Introduction to Alzheimer’s
Alzheimer’s disease is a progressive degenerative disease of the brain. It is first described by the German neuropathologist Alois Alzheimer (1864-1915) in 1905. This disease worsens with advancing age, although there is no evidence that it is cause by the aging process. The average life expectancy of a person with the disease is between five and ten years, but some patients today can live up to 15 years due to improvements in care and medical treatments. The cause of Alzheimer’s has not been discovered yet and it cannot be possible to confirm a person has Alzheimer’s until their autopsy following death.
How does Alzheimer’s develop? What causes Alzheimer’s? Well no one knows exactly the Development of this debilitating disease. But recent advances have produced several clues as to how it is born. Initially when we study the brain of an Alzheimer’s victim, we focus on two specific areas. One is the cortex of the frontal and cerebral lobes. (Ramanathan, 1997) The second is the hippocampus which is located below the cerebral cortex and responsible for short-term memory. If we study samples of these two section, we would find three irregularities which are not found in normal brain matter. These three are called neurofibrillary tangles, neuritic plagues and granulovacuolar degeneration. (Heston, 2003)
A nerve cell has numerous axons and dendrites coming out of it. A neurofibrillary tangle is when the neuron changes. A number of dendrites are missing and the nucleus is filled with protein filaments resembling steel wool. (Gelb, 2000) Although all elderly people have a few of these helix shaped bundles in their brain for they are normal indicators of aging, Alzheimer’s patients have more than usual. Their presence usually in the frontal and temporal lobes is a indication of AD.
Senile neuritic plagues are small round objects. They are masses of amyloid protein material composed of residue left over from healthy nerve endings that were broken off and decayed. Their presence near the cell further indicates something gone wrong. Neuritic plaques are the best evidence for diagnostics to make the determination of AD.
A third sign of neuron deterioration is granulovacuolar degeneration. This is when fluid-filled vacuoles are seen crowding inside the nerve cell, specifically in the triangular shaped cells of the hippocampus. This condition can only be observed in carefully sliced, stain and analyzed brain tissue. The cell having lost all it’s dendrites and nucleus soon disintegrates entirely, vanishing into the body’s waste disposal system. With the depletion of enough nerve material the brain actually shrinks, sometimes by as much as ten percent. (Bassiony, 2000) The more cells the AD sufferer loses, the more mental functions he loses. Soon the person will have limited motor skills. People who were once witty and quick on their feet were reduced to the mental status of small children.
Diagnosis of Alzheimer’s
How would you now if a person you knew has Alzheimer’s? There are certain telltale signs that point to it. There was one patient that was convinced she was suffering from AD. As proof of her condition, she bought a meeting several recent newspaper clippings, which she began to quote from memory. Obviously this person did not have the disease; she wouldn’t have memorized complex and lengthy information. But forgetting on a regular basis doesn’t indicate Alzheimer’s either.
In the initial stage, there is no clear evidence of memory trouble and deterioration in brain functions. The individual performs well on exams that test mental abilities similar to those given to measure IQ. In the second stage, the patient shows very mild memory problems with difficulty in remembering names of friends. The changes at this point are still very small. Occasionally, the patient might make a surprising statement such as inquiring about the health of a friend who everyone knows, died years ago. Only extensive psychometric testing can determine if the person’s mental ability changed. A close family member like a husband or wife might suspect something is wrong.
By the third stage, there is definite evidence of memory loss, which might interfere with job performance, the person might have difficulty competing a job that use to be routine. The person may avoid social situations because he or she realizes there’s a problem. In stage four there is clinical evidence of memory impairment when the mental status is tested by doctors. The disease has now become obvious to the family.
A sign of this stage is when the patient keeps asking the same question which has already been answered, this make daily companionship difficult because his friends and family are frustrated. By stage 5, the patient show problems with both recent and past memories, they even forget events that are important like Christmas, birthdays, friendships and interests. Judgment is failing; the individual is no longer able to select clothes for a particular weather of season and cannot match items by color. Eventually, the victim of AD may leave the water running, the stove on, or the front door open. At this point wandering becomes a major problem.
