovered In Rare Genotype

2009-01-21T05:45:00.000-08:00

Researchers at Banner Health's Sun Health Research Institute have uncovered evidence that Alzheimer's disease (AD) may be clinically confirmed in patients with apolipoprotein E2 homozygote.
The results of their study are published in the January 2009 issue of the Journal of Alzheimer's Disease.

Apolipoprotein E2 homozygote has been associated with a protective effect against AD and contributes to delaying the onset of symptoms. However previously, no significant data had pointed to clinically confirmed AD in persons with apolipoprotein E2 homozygote. The reverse is true of apolipoprotein E4. Previous studies have confirmed that apolipoprotein E4 is a predictive risk factor for AD and indicates an increased genetic risk of AD.

Clinical confirmation of the apolipoprotein E2 homozygote Alzheimer's disease finding in this study was confirmed by MRI, PET and neuropsychological evaluation and testing. AD pathology is yet to be determined and will occur at post mortem.

"Clinical diagnosis of possible AD has now become extremely accurate and is especially helpful to physicians looking for the best outcomes in treating patients," says Marwan Sabbagh, MD, Sun Health Research Institute's chief medical/scientific officer and lead investigator of the study.

"This study may hold many clues to the nature of how Alzheimer's genetics work. Although clinically rare, the information gleaned in this study allows us to ask new questions and possibly answer others," says Sabbagh.

Education Can Help Stave Off Alzheimer's Disease

2009-01-21T05:41:00.000-08:00

Even with evidence of brain plaques associated with Alzheimer's disease, highly educated individuals manage to score higher on cognitive tests. Results from this study are published in the November issue of Archives of Neurology.

Currently there exists a popular notion - the "cognitive reserve" hypothesis - that people with greater thinking, learning, and memory capabilities can delay symptom of Alzheimer's disease even as the brain is changing. Since cognitive reserve is somewhat difficult to measure, researchers use education level as a proxy. "Adjusting for level of Alzheimer disease pathological burden determined at autopsy, greater education has been associated with better cognitive function during life," write Catherine M. Roe, Ph.D. and colleagues at the Washington University School of Medicine, St. Louis. "Education interacts with Alzheimer disease pathological burden such that a greater pathological burden is required to show an effect on cognition among persons with more education."

Between 2003 and 2008, the researchers analyzed 37 individuals diagnosed with Alzheimer's-like dementia and 161 individuals without dementia. Cognitive reserve measurements included education history as well as cognitive test scores. In addition, study participants received an injection of carbon 11-labeled Pittsburgh Compound B (PiB) prior to a 60-minute positron emission tomography (PET) brain scan. This contrast compound (PiB) has been shown to stick to beta-amyloid brain plaques that are linked to Alzheimer's disease, and thus researchers could identify the disease state in each patient.

Results of the study demonstrated that there were significant difference in the level of PiB uptake among patients with different years of education and cognitive test scores. For example, individuals with beta-amyloid plaques in the brain (organs that took up higher levels of PiB) showed increased performance on tests as education levels increased. For individuals without plaques, education was not significantly associated with cognitive scores.

"The results support the hypothesis that cognitive reserve influences the association between Alzheimer disease pathological burden and cognition," conclude Roes and colleagues. "Based on autopsy data, there may be a ceiling effect when extensive beta-amyloid pathological burden is present as in late-stage dementia of the Alzheimer type. Presumably, as the Alzheimer disease pathological burden increases, a greater proportion of highly educated participants reaches the threshold for dementia and the initial advantage provided by cognitive reserve decreases. Longitudinal imaging of beta-amyloid pathology in vivo will soon allow us to determine whether these inferences from cross-sectional studies are accurate."

Potential Protection For The Brain Against Alzheimer's Disease From A Special Type Of Collagen

2009-01-21T05:38:00.000-08:00

Scientists from the Gladstone Institute of Neurological Disease (GIND), UCSF, and Stanford have discovered that a certain type of collagen, collagen VI, protects brain cells against amyloid-beta (Aβ ) proteins, which are widely thought to cause Alzheimer's disease (AD).

While the functions of collagens in cartilage and muscle are well established, before this study it was unknown that collagen VI is made by neurons in the brain and that it can fulfill important neuroprotective functions.

