Alzheimer’s disease is a degenerative brain disease that is characterized by the presence of dementia, called dementia of the Alzheimer’s type or DAT, emotional instability, and memory loss (Colman, 2001). DAT afflicts 7 percent of people over the age of 65 (Clipson, 1998), and in its most severe stage it causes severe impairment of almost all cognitive functions such as both long and short term memory, and language skills, as well as severe impairment of basic motor functions such as chewing and swallowing (Forstl, 1999). The average time from diagnosis to death is seven years (Clipson, 1998). The disease was named for Alois Alzheimer, the neurologist who first described the brain lesions associated with it (Colman, 2001).

DAT affects men and women equally, and does not appear to have any relation to racial or cultural background. However, it does seem to have a genetic background, because about 50% of children of an affected person will develop the disorder (Clipson, 1998). Some other risk factors for the development of Alzheimer’s disease have been identified, and these include the presence of Trisomy-21, or Down syndrome; ApoE4 genotype; and a history of head trauma (Hauw, 2002). There is a high correlation between severe head trauma, and senile plaques in the cerebral cortex (Ng’walali, 2002).

The exact cause of Alzheimer’s disease remains unknown. One theory, which called the amyloid cascade theory, has been the leading theory about Alzheimer’s disease for the past 15 years. That theory says that beta-amyloid is protein waste that spontaneously groups together and forms amyloid fibrils, which cause dementia because they have a neurotoxic effect on the brain (Bush, 2003).

Alzheimer’s disease is the cause of about half of all dementias, and can only be definitively diagnosed by an autopsy. The proper diagnosis of Alzheimer’s disease is based on gross and histological findings in the brain during an autopsy (Ng’walali, 2002).

An autopsy of the brain of an Alzheimer’s patient shows large quantities of senile plaques and neurofibrillary tangles in the neocortex (Skoog, 2002). Senile plaques, which are also called amyloid plaques, are deposits of insoluble beta-amyloid protein, which seem to cause neuron degeneration. In the brain of an Alzheimer’s patient, senile plaques are mostly found in the cerebral cortex, hippocampus, amygdala, and entorhinal cortex (Colman, 2001). Neurofibrillary tangles masses of neurofibrils and insoluble fibers, and they are caused by the breakdown of the tau protein. They especially occur in the hippocampus and amygdala (Colman, 2001). While the current diagnostic standards for Alzheimer’s disease are largely dependent on the observation of senile plaques as opposed to neurofibrillary tangles, the presence of the tangles can nonetheless be very helpful in making a diagnosis. There is a significantly high correlation between the presence of neocortical and hippocampal neurofibrillary tangles, and cognitive deficits in the patient (Ng’walali, 2002). Neurofibrillary tangles are insoluble masses, and they continue to exist in the extracellular space around where the nerve cells were previously, after the nerve cells degenerate. The exact cause of degeneration of the nerve cells, however, is unknown (Vickers, 2003). Other autopsy findings that are associated with Alzheimer’s disease are atrophy of the cerebrum, and enlargement of the lateral ventricles (Ng’walali, 2002).

The progression of modern technology allows for more accuracy in the diagnosis of dementia of the Alzheimer’s type, or DAT, before death occurs. That is because more ways are being invented to scan and study parts of the human brain while the patient is still alive. This allows doctors to look for some physical markers that indicate the presence of Alzheimer’s disease in order to make an early diagnosis of DAT.

The hippocampus is heavily implicated in Alzheimer’s disease, and it can be studied by way of magnetic resonance imaging, or MRI. On an MRI scan of the brain of a DAT patient, the hippocampus shows notable loss of volume, this can be estimated in two ways; by volumetric measurement of the hippocampus, and by a visual rating of the medial temporal lobe (Pelgrim-Korf, 2002). This form of evaluation has added significantly to accuracy in the diagnosis of DAT.