In stage six, understanding of languages diminishes and simple commands aren’t understood. Victims may go back to their first language if they have one. Eventually languages disappear entirely. In stage seven or the terminal stage, the victim becomes bedridden and totally dependent for all functions. He cannot speak coherently and can’t eat unassisted. Death usually occurs at this stage form aspiration pneumonia, pneumonia caused by breathing in food or other objects because the victim doesn’t remember how to swallow food safely, or from urinary infections.
Recent Research on Alzheimer’s
Some progress has been made in understanding the nature of the Alzheimer’s disease. Scientists have recently found medicine that can slow down the progress of AD. The average survival period from the time of diagnosis to death in 1985 is 10 years. Today the rate has increase a third to 15 years. (Harwood, 2000) A recent media release stated the discovery of a mutant gene called ‘triplet repeat’ disease genes. These genes produce proteins that may block from properly functioning key enzymes that are important to the production of energy in the brain. This gene was found in several diseases like AD, Huntingtons, and Haw River Syndrome as well as three other rare neurological disorders.
Another press release from the Alzheimer’s Association is one concerning the new study of an important advance toward early detection of AD. ‘Through investigations such as these, in addition to those involving apolipoprotien E (APOE), positron emission tomography (PET), and other approaches, we will improve our ability for accurate detection of individual at risks for the disease’ (Waite, 2000) said Zaven Khachaturian Ph.D., director of the Alzheimer’s Association’s Ronald and Nancy Reagan Research Institute.
Among the drugs being tested to treat AD are:
- Cholinergic agents: choline, lecithin, and the agonist (RS 86, arecholine, and bethanechol)
- Peptides: vasopressin, ACTH 4-10, naloxone
- Nootropic agents: pramiracetem, CI 911, Praxilene, Oxiratem
- other general drugs: chelating agents, Nimodipine, Vinpocetine (Alloul, 1998) most of these are still in experimental stages. Some has proved to work slightly but is generally unsafe, others has tested safe but not beneficial, but none has been both. People who offer ‘cures’ to Alzheimer’s are either frauds or ignorant. (Bootman 1996).
When people realizes that AD is a serious disease, perhaps as much as HIV, then maybe they will pay attention. The reason why there hasn’t been a cure is because scientists tries to attract grants by working on a problem that people think is serious and controversial. If there was as much attention that was paid to AIDS as there was in AD, then maybe there will be an answer.
Many people are left confused and are unsure about what Alzheimer’s disease is, how to care for Alzheimer’s patients, and how to lower their risk of getting the disease. Research has shown many different ways to lower risk. One being folate intake, another is anti-hypertensive medication, and last nanoparticle radiation is used to slow down the progression of Alzheimer’s.
The first patient of Alzheimer’s was first recorded in 1901, and was examined by Alois Alzheimer. Alois Alzheimer was an assistant medical officer at the municipal mental asylum, Frankfurt, Germany. Alois was very interested in dealing with people that have a mental illness. Alois’s first recording of symptoms of Alzheimer’s included rapid increasing memory impairments, the carrying of objects around then hiding them, jealousy towards family members, and patients being paranoid (Busschbach, 1998). Alzheimer’s disease has received and increased interest in the years since it was first discovered. This is because the affected population is growing.
Age seems to be the only clear risk factor for the disease. Researchers have also found that people who carry the gene for the protein, Apolipoprotein E4, are at a higher risk; however, no all people with the gene develop Alzheimer’s (Gray, 1993).
Mental status testing is used to help the physician determine the extent of cognitive and behavioral impairment. The patient is asked to answer questions and perform tasks. Example questions may include: “What is today’s date?” “Who is the President of the United States?” Tasks may include putting paper in an envelope, naming objects in a photo, or repeating words that have been said a couple of minutes earlier (Holmes, 1994). Brain scans provide images of the brains structures.
Computed Tomography (CT), also called Computerized Axial Tomography (CAT), or a Magnetic Resonance Imaging (MRI) are a diagnostic routine of someone who has the symptoms of Alzheimer’s. Most families are often worried about telling someone who has been diagnosed with Alzheimer’s disease. Physicians say that it is best to be hones and let the patients know exactly what is going on. The patients, if able to comprehend, are relieved to know they are not “crazy” (Cayton, 1993).