The team of investigators led by GIND director Lennart Mucke, MD, reported in a recent edition of the journal Nature Neuroscience, that collagen VI is increased in brain tissues of Alzheimer's patients.

"We first noticed the increase in collagen VI in the brain of AD mouse models, which inspired us to look for it in the human condition and to define its role in the disease," said Dr. Mucke.

The Gladstone team had profiled changes in gene expression using DNA microarrays, which provides an unbiased method for identifying key biological pathways. By comparing all of the genes that are active in disease and normal tissue, one can get valuable information on new pathways and potential therapeutic targets.

The researchers looked at the dentate gyrus, a specific area of the brain that is critical to memory and particularly vulnerable in AD, and compared the genes that were turned on and off in normal mice and a mouse model of AD. This analysis revealed the striking increase in collagen VI in the brains of mice that model AD.

Building on this initial finding, the team examined brain tissue from AD patients and normal non-demented humans and found that collagen VI expression was also higher in the AD patients. They further discovered that the cellular source of the collagen VI in the brain was neurons, the very cells that the disease attacks and that we all need to think and remember.

"These findings were really surprising and exciting to us because nobody knew anything about collagen VI in the brain," said Jason Cheng, MD, co-lead author of the study. "We were particularly curious whether collagen VI contributed to neuronal damage in AD or was produced as a defense mechanism against it," added Dena Dubal, MD, PhD, co-lead author of the study.

To answer this and other questions, the scientists carried out a series of informative cell culture experiments. These experiments revealed found that Aβ added to neurons grown in culture increased the expression of collagen VI and that this process involved the immune regulatory cytosine TGFβ. What is more, the team discovered that increasing the amount of collagen VI in the cultures effectively protected the neurons against Aβ toxicity.

"This striking protective effect suggests that increased neuronal production of collagen VI is an important component of the brain's defense against Aβ," said Dr. Mucke. "It made us really curious about the underlying mechanisms."

To clinch these mechanisms, Dr. Mucke's team examined the direct interactions of collagen VI with Aβ. They looked at how Aβ attacks individual neurons in cell culture. Small poisonous Aβ assemblies, called oligomers, bind strongly to vulnerable neurons in the brain, but in the presence of collagen VI, this binding was blocked. Using immunohistochemistry and atomic force microscopy, they showed that collagen VI and Aβ form large aggregates with each other that may sequester the smaller, more toxic Aβ complexes away from neurons.

"We are eager to explore how this kind of process might be enhanced therapeutically and how we can best leverage it for the development of more effective treatments for this devastating condition," said Dr. Dubal.

Breakthrough In Screening For Alzheimer's Disease

2009-01-21T05:36:00.000-08:00

CSIRO scientists have developed a new system to screen for compounds that can inhibit one of the processes that takes place during the progression of Alzheimer's disease.

In a paper published in the latest edition of the Journal of Alzheimer's Disease, folate is shown to be beneficial in the screening system.

Lead author, CSIRO's Dr Ian Macreadie says folate is already well known to have a protective effect against Alzheimer's disease which is believed to be caused by the loss of neurons in the brain due to a process whereby toxic multimers of a small protein called Aβ are formed.

"However, a team of scientists working within CSIRO's Preventative Health Flagship has discovered a rapid screening system to identify inhibitors of this process. Compounds that inhibit the formation of the toxic multimers may lead to the prevention or delay of the disease," Dr Macreadie says.

"Although many other research groups and drug companies around the world are trying to find compounds that act in the same way, the advance by the Flagship team involves using live yeast with the Aβ protein fused to a green fluorescent protein that comes from jellyfish.

"The significance of this development is that the yeast trial we developed could lead to the discovery of new agents which may prove useful in preventing or delaying the onset of Alzheimer's disease."

Currently Alzheimer's disease is an incurable illness and the fourth leading cause of death in people aged 65 years and over.

Although folate is abundant in foods like leafy green vegetables, pulses and liver, CSIRO studies have shown that many Australians do not consume enough folate to benefit from its ability to prevent cell damage. Folate levels can, however, be readily restored by dietary folate supplementation.

In Early Diagnosis Of Alzheimer's Disease, MRI Brain Scans Accurate

2009-01-21T05:33:00.000-08:00

MRI scans that detect shrinkage in specific regions of the mid-brain attacked by Alzheimer's disease accurately diagnose the neurodegenerative disease, even before symptoms interfere with daily function, a study by the Florida Alzheimer's Disease Research Center (ADRC) in Miami and Tampa found.