A series of MRI scans over an extended amount of time can show volume changes that occur over time, which can increase the accuracy in forming a diagnosis. However, an MRI alone cannot distinguish frontotemporal dementia, another type of dementia with symptoms similar to Alzheimer’s disease, from Alzheimer’s because the rate of atrophy is the same (Skoog, 2002).

Another reason to examine the hippocampus in an MRI is that it has been accurate in predicting future deterioration in the patient’s cognitive skills, because hippocampal atrophy has a high correlation with neuropsychological performance typical of a DAT patient, particularly with delayed recall (Pelgrim-Korf).

There are other benefits to studying an MRI in the case of suspected DAT. An MRI scan can detect other problems and diseases in the brain that might be causing the symptoms of dementia, such as brain tumors and normal-pressure hydrocephalus, among others (Skoog, 2002).

Although studying images of the brain can be extremely valuable to suggesting the presence of DAT, there are still no definite biological or instrumental markers that can be used to definitively diagnose the disease (Sorbi, 2000). An accurate diagnosistic hypothesis can be made, and there are some biological markers that can indicate Alzheimer’s disease reliably, but there is still no way to be sure of the presence of Alzheimer’s without performing an autopsy on the brain. However, there are measures that health-care professionals can take which can help lead to a reasonable diagnosis of DAT. The early diagnosis of DAT is largely based on a long process of ruling out other possible causes of the cognitive deficits.

The first signs that often characterize the onset of DAT include forgetfulness, depression, irritability, problems with any change in the patient’s routine, confusion, lapses in attention, and problems finding the right words to express a thought (Clipson, 1998). Other signs that the person might need to seek an evaluation for dementia include spatial disorientation, problems with word generation to name familiar objects, and a reduced ability to plan and organize events. The reduced ability to plan and organize may show itself in routines as familiar as preparing meals (Forstl, 1999).

The first step in the diagnosis of DAT is for the patient to go through a battery of physical examinations, neuropsychological evaluations, and laboratory tests. This is the screening phase of diagnosis, where the doctors’ aim is to identify what could be causing the patient’s cognitive deficits, and to form a diagnostic hypothesis (Sorbi, 2000). In order to get a diagnosis of dementia of the Alzheimer’s type, the patient’s cognitive deficits must be severe enough that they significantly impair occupational and social functioning, and other causes of the deficits must be ruled out (Clipson, 1998).

There are wide varieties of tests that are to be conducted in the case of suspected dementia, and the purpose of these tests is to rule out other problems that might be causing the cognitive deficits. There are also other tests that may or may not be conducted; these tests are special or supplementary, and may be used to follow up on results from the first set of tests (Sorbi, 2000).

The first tests that are to be conducted are a general physical and neurological examination of the patient, and directed anamnesis, which is an examination of the patient’s complete medical history, including whether there has been a family history of dementia. These examinations may indicate an underlying medical problem other than Alzheimer’s disease that may be causing the reduction in cognitive functioning, such as a history of hyper- or hypothyroidism, diabetes, or certain vitamin deficiencies (Sorbi, 2000). Some environmental factors must also be ruled out, such as exposure to toxins in the home environment, or a history of alcohol or drug abuse (Sorbi, 2000).

A thorough neuropsychological evaluation must also be conducted, as this evaluation will identify the cognitive deficit as well as the severity of the deterioration (Sorbi, 2000). The first set of tests to be administered is designed to be able to judge the patient’s previous cognitive abilities before the onset of dementia, so certain tests that are resistant to cerebral deterioration exist. Some examples are the best-performance method, in which the administrator uses the highest scores from all tests administered as an indication of the patient’s prior cognitive functioning. Another example is the National Adult Reading Test, because a person’s ability to pronounce irregularly spelled English words has been shown to be resistant to the deterioration associated with dementia (Clipson, 1998).

