Monday, March 1, 2010

Regressive state

On 08/12/09 at the Clara Mass Hospital during a conference when ask about Alzheimer's by Tom Thode from the observer newspaper Mr. Joseph president of the Mary Joseph Foundation reply, Alzheimer's is a thief it first robs the individual or individuals of everything then kill them slowly. Alzheimer's put the individual or individuals in a regressive state in other word it takes the individuals from an adult to a child in a regressive state in speech and behavior in this state the individuals cannot do anything for themselves, the individuals have to depend completely on their caregivers to feed and clean them, while they may be also in pain and cannot say.

When ask, what causes Alzheimer's he stated no one fully know but we can see inside the brain of individuals and the damage Alzheimer's disease causes.
Inside the brain
In several cases I observed about 81 percent develop dementia/Alzheimer's. Loneliness seem to play a big role in triggering the disease more rapidly than usual...Looking at three individuals Mr. Carl Thomas. Tracy Richard and Ann Thompson, in each case shortly after these individuals had left alone to live on their own dementia came on rapidly then after a short time full blown Alzheimer's. Could it be the love, closeness and comfort they had with their wife, husband and children before which may causes the disease to be suppress.

What is Alzheimer's?Alzheimer's is a progressive, degenerative disorder that affects the brain, it damages the brain cells responsible for intellectual functioning in the brain, including memory, intelligence, judgment and speech ... Alzheimer's lead to the loss of mental and physical functions.

Today a rare and aggressive form of Alzheimer's can happens in some people in their 30's and 40's.

Individuals with Alzheimer's loose their ability to perform the basic tasks that are part of every day life and up requiring constant care and supervision.

Alzheimer's statistics

* Over 8 million people in the United States and well over 30 million world wide suffer from Alzheimer's.

*Every 22 second someone some where in the world gets Alzheimer's disease.

*The average course of the disease from the time it is diagnosed to death is about 4 to 7 years.

Remember anyone can get Alzheimer's, many individuals who get Alzheimer's disease in the third world countries do not have anyone to take care of them so many ends on the street and in homes for the insane and crazy individuals only to get mistreated by other people.

Alzheimer's cost

The national tab for caring for individuals with Alzheimer's disease is estimated at well over $100 billion annually, and by 2050 it will be over $ 450 billion annually.

Alzheimer's disease costs U.S. businesses more than $80 billion annually, stemming from lost productivity and absenteeism by primary caregivers, and insurance costs.

The annual cost of caring for one individual with Alzheimer's disease in America ranges from nearly $18,800 to more than $43,000 today depending on the stage of the disease.


Alzheimer's find out more
Individuals with early-stage Alzheimer's account for about half of all Americans afflicted with the disease.
Until recently, doctors assumed there wasn't much to be done once a person was diagnosed with Alzheimer's patients were sent home with kind words, drugs that had a mild impact on symptoms and perhaps some advice on how to deal with the inescapable changes in their brains and the inevitable changes in their lives.
Now for example, the studies in mice engineered to carry the human gene for Alzheimer's, one, published in the Journal of Neuroscience, showed that the simple act of learning could have a profound impact on the buildup of the distorted proteins that cause memory loss in both humans and mice afflicted with the disease, Scientists form that mouse that had periodically been forced to learn to navigate a maze ended with fewer plaques and tangles of protein than intellectually idle ones.
So far, there's no proof that mental exercises can stave off Alzheimer's, but growing evidence suggests that it might be possible to slow down the disease impact. This doesn't necessarily mean that the mental activity prevents Alzheimer's. It's always possible that the people with the healthiest brains were able to stay more mentally active. Still Scientists say, the research does suggest that mental activity might help slows the symptoms.
Today Scientists are saying information stored in episodic memory is like the narrative of a short story. This kind of memory depends on the hippocampus, a part of the brain hit hardest by Alzheimer's. The brain regions involved in another kind of memory ... procedural memory... are less affected by the disease. Procedural memory is what allows us to learn a difference subject or language.
Alzheimer's. As the disease progresses, it robs the individuals of their memories and changes how they both think and behave. It's ultimately fatal.
Experts in the field of dementia/Alzheimer's had a meeting in Washington, DC 09/16/07 on dementia/Alzheimer's disease and its coming destructive progressive behavior to so many worldwide...It is very critical for Scientists Dr. Thomas Hall stated from W.H.O to find a cure or maintain it. More than 30 million people today have this brain wasting disease and this number will quadruple, to over 130 million by 2050. By 2050 1 in 78 persons worldwide especially those in the third world countries who will see a rapid increase in Alzheimer's disease. The problem today in most cases is Alzheimer's disease is very difficult to detect until it has progressed from mild memory loss to clear impairment. Patients eventually lose all ability to care for themselves.
Who may get Alzheimer's
Experts now said those who most often are anxious or depressed were 40 to 50 times more likely to develop mild cognitive impairment, a form of memory loss that is often a transitional stage between normal aging and dementia. Not only are these individuals losing cognition, but they are showing many of the changes in the brain that associated with Alzheimer's disease.
In early studies, some Scientists found people who are more prone to distress are more likely to develop Alzheimer's disease than their more carefree counterparts.
People with mild cognitive impairment have some trouble remembering things, but they do not have significant disability.Not all people with this problem develops Alzheimer's disease, a much more serious impairment, about 20 percent do, according to several scientific reports.

