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Alzheimer's disease is the third most common cause of death in developed countries after heart disease and cancer. Alzheimer's disease increases with age and with the increasing age of the population in developed countries it is believed that the worldwide number of Alzheimer's disease will increase from 12million in 2000 to 50million by 2050.
Alzheimer's disease is named after Dr Alois Alzheimer. In 1906, Dr Alzheimer noticed changes in the brain tissue of a woman who had died of an unusual mental illness. Her symptoms included memory loss, language problems, and unpredictable behaviour. After she died, he examined her brain and found many abnormal clumps amyloid plaques and neurofibrillary tangles. Plaques and tangles in the brain are two of the main features of Alzheimer's disease. The third is the loss of connections between neurons in the brain  .
Vulnerable brain regions include the amygdala as well as the hippocampus and areas around the hippocampus, and affected cell populations include cortical pathways involved in catecholaminergic, serotonergic and cholinergic transmission.
The pathology of Alzheimer's disease refers to the essential nature of disease, especially changes in body tissues and organs that are caused by disease andÂ the structural and functional signs of disease.
In the course of this essay I would focus on the clinical signs and symptoms of AD, how AD, can be differentiated from other types of dementia and conditions and how AD is diagnosed. The two pathological hallmarks in identifying AD, the likely causes of AD, and changes in tissues as a result of AD would also be analysed, as well as a brief treatment and prevention strategy
Symptoms and signs of Alzheimer's disease
This section focuses on the signs and symptoms of Alzheimer's disease, which can be grouped into the early signs, the signs and symptoms as the disease progresses and the later symptoms and clinical signs. The clinical signs and symptoms of moderate type Alzheimer's disease and severe Alzheimer's disease would also be considered.
Early clinical signs and symptoms
In the early stages of Alzheimer's disease, short-term memory begins to decline when the cells in theÂ hippocampusÂ degenerate. Signs and symptoms in the early stages include;
Simple forgetfulness of recent events such as things done the day before, which often can be confused with age-related memory problems, although, their long-term memory is relatively preserved as they can remember long past events.
Repeated old stories, they start to retell old stories, remembering the stories but not remembering they have told it.
Behaviour changes that resemble depression. 
Signs and symptoms as the disease progresses
As Alzheimer's disease progresses, brain tissue shrinks. However, theÂ ventricles are noticeably enlarged. The signs and symptoms as the disease progresses include;
Forgetfulness which starts to affects routine activities such as every day chores which was performed without a problem before. Cooking becomes a problem especially if unexpected interruptions occur.
Patients get lost in their own neighbourhood
Solving simple mathematical problems such as household accounts is not possible anymore
Their personality changes as they begin to behave in a manner unexpected of them, active people lose interest in their hobbies and financially intelligent people start to overspend.
Self-neglect, apathy and loss of interest in life
Patients are aware of memory problems so they try to compensate by letting someone else talk and make decision for them or by setting reminders.
Patients might become aggressive as a result of anxiety and frustration. 
Later clinical signs and symptoms
Advancement of the disease leads to the death of more nerve cells and subsequent changes in behaviour, such as wandering and agitation. In the final stages, people may lose the ability to feed themselves, speak, recognize people and control bodily functions. Memory worsens and may become almost non-existent.
The later signs and symptoms resulting in moderate or severe Alzheimer's disease are considered. Changes in memory and behaviour become more noticeable.
Patients become incapable of organising their thoughts, not able to follow instructions written by other people and memory gaps are filled with stories they make up. They become more confused as they cannot recognise their family members and friends. The repetition of old stories degenerated into repeating just words or statements.
In moderate Alzheimer's disease, as the patient memory and behaviour continues to deteriorate, the efforts to compensate fail.in this stage, damage occurs in areas of the brain that control language, reasoning, sensory processing, and conscious thought. Memory loss and confusion increase. They may be unable to learn new things, carry out tasks that involve multiple steps (such as getting dressed), or cope with new situations. They may have hallucinations, delusions, and paranoia, and may behave impulsively. The repetitive behaviour also extends to pointless movements such as pacing restlessly. They Lose insight and judgement which can lead to safety problems, antisocial behavioural patterns and inappropriate sexual behaviour may develop. Patients become more dependent on their care as they require constant help.