The study, reported earlier this month in the journal Neurology, adds to a growing body of evidence indicating MRI brain scans provide valuable diagnostic information about Alzheimer's disease. The findings are important in light of many new disease-modifying drugs in trials -- treatments that may prevent mild memory loss from advancing to full-blown dementia if administered early enough.

"We advocate, based on these findings, that the criteria for the diagnosis of Alzheimer's disease should include MRI scans," said the study's lead author Ranjan Duara, MD, medical director of the Wien Center for Alzheimer's Disease and Memory Disorders at Mount Sinai Medical Center who is affiliated with the University of Miami Miller School of Medicine and University of South Florida College of Medicine. "By incorporating MRIs into the assessment of patients with memory problems, early diagnosis can be standardized and done far more accurately."

"This study demonstrates that MRI brain scans are accurate enough to be clinically useful, both in diagnosing Alzheimer's disease itself at an early stage and in identifying people at risk of developing Alzheimer's," said Florida ADRC Center Director Huntington Potter, PhD, a neuroscientist at the Byrd Alzheimer's Center and Research Institute, University of South Florida.

Alzheimer's disease, the most common cause of dementia, is characterized by memory loss, disorientation, difficulty with reasoning and the decline of language and thinking skills. Alzheimer's is diagnosed by a process of elimination since many other diseases and related disorders can mimic its symptoms, and autopsy is currently the only definitive way a diagnosis can be confirmed. The diagnosis often includes a medical history, mental status tests, neurological evaluations and blood tests. Physicians typically use brain scans only to exclude conditions that can also cause memory deficits, such as strokes and brain tumors.

The Florida researchers used a new visual rating system to evaluate the severity of shrinkage, or atrophy, in the brain's medial temporal lobe - specifically in three structures essential for the conscious memory of facts and events. They compared the MRI brain scans of 260 people - a group with probable Alzheimer's disease, two groups with varying degrees of mild cognitive impairment (mild memory problems), and a control group of normal elderly with no discernable memory loss. They found that scores generated by this MRI-facilitated test accurately distinguished each group from the other and correlated with the types of memory problems most frequently caused by Alzheimer's disease. The more extensive the brain atrophy, the more advanced the clinical stage of Alzheimer's disease.

The researchers even found brain atrophy in some people without memory complaints at the study's onset who demonstrated memory decline when assessed a year or two later. This suggests MRIs could predict who will get the disease well before signs of dementia become apparent by other diagnostic methods as well as rule out an Alzheimer's diagnosis in people experiencing memory problems, Dr. Duara said. "If you don't have changes in these three particular areas of the brain, then you don't have Alzheimer's."

Researchers at centers like Miami's Wien Center and USF's Byrd Institute are developing new Alzheimer's drugs that attack mechanisms leading to the death of nerve cells and their connections. The emergence of these disease-modifying treatments has made an earlier diagnosis of Alzheimer's increasingly important, Dr. Duara said. "Having an accurate diagnosis will allow us to start using drugs earlier. The earlier treatment begins, the more likely you are to stop disease progression and benefit the patient."

Most participants in the MRI study were enrolled in the clinical arm of the Florida ADRC, which is supported by a grant from the National Institute on Aging.

The Florida ADRC, the first statewide, multi-center ADRC in the United States, was critical for the successful implementation of the study, said Dr. Potter, the study's senior author. "To validate any new diagnostic test or treatment, you need a large number of diverse volunteers for good comparisons. Alzheimer's research is a partnership between the scientific community and study volunteers; we need both to solve the complexities of Alzheimer's disease."

Diagnostic criteria for depressive episode

2008-11-14T02:08:00.000-08:00

The main symptoms:
• lowering of mood, evident in comparison with the inherent patient norm, the dominant daily, and most of the day and continued at least 2 weeks regardless of the situation;
• marked reduction of interest or pleasure from activities that are usually associated with positive emotions;
• reducing energy and increased fatigue.
Additional symptoms:
• reducing the efficiency of focus;
• lowering self-esteem and sense of self-doubt;
• idea of guilt and self-effacement (even in light depressions);
• dark and pessimistic vision of the future;
• ideas or actions relating to self or suicide;
• disturbed sleep;
• broken appetite.
It should be noted that depression at the moment remains the most common mental disorder that requires adequate drug therapy. It is widespread depression leads on the one hand, to underestimate the role of development in the clinical picture of various diseases, including dementia, on the other - to hyper diagnostic depression and inadequate appointment of antidepressants.