Patients with Alzheimer’s disease are prone to a number of accidents. This makes caring for Alzheimer’s patients somewhat difficult. In the early stage traffic accidents are often and alert that an individual’s mental function are decreasing. Common driving problems include becoming lost and failing to stop at traffic lights or stop signs. This is what happened to my grandmother. Also in stage one, patients often lose their way. Many have gotten on trains or buses and some found wandering miles away from home. My grandmother tried to walk out of her nursing home one night because she said someone had kidnapped her and she was trying to get home. Poor Judgment and gullibility are also included in stage one (Cavallo, 1997).
In the second stage, patients with Alzheimer’s main accidents are repeated falls and a number of personal injuries. The Alzheimer’s patient reacts more slowly, which makes it difficult for him/her to regain their balance. Caregivers need to make sure the patient’s surroundings are free from hazards. Fire hazards, bathing, poisonings, medication, wandering, and pica are included in this stage. Many patients are not aware of the mentioned hazards and can easily cause harm to themselves (Knapp, 1998).
In the last stage, the patient has a number of physical disabilities in addition to his mental impairment. Because of this, he/she is much more at risk of falling becoming incontinent, and becoming dehydrated. Safety and accident prevention for patients with Alzheimer’s disease pose many difficulties for the caregivers. Being away of potential hazards and realizing that the patient can no loner be responsible for his/her own safety is the first step in preventing accidents Providing a safe environment, either at home or in the nursing home, can lessen the strain on caregivers. Patience is required to make an environment safe yet stimulating for patients with Alzheimer’s disease (Hux, 1998).
Researchers say that an intake of folate at or above the recommended daily allowances of 400 mcg may reduce the risk of developing Alzheimer’s disease by up to 55% (Nagaratnam, 1998). You can either achieve this by taking a folic acid pill or eating lots of fruits and veggies. Eating all the healthy foods that contain folate leads to a very healthy life, both physically and mentally. The study compared diets of non-Alzheimer’s disease patients, 579 primarily white women and men at the age 60 or older, comparing the nutrient intake of those who later developed Alzheimer’s to the intake of those who did not progress to the disease (Volicer, 1994).
Participants were followed for up to 14 years. During this study, 57 developed Alzheimer’s. Those with higher intake had lower rates of the disease (Weinberger, 1993). The only question this study produces is does folate have an effect on Alzheimer’s. It was stated, but not proven in full explanation. Researchers also have stated that anti-hypertensive’s may reduce the risk of getting Alzheimer’s. Researchers in Utah did a long-term survey where 3,308 participants were interviewed, and all were 65 years and older. 90% of the interviewed were Mormons. They were asked medical history and medications that they were using all were considered Alzheimer’s free (Weiner, 1998).
A couple of years later, the participants were tested over, in which one hundred had developed the disease. The study shows that among the participants, the ones that were anti-hypertensive users had a risk reduction in getting Alzheimer’s. The question that this study seems to leave out, in my opinion, is that could sex, age, race, or any factor in that nature with the use of an anti-hypertensive make the risk less or more. This was not mentioned in this research.
Last is the research on nanoparticle radiation, and how it may slow Alzheimer’s disease. Chemists in Chile and Spain have identified a treatment they say has the potential to destroy beta-amyloid fibrils and plaque-hypothesized to contribute to mental decline; the researchers call their method a type of “molecular surgery”, and it could halt or slow the disease’s progress with out harming healthy brain cells (Whitehouse, 1997).
Using test tube studies, the scientists attached gold nanoparticules to a group of beta-amyloid fibrils, incubated the resulting mixture fro several days, and then exposed it to weak microwave fields for several hours. The fibrils dissolved and remained so for a week after being irradiated, indicating that the treatment not only was effective at breaking up the fibrils, but resulted in a lower tendency of the proteins to build up again.
The symptoms are not the same in each person. Some people develop symptoms very fast. For instance they start off having short loss of memory then all of a sudden they get to the point where they can not remember much of anything. Others it can take 8 to 10 years for the symptoms to get worse (1998-2003 Mayo Foundation for Medical Education and Research (MRMER)). Some people just mistake some of these things with old age. They feel that just because they are forgetting things, feeling tired or losing things that they are just getting old and they do not seek attention from their doctors. This could end in a very difficult situation for them and their loved ones. By seeking advice from a doctor, a person with Alzheimer’s disease can prolong their lives and be able to enjoy everyday things.