Questions ask by most people

  1. How can we tell if memory loss is caused by Alzheimer's disease?
  2. Are there any symptoms I should watch for and report?
  3. What should I expect if it is Alzheimer's disease?
  4. When should I come back for another visit?
  5. Where can I go for more information?
  6. If the memory loss is caused by Alzheimer's disease, which treatment is most appropriate?
Here are some of the symptoms
  • Short-term memory loss, like repeating the same question several times.
  • Trouble remembering easy words, like saying "that thing I write with" instead of "pen or pencil ."
  • Not wanting to do things you usually enjoy doing such as cooking.
  • Making bad judgments, like turning the heat up too high, leaving the stove, walking out into the pouring rain without an umbrella, forgetting where you put your keys, to eat, or giving lots of money to a stranger for no reason, getting lost.
  • Extreme personality changes, mood swings and getting upset easily.
  • Confusing things and people from the past with things and people from the present.
The latest test, and research suggests that chronic stress may harm parts of the brain responsible for responding to stress ... an area that is also associated with memory.
Studies have shown that while these medications such as Namenda and Aricept don't stop or slow down the disease, they can tune up the brain but they cannot stop Alzheimer's disease. There are no cure for Alzheimer's disease today on the market any where in the world.
We at the Mary Joseph Foundation are working with several organizations and doing everything possible to help find a cure for this deadly disease while at the same time we are helping patients who have Alzheimer's disease by giving them rooming, loving care, foods, vitamins, Memory Companion and removing them from the street who are homeless and from mental disturb homes and care for them. Our services are FREE.
Our mission
The Mary Joseph Foundation is interested in building relationships with more companies here in America to help increase awareness of dementia/Alzheimer's disease, our organization generates funds to further our mission.

We are eager to work with you and your company to explore how the Mary Joseph Foundation can best support your business goals and objectives. There are several ways we can work together include cause-marketing programs, product royalty promotions, ads and special events here in America and abroad.

Our mission is to eliminate dementia/Alzheimer's disease and to provide the best care and support to those living with Alzheimer's disease here in America and around the world.

Mary Joseph Foundation a non-profit international organization.
Register with the Federal government and incorporated in the state of New Jersey.

Monday, January 4, 2010

Progressive memory loss.

 

This is the hallmark of Alzheimer's disease. Initially, only short-term memory is impaired, and the person merely seems forgetful. But because short-term memory is essential for absorbing new information, the impairment soon interferes with the ability to interact socially and perform one's work. Long-term memory may be retained longer, often in great detail, but it becomes fragmented as the disease progresses. Toward the final stage, people with Alzheimer's may be unable to recall their own names.

The cerebral cortex

The third level of the brain is the cerebral cortex, commonly called the "gray matter." The cerebral hemispheres contain two specialized regions, one dedicated to voluntary movement and one to processing sensory information. But most of the gray matter is the association cortex, which becomes progressively larger as animals move up the evolutionary ladder. The association cortex is the region of conscious thought: It is where you store memory and language skills, process information, and carry out creative thinking.

Inside the brain

Inside the brain
In Alzheimer's disease, brain cells die and neuronal connections wither in all parts of the brain, but especially in the hippocampus and the amygdala — important parts of the limbic system that coordinate memory storage and recall — and the cerebral cortex, the seat of higher-level thinking, memory, and language.

A micro view of the brain

Up close, the brain is a web of interconnecting cells called neurons. How these cells communicate and what happens when these cells die form the basis of our understanding of brain disease.

How brain cells communicate

The neuron is the brain's basic unit for processing information. The human brain contains an incredible number of neurons — about 100 billion, give or take 10 billion. The neuron is a unique cell in activity and appearance. It generates both electrical and chemical signals, making it able to communicate quickly with distant neurons. Instead of the compact shape typical of other cells in the body, the neuron is like an oak tree with giant branches stretched out. Each neuron has a body containing a nucleus, one long fiber called an axon, and many shorter branching fibers called dendrites.

The neuron is both a receiver and a transmitter. When a neuron receives a signal, it generates an electrical impulse. This impulse travels through the neuron and down the axon to its end (the axon terminal). The signal is then passed on to other neurons. Viewed under a microscope, neurons look like a dense forest of trees whose branches are so closely intertwined that they appear to touch. But when the details are highlighted with a silver stain, it is clear that each cell is separated from its neighbors by tiny gaps called synapses. Because the electrical signal cannot bridge this space, some other mechanism is required for a neuron to communicate with its neighbors. This is where the neuron's chemical signal comes in.

Stored in the axon terminal are chemical messengers called neurotransmitters. The electrical impulse opens tiny pores in the axon terminal, allowing a supply of neurotransmitters to flood into the synapse. The chemical then attaches to receptors on a neighboring neuron. What happens next depends on whether the neurotransmitter has an exciting or inhibiting effect on the neuron.