Fruit and vegetable juices help prevent Alzheimer's

2008-11-14T01:43:00.000-08:00

Drinking fruit and vegetable juice several times a week may help prevent Alzheimer's disease, showed the results of a new study, reported AFP.
The study was conducted 9 years in Seattle and has affected nearly 2 thousand people, led by professor at the University of Tennessee (USA) Key Dej. People filled out questionnaires about their lifestyles and preferences in foods. The state of health was recorded.
Research has shown that the risk of developing Alzheimer's disease is reduced by 76% among those who used the fruit or vegetable juice at least three times a week. Among those who used the juice once a week, the risk of the disease decreased by 16%.
Earlier Society believed that the prevention of Alzheimer's great role played by vitamins C and E. But now it is clear that the case not only in them. The author of the study believed that the disease could hinder development and natural antioxidants - polyphenols contained in tea, wine and soke.
Remarkably, the study did not identify any specific fruit or vegetable juices that help prevent Alzheimer's disease better than others.
Alzheimer's - a progressive disease in which patients gradually lose their memory and become unable to care for themselves. Medicines for him does not exist, modern drugs provide only temporary improvement.
It is believed that the disease causes sticky protein called beta-amyloid. It is contained in the brain, but healthy cells are able to get rid of its surplus. However, in patients with Alzheimer beta-amyloid accumulates, forming lump, which cover the cage.
In the U.S. Alzheimer's affects about 4.5 million people in Western Europe - 5.4 million.

Alzheimer's Disease: I think more

2008-11-14T01:22:00.001-08:00

The most terrible disease XXI century may become senile marauds. Life expectancy in developed countries is constantly growing: the projections demographers, for example, half of girls born in 2000, live to 100 years. At the same time, after 65 years, the man threatened senile dementia - Alzheimer's disease. If scientists did not find drugs against the disease, it has been 50 years in the world will be 45 million marauds - more than cancer patients.
The American scientist Steven Austad believes that the average person will survive until the 150 the anniversary because, in his view, thanks to modern technology will soon be constructed of high quality and biologically adapted to the body «spare parts». According to another American scientist Jay Olshansky, the average length of human life in the XXII century, despite the gene therapy and cloning, will not exceed 130 years.
Studies have long shown that they have achieved so old age thanks to good health, and many continue to keep it until the end of his days
Long, who studied Dr. Thomas Perlz from Harvard Medical School, managed to avoid many of senile diseases - stroke, cardiovascular disease and others. According to Dr. Perzl sharp rise in long-livers in the United States over the past 10 years caused massive changes in lifestyle: Americans have to monitor their weight is healthy food, less smoke and more in sports. It is the combination of good heredity, a good environment and healthy lifestyles, according to scientists, and ensures longevity.
Physiology of aging studies have shown that the aging process involves two closely related system of the body: endocrine (hormone responsible for the formulation) and immunity (protecting the body against infection). From the age of the body resistance to disease drops. Scientists attribute this to age in violation of endocrine balance: a substance produced by the beginning of a larger, others - in smaller numbers. So, even if the medicine man learns to replace all the fastest frayed organs (heart, lungs, liver), it is unlikely to make him immortal.
Another more wear body, which can not yet be replaced - it is the brain. According to Lynn Adler, a pioneer in the study of long-livers in the United States, the most important problem associated with aging - a violation of the functions of the brain and senile dementia caused by the disease, first described in detail by German doctor Alloiz Alzheimer and called his name.

Medicines for Alzheimer's disease already on the way

2008-10-16T02:38:00.000-07:00

Scientists from Edinburgh University of St. Andrews (University of St Andrews)
find a way of blocking the processes that lead to the development of Alzheimer's disease - reports Daily Telegraph.