In severe Alzheimer's disease as the disease spreads through theÂ cerebral cortex judgment worsens, emotional outbursts may occur and language is impaired. The patient is unable to recognise themselves, as their speech is incomprehensible, they often become mute. By the final stage, plaques and tangles have spread throughout the brain and brain tissue has shrunk significantly. They become uncooperative and difficult to manage, refusing to go to the bathroom or eat. They lose weight and have an emaciated appearance; often they are weak and cannot stand alone. Their gait is unsteady and falls are common. The patient becomes bedridden and incontinence of urine and bowels appears. Infections and sometimes seizures are frequent, and at this stage patients require Constant full time care.
How Alzheimer's disease is differentiated from other Dementias and conditions.
Alzheimer's disease can be difficult to diagnose as it can be mistaken for depression or dementia and age related problems in the early stages of the disease. In the later stages the presence of multiple pathologies makes the differential diagnosis complicated. Therefore AD has to be differentiated from the other various types of dementia before it can be diagnosed, by a process of elimination. Other dementias and conditions to be eliminated from include;
Vascular dementias, Lewy body dementias, Frontal lobe dementia, Subcortical dementia, Metabolic-toxic dementias
Infections, Alcohol, drugs or medicines, Depression and delirium.
How Alzheimer's disease is diagnosed.
Alzheimer's disease can be conclusively diagnosed only after death by relating clinical course with an examination of brain tissue and pathology in an autopsy. But when the patient is alive doctors now have several methods to help them determine fairly accurately whether a person who is having memory problems has "possible Alzheimer's disease" (dementia may be due to another cause) or "probable Alzheimer's disease" (no other cause for dementia can be found). To diagnose Alzheimer's, doctors:
ask questions about the person's overall health, past medical problems, ability to carry out daily activities, and changes in behaviour and personality
conduct tests of memory, problem solving, attention, counting, and language
carry out medical tests, such as tests of blood, urine, or spinal fluid
Perform brain scans, such as computerized tomography (CT) or magnetic resonance imaging (MRI) and SPECT. 
The disease (early onset) must start after 40 years of age and the late onset usually after 65years of age. These tests listed above may be repeated to give doctors information about how the person's memory is changing over time. The diagnosis is supported by the finding of progressive worsening of specific cognitive function, dysphasia, dyspraxia, agnosia, altered behaviour, and family history of AD. Usually brain atrophy is seen on CT and SPECT scanning shows reduced temporal lobe blood flow.
Early diagnosis is beneficial for several reasons. Having an early diagnosis and starting treatment in the early stages of the disease can help preserve function for months to years, even though the underlying disease process cannot be changed. Having an early diagnosis also helps families plan for the future, make living arrangements, take care of financial and legal matters, and develop support networks. In addition, an early diagnosis can provide greater opportunities for people to get involved in clinical trials. In the clinical trial, scientists test drugs or treatments to see which are most effective and for whom they work best  .Â
There are two major diagnostic manuals for the clinical diagnosis of AD, the NINCDS-ADRDA (McKhann et al. 1984) criteria and the DSM-III-R (American Psychiatric Association, 1987). These two manuals are compatible and the criteria are shown in the appendix.
Causes of Alzheimer's disease
This section focuses on the tissues changes caused by Alzheimer's disease such as the formation of amyloid plaques and neurofibrillary tangles and the excessive loss of neurone and neurotransmitters. The risk factors associated with Alzheimer's disease such as age, genetics and environment will also be considered.
The post-mortem brain of a patient with AD often shows marked atrophy in the temporal lobe and the parietal lobe. The occipital lobe is not affected by the disease but the frontal lobe is relatively spared. There is an overall shrinkage of brain tissue. The grooves in the brain (sulci) are noticeably widened and there is shrinkage of the gyri, the well-developed folds of the brain's outer layer. [ CLOSE WINDOW ]
Microscopically, there is significant loss of neurons, in addition to shrinkage of large cortical neurons. Many investigators believe that loss of synapses, in association with shrinkage of the dendritic tree of large neurons, is the critical pathological substrate. The neuropathologic hallmarks of AD are neuritic plaques and neurofibrillary tangles , although these lesions are not unique to AD and can be found in other neurodegenerative disorders and in clinically normal individuals as well. Classic neuritic plaques are spherical structures consisting of a central core of fibrous protein known as amyloid that is surrounded by degenerating nerve endings.