How nerve cells communicate

How nerve cells communicate
  1. Electrical signal travels down axon of neuron.
  2. Chemical neurotransmitter is released.
  3. Neurotransmitter binds to receptor site.
  4. Signal continues into new neuron.
  5. Reuptake occurs; neurotransmitter is transported back into the cell that released it.
An excitatory neurotransmitter passes the message on by creating an electrical impulse in the cell that receives it, and the process of electrical-to-chemical signaling is repeated. But if an impulse were to be transmitted to every neuron in the brain, the result would be chaos; much like a power surge can cause a short circuit, neurons firing all at once would cause a prolonged epileptic seizure. To safeguard against this happening, inhibitory neurotransmitters suppress communication to neighboring neurons.

Of the more than 20 chemical messengers discovered thus far, a few are fairly well understood. Several of them are involved in memory, including acetylcholine, serotonin, and dopamine. Many of these neurotransmitters have additional functions; for example, serotonin helps regulate sleep and sensory perception, while dopamine helps regulate movement.

As biological processes go, the speed of thought is rapid (although slow compared with a computer). Electrical impulses in some neurons reach speeds of nearly 200 mph, and transmission from cell to cell takes about a thousandth of a second. In addition, one nerve cell may have more than 1,000 synapses and, with a single impulse, can transmit simultaneously to all its neighbors.

Plaques and tangles

Plaques and tangles
The brains of Alzheimer's patients contain neurofibrillary tangles inside neurons and clumps of fibers called neuritic plaques outside of neurons. A set of enzymes, called secretases, in the neurons cause plaques to form. The secretases snip pieces from a large amyloid precursor protein (APP), leaving behind fragments of amyloid proteins that snarl and clump with the debris of dying neurons (pieces of dendrites). In contrast to the neuritic plaques, neurofibrillary tangles form within neurons and are composed of aggregates of a different protein known as tau.
Beta-amyloid is a peptide composed of approximately 40 amino acids. Research has shed light on the chemical process responsible for the formation and deposit of this sticky, starchlike protein in the brains of Alzheimer's patients. This understanding has prompted pharmaceutical companies to start manufacturing drugs to block the formation of amyloid deposits (see "Amyloid production blockers").

These tangles and plaques, first described by Alois Alzheimer in 1907, have been the main focus of research for decades, and for good reason: The worse the mental deterioration, the more amyloid and tangles are found in brain tissue. The prevailing view among neurologists used to be that these deposits caused the mental changes in Alzheimer's disease.

However, tangles and plaques are not unique to this condition. Some are found in other dementing disorders, and a few are scattered about in the brains of healthy middle-aged and elderly people. Some neuroscientists have wondered if these occasional deposits might explain the mild forgetfulness associated with normal aging, but studies have cast doubt on this theory.

Studies now indicate that dementia in Alzheimer's patients is caused by the shrinkage and death of neurons and synaptic loss, not by tangles and plaques themselves. However, according to the leading hypothesis, amyloid deposits play an early role by setting in motion a cascade of biochemical events that causes the cells to shrink and die.

With advances in technology enabling them to count neurons, neuroscientists were able to make this discovery by examining brain tissue from 10 people with normal brain function who died after age 60. All the samples contained about the same number of neurons in an area of the association cortex richly supplied with nerves from the sensory region. For the first time, scientists had a standard for defining how many neurons were "normal" in the human brain. Furthermore, this finding indicated that neuron loss was not a product of normal aging.

Next, the researchers compared the normal samples with brain tissue from 10 people with Alzheimer's and discovered, on average, a 41% reduction in the number of neurons. And the longer dementia had been present, the fewer neurons were found. There was also a correlation with neurofibrillary tangles: People with the greatest neuron loss had more tangles, about 95% of which were inside the remaining neurons. However, loss of neurons was dramatically greater than the number of tangles.

The researchers offered "housekeeping" as a possible explanation for this discrepancy: Molecules that clear away dead cells in the body eventually removed the tangles. When they counted neuritic plaques, the researchers found no relationship with either neuron loss or disease duration, reinforcing the view that neuronal dysfunction and death cause dementia. Although tangles and plaques are still considered the diagnostic hallmarks of Alzheimer's disease, synaptic loss and neuron death correlate best with dementia.

Experts also believe that decreased levels of the neurotransmitter acetylcholine, a chemical that bridges synapses between neurons that affect memory, also contribute to the memory loss of Alzheimer's disease. In the cortex and hippocampus, where this neurotransmitter is needed for memory and learning, the acetylcholine-producing neurons (called cholinergic neurons) are normally plentiful. But of the several types of neurons that can degenerate in Alzheimer's disease, the cholinergic neurons are especially hard hit. As acetylcholine production falls in the cortex and hippocampus, dementia becomes progressively worse. By the time someone with Alzheimer's disease dies, the cortex may have lost 90% of its acetylcholine.

Other neurotransmitter abnormalities may also be present. Reduced levels of serotonin and noradrenaline have been found in some people with Alzheimer's disease. Imbalances among these and other neurotransmitters could explain why some patients experience sensory disturbances, depression, sleep problems, aggressive behavior, and mood swings.

Mary Joseph Foundation