Scottish scientists together with their American colleagues have made a big step towards rede development mechanisms of Alzheimer's - degenerative diseases of the central nervous system, which gradually decreases intellectual activity and the brain suffers memory. Only in the United States of Alzheimer's disease affects 4 million people in Britain - half a million, mostly elderly. The disease is characterized by deposit amyloid protein in the brain - as the surrounding neurons education plaque, and within neurons in the formation of interlocking neyrofibrillyarnyh - these processes kill brain cells. On
cellular level essence of the disease is that amyloid «closes» at the castle enzyme, called amyloid-beta alcohol- dehydrogenase (Amyloid Beta Alcohol Dehydrogenase, ABAD), blocking its action.

Scientists managed to develop a chemical compound that prevents amyloid protein interact with brain cells. To understand how amyloid introduces himself in the box at St. Andrews have created three-dimensional model of ABAD. When the mechanism was understood, was a chemical trap - peptide, which attracted amyloid protein and «offered» him to join him, but not to ABAD. If amyloid has been introduced into the structure of ABAD, then the trap helped to be disconnected from the amyloid protein molecules ABAD and introduced into the structure of peptide.

Scientists have studied opportunities peptidnoy traps on laboratory mice and found that those animals that suffer from memory after memory of the drug seriously improved. Also they have recovered the ability to learn.

According to Frank Gunn-Moore (Dr Frank Gunn-Moore), a professor of biology at St. Andrews, «We have shown that it is possible to stop some signs of the development of Alzheimer's disease». The study, he said, provides a possible key to the treatment of disease, especially - in the early stages. However, according to Gunn-Moore, you will need to at least three years to convert peptide trap in the real drug, and several more years - to test its ability to humans.

The Fund support for research of Alzheimer's (Alzheimer's Research Trust) has been called the results of the study «exciting». Dr. Susanne Sorensen (Dr Susanne Sorensen), director of the Research Society of the fight against Alzheimer's disease (Alzheimer's Society), said that the results of the study added an important piece of knowledge to razgadke nature of the disease and offer a possible way of treatment.

Alzheimer determined by blood

2008-10-16T02:33:00.000-07:00

The company Power3 Medical Products, USA, has developed a test for the identification of Alzheimer's disease at an early stage of the analysis of blood, reports BBC News.

Suffers from Alzheimer's disease about 2-5% of people over 65 years and up to 20% of people over 85 years. It destroys the conscience, is absurd and beyond death. Now Alzheimer's disease, and other neurodegenerative disease, identified only when symptoms become pronounced.

The test NuroPro defines Alzheimer's disease, and Parkinson's disease and amyotrophic lateral sclerosis (Gehrig's disease) on the levels of 59 biomarkers - blood proteins. Clinical trials that have already brought together 180 people, showed the success of the test in 70% of cases.

Last summer the company intends to issue a test of free sale in Greece, by the end of the year - in the United States.

While Alzheimer's disease is considered incurable, but scientists have announced razgadke mechanism for its development as well as taking a drug that can remove the symptoms of the disease at an early stage in 10 minutes.

Alzheimer's sparing no good and educated

2008-10-16T02:31:00.001-07:00

Alzheimer's sparing no good and educated

Good people with a high degree of self-leading regular lives, less prone to the development of Alzheimer's disease, just as people with higher education; to the conclusions reached American and Swedish researchers, whose article published in the journal «General Psychiatry»
( «General Psychiatry») and «Neyrologiya» ( «Neurology»).

The first conclusion made by doctors at the University Medical Center Rasha (Rush University Medical Center) in Chicago, USA. They examined the health status of some thousands of Catholic monks and priests (an article in the magazine «General Psychiatry» quotes Reuters). It turns out that among most of which were measured, good life and restrict themselves to food and bodily pleasure (that is, have a high level of self), the number of patients with Alzheimer's disease was very low, much lower than that of ordinary people. In the surveyed group has not been a single case of dementia since 1994.

Data obtained from the survey of monks, researchers compared the data with ordinary people, who were asked to evaluate themselves on a scale «good» and the self (in the latter case it was necessary to put yourself from 0 to 48 points). The average level of self was 34 points. As it turned out, people with high self (who scored 40 points or more) to 89% less likely to suffer Alzheimer's than those who had low self (28 points or less).

As suggested by the authors of the report, high levels of self allows people a long time to deal with the approaching dementia syndromes: cognitive failure and mild cognitive decline (they are the two main symptoms of Alzheimer's disease). People with high self-accustomed to cope with difficulties, and can for some time to cope with the disease, believed to University Medical Center Rasha.