The exact cause of Alzheimer’s disease is still uncertain. Most researches today believe the immediate cause of Alzheimer’s disease is the abnormal build-up in the brain of a substance called amyloical beta peptide. In the early 1980’s some researchers found aluminum in the cores of senile plaques. The fact that aluminum was found close to AB deposits in senile plaques suggested that it might be a cause of Alzheimer’s disease. They found high aluminum levels in the blood of dialysis patients, who sometimes developed Alzheimer’s disease. They began to look for aluminum in the brains of Alzheimer’s patients.
Some studies did in fact find high aluminum levels in the brains of patients. However, just as many of their studies found that there was no aluminum in the brains of patients. Other metals, such as silica, iron and zinc were also found in senile plaques, along with the aluminum. With these results there was a doubt that aluminum was the cause of Alzheimer’s disease. Scientists also believe that the brain chemical call acetylocholine helps memory work.
They also suspect that not having enough of this chemical plays a role in Alzheimer’s disease. Although they don’t really know what causes Alzheimer’s disease, they do know physical changes take place in the brain (Gutterman, 1999) This disease effects brain cells called neurons, this is what makes us think, remember, and speak. When people grow older sometimes deposits form called plaques and tangles. But in Alzheimer’s patients they have found that they have many more of these deposits, which causes them to have trouble thinking, remembering, and doing everyday tasks that were at one time simple for them.
There is no simple physical or mental test to find out if a person has Alzheimer’s disease. Healthcare providers combine many methods to diagnose Alzheimer’s disease, beginning with a medical history and a physical examination of the person thought to have Alzheimer’s disease. They also check on the family history of patients, people who have had a immediate family member that has had the disease have a higher chance of getting Alzheimer’s disease. After age 65 the chances of getting Alzheimer’s is higher. Although it is very rare Alzheimer’s disease can also affect people under the age of 50. Studies also show that women have a higher risk of getting Alzheimer’s then men do.
A complete exam may include tests of memory, attention, language, judgment, and problem solving. They may ask the individual, a family member, or a close friend about this person’s ability to do daily activities such as: Eating, Bathing, Walking, Dressing, Shopping, Cooking and using the phone. Often the doctor or other healthcare provider will recommend that a diary be kept of the person’s symptoms and behavior over time to keep track of any changes. Changes in mental and physical function are very important in making a correct diagnosis. Healthcare providers may use various tests to make sure their diagnosis is correct.
There are three main stages in Alzheimer’s disease. The mild stage is the early stages of Alzheimer’s disease, this is when the person starts to lose there short term memory. They may also complain of losing things or forgetting names of people they are close to. They may forget places they need to go, things they need to do, people they need to call or that just called them. They may be walking across the room and forget where they are going and why they are even there in the first place.
This stage of Alzheimer’s, people are still able to live on there own but may need some help. The moderate stage of this disease is where people tend to need more help with most everything. Those around them also start to notice more clearly the problems the person with Alzheimer’s disease is having. They need help with basic self care and cleaning house, doing yard work becomes more of a problem to them. Cooking and also dressing themselves is harder without help.
They tend to get more frustrated, due to the fact that they need helping doing things they were once able to do on their own. They also may start to get angry and they fear new surroundings and people. They also may become suspicious or paranoid. Although their loved ones see what is going on, people with Alzheimer’s do not realize at the time or sometimes at all what they have said or done.
The last stage is the severe stage of Alzheimer’s. This is the worse stage for them and those around them. They become unable to feed themselves, therefore causes weight loss and malnutrition. They may also have a hard time controlling there bowels or bladders. In this stage people with Alzheimer’s forget pretty much everything. They don’t remember who people are, or even who they are. They forget where they are and what they are doing altogether.
They also have a hard time of saying simple words. They may be trying to say one thing and it comes out as something different. Sometimes they lose there ability to even speak. When loved ones come around they know that you mean something to them, but they don’t know how or who you are. People with Alzheimer’s can live for 7 to 10 years, others live for as many as 20 years beyond there diagnosis.