Amyloid Plaques consists of deposits of insoluble short fragment peptide (beta-amyloid), of a large transmembrane protein called amyloid precursor (APP). In a normal circumstances APP is cut in a two-step process to which leads to the formation of short soluble fragments which are thought to have neuroprotective properties  . However in AD patient APP is cut in a two-step process to form beta-amyloid which aggregates outside the nerve cell overtime and form plaques. Beta-amyloid assumes different conformations, which are capable of different biological activities. It has the ability to interfere with signal transduction processes and disturb normal neuronal function.
The brain aging and neurodegeneration can be resolved into distinct phases; the successful aging phase, the initiation phase and the propagation phase. Beta -amyloid at sublethal concentrations can interfere with activity dependent plasticity through suppressing CREB regulation, a key transcription factor in learning and memory. In the propagation stage, degenerative mechanisms become prominent and progressively irreversible. Beta-amyloid plays a major role in initiating propagation and driving it, because beta-amyloid can augment so many degenerative mechanisms, including the ability to activate caspase death receptors. 
Neurofibrillary tangles are insoluble helical fibres found inside the brain's cells. These tangles consist primarily of an abnormal form of tau protein in Alzheimer's disease. Tau is a long intracellular protein which forms part of a structure called a microtubule. It holds together microtubule's which helps transport nutrients and other important substances from one part of the nerve cell to another. Microtubules constantly change and tau protein has the ability to detach and reattach. In Alzheimer's disease tau protein is detached from microtubules and undergoes phosphorylation that prevents it from reattaching. This leads to the decay of microtubules and the accumulation of phosphorylated tau. The phosphorylated tau forms paired helical filaments (PHFs) with itself and becomes insoluble. The (PHFs) accumulate in axons and dendrites of the neurones to form neuropil threads. The microtubules collapse and the filling of the cell with tangles lead to cell death.
Amyloid plaques appear mainly in the association cortical regions of the brain and invade the hippocampus and medial temporal lobe structures in the late stages of the disease. Neurofibrillary tangles appear first in the medial temporal regions and then spread to the association cortical areas of the brain. Amyloid plaques are only a by-product of AD while tangle formation is associated with the clinical symptoms of AD (Braak staging).
AD is a multifactorial disease. Many factors increase the risk of developing AD. Advanced age is the strongest risk factor. Diabetes, atherosclerosis, high blood pressure, vitamin deficiencies, and low education are known to increase the risk of developing AD. Genetic factors such as ApoE4, may also contribute. ApoE4 is a variant of the ApoE lipoprotein; this variant is associated with an elevated risk of AD. However having this variant of ApoE gene does not mean the patient will develop AD, but if AD appears the disease will begin earlier, develop faster, with more plaques and tangles. 
There is no treatment for AD. The only available medication is symptomatic (cholinesterase inhibitors such as donepezil, rivastigmine and galantamine). Preventive measures can be taken to reduce the risk of AD
In conclusion AD is an irreversible dementia that eventually leads to the death of the patient. As the disease progresses patients lose their memories and personality, people with Alzheimer's will need more support from those who care for them. Eventually, they will need help with all their daily activities. AD is a multifactorial disease. There are many current theories as to what triggers the onset of Alzheimer's disease. There seem to be many contributing factors lying at the root of this disease, and the acquisition of Alzheimer's seems to have both environmental and genetic foundations. Regardless of the cause, the main pathology of Alzheimer's dementia remains the same: toxic levels of extracellular amyloid plaques build up in the brain, and destroy those regions next to the accumulation sites. There are no current treatments for AD, and the available drugs only provide symptomatic relief for a small number of patients. Therefore the diagnosis of AD only means the prospect of long-term suffering for patients and relatives.
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