The second interesting discovery made by scientists Karolinska Institute (Karolinska Institute) in Stockholm, Sweden. According to their data, the risk of the disease Alygeymera also directly linked to the level of education rights (article in the magazine «Neyrologiya» quotes Reuters).

According to the authors of the report, people who have 6-8 grades of education, ill with Alzheimer's disease at 43% less than those who had studied only five years or less. And among those who studied at the School of 9 or more years or have tertiary education, the risk of developing dementia is reduced by 84%. «Low level of education clearly increases the risk of dementia», no doubt Tiya Ngandu (Dr. Tiia Ngandu) from the Karolinska Institutet. According to her, people with high IQ, even feeling the first syndromes approaching Alzheimer's disease are able to resist, unlike those who had not previously engaged in intellectual activities. These findings are directly correlated with data obtained by American researchers.

According to the World Health Organization, from Alzheimer's disease worldwide suffer about 18 million people. As has been reported around the world, among the factors that increase the risk of developing the disease, known as smoking and loneliness.

Alzheimer DISEASE

2008-10-16T02:08:00.000-07:00

Alzheimer DISEASE, degenerative brain disease, progressive decline reflected intelligence. First described by German physician A. Alzheimer in 1907, the disease is a common form of acquired dementia (dementia). Only in the U.S. Alzheimer's affects about 1.5 million. Of a total of 1.3 million people in the U.S. in nursing homes, 30% of people with Alzheimer's disease.

This disease affects people regardless of ethnicity or socioeconomic status. Most early disease recorded in 28 years, but usually manifests itself after 40-50 years. Although Alzheimer's disease often remains unknown, it ranked fourth among causes of death: in the U.S. die from it, it seems, more than 100 thousand people a year.

Alzheimer's was first described in people younger than 65 years, so the sooner it is called presenile dementia. It also mistakenly viewed as a manifestation of aging or as a «sclerosis» cerebral vessels. In fact, the disease associated with degeneration of nerve cells (neurons) and not the defeat of blood vessels.

Symptoms of Alzheimer's are diverse. Among them - a gradual decline in memory and attention, a violation of thinking and the ability to learn, disorientation in time and space, difficulty in selecting the words, the difficulties in communication, personality changes. Symptoms of dementia gradually progressing, leading eventually to the patient completely loses the ability to self and dies. The process of disintegration of the psyche may take several years, bringing suffering to the patient and his family.

Diagnosis. There is no test that would accurately diagnose Alzheimer's disease. Therefore, the doctor must exclude other causes symptoms of dementia diseases, especially those that may be cured, namely, tumors, trauma, infection, metabolic diseases, overdose of drugs, as well as psychiatric disorders such as depression or disturbing syndromes. Even after the exclusion of other diseases diagnosed with Alzheimer's disease remains conjectural. Confirm it can only microscopic examination of brain tissue, which usually posthumously. Only occasionally, the study conducted from a living person, which makes biopsy, and take small samples of brain tissue.

Changes in the brain, confirming the diagnosis of Alzheimer's disease, mostly identified in the outer layer of the brain (Korea) and the hippocampus, which lies deep in the hemisphere, and plays an important role in memory. In the microscopic study of these brain areas are found neurofibrillar glome and neyriticheskie plaque. Klubochki consist of the pathological changes of neurons containing abnormal proteins. Plaques represent areas of sediment in the intercellular space uglevodnyh-protein complexes - amyloid. The more in the brain and klubochkov blyashek, the more intelligent expressed violations.

Biochemical studies show that when Alzheimer's disease in the brain becomes much less acetyl transferring enzymes - an enzyme necessary for the synthesis of acetylcholine. The latter is neuromediator, and substance, which transmit the initiation of the one cell to another, and participates in the process of memory.

Treatment. Temporarily suspend or slow the progression of the disease through drug able takrina, but full recovery is now impossible. Therefore, mainly symptomatic treatment. Patients and their families to help adjust to the disease. We need to strive to maintain the patient may be more active lifestyles. If you have any nonsense, institution or other changes in behavior assigned medication.

The reason for Alzheimer's disease is unknown. Currently, numerous studies aimed at clarifying the role of viral infection, heredity, pathological immune responses, environment factors and toxic substances in the development of the disease.