Alzheimer’s disease is a degenerative brain disease. It is caused by a slow break down of the brain cells. This is caused by unknown reasons but it is believed to be caused by renegade proteins surrounding and destroying brain cells. AD is actually quite random toward its victims. The greatest risk factor for the disease is age. Alois Alzheimer, a German physician, first discovered Alzheimer’s disease in 1906. The first recorded case of Alzheimer’s disease was a 55-year-old woman. She was admitted to the mental asylum where Alzheimer worked when she was 51 and slowly deteriorated over her 4 years there. After her death, Alzheimer performed an autopsy in which he found a small, shrunken brain. This was the start of Alzheimer’s research.
Since its discovery, Alzheimer’s disease hasn’t evolved much. It’s much more common now and the symptoms are slightly enhanced, but the disease is relatively the same. The number of people with Alzheimer’s disease is expected to increase dramatically as the baby boomers age, and by 2050 it is believed that there will be over 14 million Americans with AD. Some scientists believe that Alzheimer’s disease may be caused by a mutation of a gene on chromosome 14; this mutation is related to about 8% of all Alzheimer’s cases. According to the Alzheimer’s disease and Referral Center statistics up to 4.5 million Americans suffer from AD.
The disease usually begins after age 60, and risk goes up with age. While younger people also may get AD, it is much less common. About 3 percent of men and women ages 65 to 74 have AD, and nearly half of those age 85 and older may have the disease. The early stages of the disease are often viewed as the consequences of aging, so Alzheimer’s often goes undiagnosed.
There are several stages to Alzheimer’s disease. In the early stages people forget recent events, but they clearly remember things that happened many years ago. In the later stages of the disease, people can no longer remember past events and often do not recognize their family members. Some victims do not even recognize themselves. Alzheimer’s victims often suffer from impaired judgment. They may touch a hot stove burner not remembering that it can burn them.
There have been cases where people with Alzheimer’s disease nearly starve because they forget to eat for days. The disease can also cause people to be very tired. Patients may also have trouble with place and time. They may not recognize their own home of many years, and they may confuse morning with afternoon. Some patients with Alzheimer’s disease will revert back to an almost child-like state. Some of the victims are very angry and aggressive while others are very calm and quiet. How fast the disease advances varies from person to person.
Eventually, most people with Alzheimer’s disease become unable to care for themselves. Alzheimer’s disease is not the direct cause of many victims’ deaths. The disease renders the patients bedridden and in their weakened condition they catch viruses such as pneumonia. AD can kill though because in advance stages the victim’s brains cannot perform life sustaining functions. Alzheimer’s does not occur more in men or woman, but the disease is more prone to Caucasian people.
Out of all the cases of Alzheimer’s in the United States, about three-fourths of them are white people. Scientists do not know why this is, because African American brain cells are the same as those of white people. Some scientists say that Alzheimer’s disease is genetic, and it may be. Scientists say that if the disease is genetic, then it only occurs in every 4th or 5th generation, but that the disease must be “turned on” by some outside factor.
Doctors can’t seem to figure out what the outside factor is. Some scientists even believe that Alzheimer’s may be caused by an excess of estrogen in the brain. Alzheimer’s disease is considered non-reversible. Many of the symptoms can be treated, but not the actual disease. To date, no chronic degenerative disease, Alzheimer’s or others, can be cured. Most therapies currently being used are experimental.
The drugs Tacrine and Donepezil are the only two drugs proven effective in slowing the progress of Alzheimer’s disease, and even they only have a temporary effect. Selegilin, the drug used to treat Parkinson’s disease, has been shown to delay symptoms of Alzheimer’s by about seven months in test cases, but doctors are not sure if this drug is safe for people yet. Some doctors suggest for people to take one ibuprofen a day, to help lower the risk of developing Alzheimer’s disease. Daily supplements of vitamin E can help too. Thanks to medical breakthroughs and healthier lifestyles, Alzheimer’s patients can live longer then ever.
