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Dementia is a brain disorder that seriously affects a person¶s ability to carry out daily activities. The most
common form of dementia among older people is Alzheimer¶s disease (AD), which initially involves the parts
of the brain that control thought, memory, and language. Although scientists are learning more every day, right
now they still do not know what causes AD, and there is no cure.

Scientists think that as many as 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 5 percent of
men and women ages 65 to 74 have AD, and nearly half of those age 85 and older may have the disease. It is
important to note, however, that AD is not a normal part of aging.

AD is named after Dr. Alois Alzheimer, a German doctor. In 1906, Dr. Alzheimer noticed changes in
the brain tissue of a woman who had died of an unusual mental illness. He found abnormal clumps (now called
amyloid plaques) and tangled bundles of fibers (now called neurofibrillary tangles). Today, these plaques and
tangles in the brain are considered signs of AD.

Scientists also have found other brain changes in people with AD. Nerve cells die in areas of the brain
that are vital to memory and other mental abilities, and connections between nerve cells are disrupted. There
also are lower levels of some of the chemicals in the brain that carry messages back and forth between nerve
cells. AD may impair thinking and memory by disrupting these messages.

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Alzheimer¶s disease is characterized by progressive cognitive decline and memory loss. Individuals who
suffer from Alzheimer¶s Disease will have difficulties with activities of daily living and need full time
assistance in the later stages of the disease. It accounts for 50-60% of all dementia cases in the elderly.
Alzheimer¶s is a unique condition that is not the result of common aging and natural senility.

The brain tissue in Alzheimer¶s patients has a specific pattern of degeneration marked by senile plaques
and neurofibullary tangles. There is also a loss of neurons in the cerebral cortex, hippocampus, and subcortical
structures, such as the locus caeruleus and nucleus raphe dorsalis. An increase in beta-amyloid proteins is
thought to contribute to the disease as well. This increase is pararlleled with a marked decrease in brain
neurotransmitters, with acetylcholine being affected the greatest.

The distinct cause of Alzheimer¶s disease is not completely known. There is a familiar pattern in 15-
20% of the cases. For the other 80-85% of cases there are several causal relationships. A genetic etiology is
suspected in some individuals, due to findings of an increase in certain proteins in the brain that are coded for
on specific chromosomes (1, 14, 19, and21). The most significant findings are with the protein apolipoprotein
E. Certain forms of the protein (e4-type) are linked with greater incidence, while one form (e2-type) is
associated with a more protective effect.Environmental factors are also suspected to play a role in the
development of Alzheimer¶s disease with specific attention to heavy metal toxicity, oxidative damage, and
abnormal hormone metabolism.




Scientists do not yet fully understand what causes AD. There probably is not one single cause, but several
factors that affect each person differently. Age is the most important known risk factor for AD. The number of
people with the disease doubles every 5 years beyond age 65.

Family history is another risk factor. Scientists believe that genetics may play a role in many AD cases.
For example, early-onset familial AD, a rare form of AD that usually occurs between the ages of 30 and 60, is
inherited. The more common form of AD is known as late-onset. It occurs later in life, and no obvious
inheritance pattern is seen in most families. However, several risk factor genes may interact with each other and
with non-genetic factors to cause the disease. The only risk factor gene identified so far for late-onset AD is a
gene that makes one form of a protein called apolipoprotein E (ApoE). Everyone has ApoE, which helps carry
cholesterol in the blood. Only about 15 percent of people have the form that increases the risk of AD. It is likely
that other genes also may increase the risk of AD or protect against AD, but they remain to be discovered.
Scientists still need to learn a lot more about what causes AD. In addition to genetics and ApoE, they are
studying education, diet, and environment to learn what role they might play in the development of this disease.
Scientists are finding increasing evidence that some of the risk factors for heart disease and stroke, such as high
blood pressure, high cholesterol, and low levels of the vitamin folate, may also increase the risk of AD.
Evidence for physical, mental, and social activities as protective factors against AD is also increasing.
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Primary dementias are degenerative disorders that are progressive, irreversible, and not due to any other
condition. Specific disorders are dementia of the Alzheimer¶s type (DAT) and vascular dementia (formerly multi-infarct
dementia). Dementia of Alzheimer¶s type demonstrates progression of symptoms from the initial stage, which is
characterized by mild cognitive deficits in the area of short-term memory and accomplishment of goal-directed activity, to
the final stage in which profound impairment occurs in the areas of cognition and self-care abilities. Research is ongoing.
Dementia of Alzheimer¶s type believed to have multiple causative factors.
1. Genetic Factors:
2 Familial Alzheimer¶s disease is associated with abnormal genes on chromosomes 1, 14, and 21. In particular, with
genes located on these chromosomes (1 and 14) that encode for amyloid precursor protein which leads to
mutation of the amyloid beta-peptide in plaques.
2 A specific cholesterol-bearing protein, apolipoprotein E4 (Apoe4), is found on chromosome 19 twice as often as
people with DAT as in general population.
2. Biochemical and brain structure factors:
2 The neurotransmitter acetylcholine has been implicated in terms of relative deficit and/or receptor abnormalities
as related to Alzheimer¶s disease.
2 Autopsy findings reveal presence of brain changes, that is, the presence of amyloid plaques and neurofibrillary.
2 Additional areas of investigation includes: slow viral infection, autoimmune processes, and head trauma.



 
Occur as a result of another pathologic process.
1. Infection-related dementias
2 Acquired immunodeficiency syndrome
2 Chronic meningitis
2 Creutzfeldt-Jakob disease
2 Progressive multifocal leukoencephalopathy
2 Postencephalitic dementia syndrome
2 Syphilis
2 Subacute sclerosing panencephalitis
Tuberculosis
2. Subcortical degenerative disorders
2 Huntington¶s disease
2 Parkinson¶s disease
2 Wilson¶s disease
2 Thalamic dementia
3. Hydrocephalus
4. Vascular dementias
5. Traumatic conditions, such as post traumatic encephalopathy and subdural hematoma.
6. Neoplastic dementias
2 Glioma
2 üeningioma
2 üeningeal carcinomatosis
2 üetastatic deposits
7. Inflammatory conditions, such as sarcoidosis, systemic lupus erythematous, and temporal arteritis.
8. Toxic conditions, such as alcohol-related syndrome and iatrogenic dementias
9. üetabolic disorders
2 Anemia¶s
2 Deficiency states
2 Cardiac or pulmonary failure
2 Hepatic encephalopathy
2 Porphyria
2 remia