There are several neuropsychological tests that might be conducted to assess the severity of the patient’s cognitive disability include measures of intelligence. These include the Wechsler Adult Intelligence Scale-Revised; evaluation of the patient’s visual-spatial functioning and visual memory by tests such as the Rey Complex Figure Test; and tests to measure the patient’s verbal memory by tests like the Rey Auditory-Verbal Memory Test (Clipson, 1998). While the neuropsychological evaluation alone is not enough to make a diagnosis of dementia, it can document the reduced cognitive functioning in multiple domains, which is part of the required diagnostic criteria for dementia (Sorbi, 2000).

The Rey Complex Figure Test evaluates the patient’s visual-spatial functioning, and visual memory. This test scores visual-spatial functioning by requiring the patient to copy a fairly complicated line drawing, and is then scored for accuracy and completeness (Clipson, 1998). The Rey Auditory-Verbal Memory Test, as the name implies, evaluates the patient’s verbal memory. This test works by having the patient listen to a list of fifteen words during several trials, and then recall what the words were. The results are scored by how many of the original words the patient can recall. This test is designed to show problems with the patient’s short-term memory (Clipson, 1998).

Another neuropsychological test that may be administered is called the Trail-Making Test. This test is designed to measure all types of cognitive dysfunction. There are two steps to this test. In the first step, the patient connects circles containing the numbers one through 25, in order. In the second step, the patient again connects circles, but this time some of the circles contain numbers and some contain letters, and the patient has to connect them in order, alternating between numbers and letters (Clipson, 1998).

There are also several laboratory tests that should be routinely conducted when DAT is suspected. The tests that should be conducted include electrolyte levels, erythrocyte sedimentation rate, glycaemia, azotaemia, creatinimaemia, thyroid function, blood vitamin B12 and folate levels, and syphilis serology. There are several other tests that may be conducted depending on the individual patient, and these include hepatic function, serology for HIV-1, urinary metabolites of drugs of abuse and urinary excretion of heavy metals, chest X-rays, and blood gas analysis (Sorbi, 2000). The reason that these laboratory tests must be conducted is that misdiagnosis of dementia is a common problem, and it is important to make sure that the patient’s symptoms are not being caused by a reversible medical condition (Clipson, 1998).

Investigating the content of the patient’s cerebrospinal fluid can offer clues to aid in a diagnosis also. For instance if there is a change in the cerebrospinal fluid that shows a decrease in beta-amyloid and an increase in tau protein, it is reasonable to suspect Alzheimer’s disease. However while cerebrospinal fluid levels can indicate the presence of Alzheimer’s, they cannot discriminate between Alzheimer’s, vascular dementia, and Lewy-body disease (Skoog, 2002).

The next step in the diagnosis of DAT, if all other possible diagnoses have been ruled out, is to exclude vascular dementia. If vascular dementia can be ruled out as a diagnosis, then the patient is suffering from a primary degenerative disorder, of which Alzheimer’s disease is the most widespread (Sorbi, 2000).

In conclusion, Alzheimer’s disease is a degenerative disease characterized by cognitive defects including dementia, and the presence of both senile plaques and neurofibrillary tangles in the cortex. The exact cause of Alzheimer’s disease remains a mystery. Alzheimer’s affects men and women equally, and there seems to be no connection to the patient’s race or ethnic background. While diagnostic accuracy has improved, by way of using MRI scans and certain laboratory tests as well as neuropsychological evaluations, there is still no way to be certain of the presence of Alzheimer’s disease without conducting an autopsy of the brain. The diagnosis of dementia of the Alzheimer’s type, or DAT, is essentially a long process of ruling out other medical and environmental problems that could cause the dementia. One can only hope that continuing research into the underlying chemistry of the disease will one day turn up a successful way to treat individuals suffering from the disorder.

Bush, A. I. (2003) The metallobiology of Alzheimer’s disease. Trends in Neuroscience. Retrieved April 7, 2003, from http://www.sciencedirect.com.