There are no screening tests for Alzheimer’s disease. In fact, brain tumors, blood clots, hypothyroidism and vitamin deficiencies have all been mistaken for Alzheimer’s. The reason for these mix-ups is that a head scan can not show Alzheimer’s disease until well in to the disease. If the tumors or clots are small enough they might not be seen either and can produce nearly the same results. Alzheimer’s disease is a serious and growing medical, social and economic problem. It affects millions of people in the United States and millions more around the world. When we look at elderly people and cast them off as crazy or senile we should stop and consider the root of their problems. We know more about the disease now then at any other time in history. Doctors are closer to a cure then ever, but until there is a cure for Alzheimer ‘s disease, we are all at risk
The major development that leads to Alzheimer’s disease is the build up of amyloid plaque. Amyloid plaque is term referring to the clustering the peptide (protein) amyloid beta. The presence of amyloid plaque can be detected post mortem and is integral in the diagnosis of Alzheimer’s disease. The amyloid beta protein is itself a segment of a much larger protein known as amyloid precursor protein (APP). APP is a normal neurone membrane protein that is synthesized within the cell, transported to the cell membrane then later broken down.
There are two major pathways of enzyme cleaving involved in the breakdown of amyloid precursor protein. It is only one of these pathways that leads to the formation of the amyloid beta peptide. The enzymes that cleave APP are known as secretases. Alpha (a) secretase and beta (B) secretase initially compete to cleave the APP. If a-secretase cleaves the amyloid precursor protein, there is no amyloid beta produced. If however the b-secretase succeeds, the APP can be further cleaved by gamma (y) secretase to form either one of two variants of amyloid beta protein.
The amyloid plaque collects on blood vessels in the brain and also on the membrane surfaces of neurons, ultimately leading to their death. The plaques binding onto and inserting themselves into the neuron membranes interferes adversely with the cells usual function and also facilitates leaking of extracellular substances into the cell, leading to neuron dysfunction and death.
In Alzheimer’s disease, the immune response of the body often does more to further the disease rather than fight it. Astrocytes and microglia are glial cells of the central nervous system. These cells are major participants in the immune response that the nervous system undergoes. In the course of Alzheimer’s disease, astrocytes become activated and initiate a inflammatory response mediated by prostaglandic and arachidonic acid.
These acidic conditions enhance the aggregation of amyloid beta, stabilising and accelerating the formation process of Aß plaques. The microglia serve a similar function to that of macrophages outside the brain. These are phagocytic cells that destroy pathogens and cellular debris within the central nervous system. They are usually scarce but multiply rapidly in response to injury or infection, gathering around the amyloid beta plaques.
The activation of microglia by Aß causes them to synthesize inflammatory cytokines such as InterLeukin-1B (IL-1B). This cytokine IL-1B then aggravates the immune response even further by promoting the synthesis of amyloid precursor protein (APP), and promoting the production of amyloid beta (Aß) binding proteins by astrocytes. Activated microglia also produce free radicals that are damaging to the neurons. The various processes that take place in the immune response can ultimately lead to more amyloid plaque building to cause more neuron death.
A major cause of neuron death associated with Alzheimer’s disease is the formation of NeuroFibrillary Tangles (NFT). NFT’s are pathological build ups of proteins found in the cytoplasms of neurons in the cerebral cortex. They are most common in the temporal lobe structures and can be clearly identified after death through use of microscopes. Substances needed for cell regulation and nutrition of the cells are transported along microtubules with neurons.
As nerve cells are among the largest cells in the human body, the structural integrity of the microtubules is vital for normal cell function. Tau is a microtubule associated protein that is integral in maintaining the structural integrity of the microtubules. Tau is the protein affiliated with the development of NFT’s. In Alzheimer’s disease, the Tau proteins become abnormally hyper-phosphorylated and lose their capacity to bond to microtubules. Instead, the proteins bind to one another, knotting and aggregating themselves into insoluble tangles. Due to this knotting, the microtubules within a neuron become no longer functional. A neuron packed with NFT’s rather than functional microtubules cannot maintain life and quickly die.
Changes in the brain characteristic of Alzheimer’s disease range from atrophy of actual brain tissue, increased levels of immune response related cells such as microglia, reduced levels of many neurotransmitters and formations of amyloid plaque buildup and neurofibrillary tangles. Neurons are the main functional units of the nervous system, without them the system cannot function. This Gradual loss of neurons is what leads to the eventual dementia of Alzheimer’s patients. Alzheimer’s disease destroys the brains structure through the death of neurons, this destruction of the brains structure inevitably begins to lead to loss of brain function and eventually the loss of any ability to think or even to recognise that one is still alive.
For decades, Scientists have been trying to unravel the mystery of what exactly causes AD. Professor John Edwardson at the neurochemical pathology unit of Newcastle-upon-type General Hospital studied the belief of how Aluminium causes AD. His research team noticed that in areas of an AD patient’s brain, there were traces of aluminium. After this observation, he conjured up the aluminium theory which claimed aluminium was the reason for AD.
To justify his theory, Edwardson noted how patients of renal dialysis (a disease affecting the kidney) used to take large amounts of aluminium to treat their disease was seen to have a higher risk of developing AD than those treating it from the water supply. However other researches argued that aluminium is not a cause for AD saying that it (aluminium) was naturally present in older people who were not suffering from AD. The excess of aluminium found in AD patients is also very small. The Aluminium theory is still very controversial and needs further research because everyone is exposed to this due to it being present in the environment. Scientists are still trying to figure out why aluminium may cause people to have AD and how it got there.
A study by the University of Washington published in 2003 showed how people who stress a lot are more likely to develop AD than those who do not. Robert S.Wilson, PHD of Rush University Medical Centre in Chicago and his research team were responsible for this study. He says “Since chronic stress has been associated with changes in the hippocampus area of the brain and problems with learning and memory, we wanted to test the theory that psychological distress may affect the risk of developing Alzheimer’s disease.” (Katchaturian, 2005) 797 people with an average age of 75 were evaluated when they started the study and then on an annual basis.
They were tested on their level of how prone they were to stress with a reliable rating scale and had to rate how much they agreed with statements such as ‘I am not a worrier,’ and ‘I often feel tense and jittery’ using words such as strongly disagree, disagree etc. About 4.9 years later, 140 participants of the study developed AD. 90% of these people admitted to frequently feeling stressed. Once the researchers received these results, they then investigated whether frequent distress was a symptom of AD or an actually cause of it. To do this, they studied the brains of 141 people who had died during the course of the study. Out of 141, 57 passed the test of having probably AD. However, researchers found that distress was not related to the biology of an AD patient’s brain (involves plaques, tangles etc.) Therefore, this means that frequent stress is a co-factor that leads to AD.
In conclusion Alzheimer’s disease is a very serious condition that affects many people. They do not know what causes this disease or why people get it. It is due to the fact that there is a chance for anyone to get this disease. People must take precautions and seek the advice of healthcare professionals to be tested for this disease. This way they have a chance to go on living there lives for as long as possible. If they do not seek care then they have a lesser chance of living a longer life.
Alzheimer’s disease is a complex disease that science has researched for years. It is a tragic disease that not only affects the sufferer, but also their family. Alzheimer’s disease is a thief of hearts, souls and memories. Although research has been done to find out about what exactly causes the disease, a lot more of this needs to be done to find out how the tangles and plaques Dr Alzheimer discovered got there in the first place. After all, these are the two main things that destroy the brain. More research about plaques is especially needed as this damages many of the brain’s regions such as the parietal lobe, frontal lobe, hippocampus, amygdala and temporal lobe. In terms of prevention, Dr Valenzuela and the team at Colombia University have done a fine job in showing people how AD could actually be prevented.
Dr Valenzuela’s research has effectively addressed the reason why people should eat healthily and the team at Columbia University’s study has explained why stress should be avoided as much as possible. For decades, scientists have tried and tested various forms of treatment for AD patients but have so far been unsuccessful. However, with the PBT2 pill regarded as ‘the major breakthrough’ and the nasal spray proven to be amazing, one can only hope that Alzheimer’s will be cured someday. Something needs to be done about Alzheimer’s disease sooner or later as the ‘Alzheimer’s Australia’ organisation’s statistics show that this condition in people is becoming more common and is expected to outdo the depression illness’ numbers very soon.
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