Dementia (cont.)
What Conditions Are Not Dementia?
Age-related cognitive decline. As people age, they usually experience slower
information processing and mild memory impairment. In addition, their brains
frequently decrease in volume and some nerve cells, or neurons, are lost. These
changes, called age-related cognitive decline, are normal and are not considered
signs of dementia.
Mild cognitive impairment. Some people develop cognitive and memory problems
that are not severe enough to be diagnosed as dementia but are more pronounced
than the cognitive changes associated with normal aging. This condition is
called mild cognitive impairment. Although many patients with this condition
later develop dementia, some do not. Many researchers are studying mild
cognitive impairment to find ways to treat it or prevent it from progressing to
dementia.
Depression. People with depression are frequently passive or unresponsive,
and they may appear slow, confused, or forgetful. Other emotional problems can
also cause symptoms that sometimes mimic dementia.
Delirium. Delirium is characterized by confusion and rapidly altering mental
states. The person may also be disoriented, drowsy, or incoherent, and may
exhibit personality changes. Delirium is usually caused by a treatable physical
or psychiatric illness, such as poisoning or infections. Patients with delirium
often, though not always, make a full recovery after their underlying illness is
treated.
What Causes Dementia?
All forms of dementia result from the death of nerve
cells and/or the loss of communication among these cells. The human brain is a very complex and intricate
machine and many factors can interfere with its functioning. Researchers have
uncovered many of these factors, but they have not yet been able to fit these
puzzle pieces together in order to form a complete picture of how dementias
develop.
Many types of dementia, including AD, Lewy body
dementia, Parkinson's dementia, and Pick's disease, are characterized by
abnormal structures called
inclusions in the brain. Because these inclusions, which contain abnormal
proteins, are so common in people with dementia, researchers suspect that they
play a role in the development of symptoms. However, that role is unknown, and
in some cases the inclusions may simply be a side effect of the disease process
that leads to the dementia.
Genes clearly play a
role in the development of some kinds of dementia. However, in AD and many other
disorders, the dementia usually cannot be tied to a single abnormal gene. Instead, these forms of dementia appear to result from a
complex interaction of genes, lifestyle factors, and other environmental
influences.
Researchers have identified several genes that influence
susceptibility to AD. Mutations in three of the known genes for AD - genes that
control the production of proteins such as amyloid precursor protein (APP), presenilin 1,
and presenilin 2 - are linked to early-onset forms of the disease.
Variations in another gene, called apolipoprotein E
(apoE), have been linked to an increased risk of late-onset AD. The apoE gene
does not cause the disease by itself, but one version of the gene, called apoE
epsilon4 (apoE E4), appears to increase the risk of AD. People with two copies
of the apoE E4 gene have about ten times the risk of developing AD compared to
people without apoE E4. This gene variant seems to encourage amyloid deposition
in the brain. One study also found that this gene is associated with shorter
survival in men with AD. In contrast, another version of the apoE gene, called apoE E2, appears to protect
against AD.
Studies have suggested that mutations in another gene,
called CYP46, may contribute to an increased risk of developing late-onset
sporadic AD. This gene
normally produces a protein that helps the brain metabolize cholesterol.
Scientists are trying to determine how beta amyloid
influences the development of AD. A number of studies indicate that the buildup of this protein
initiates a complex chain of events that culminates in dementia. One study found
that beta amyloid buildup in the brain triggers cells called microglia, which
act like janitors that mop up potentially harmful substances in the brain, to
release a potent neurotoxin called
peroxynitrite. This may contribute to nerve cell death in AD. Another study found that beta amyloid causes a protein called
p35 to be split into two proteins. One of the resulting proteins triggers
changes in the tau protein that lead to formation of neurofibrillary tangles. A
third study found that beta amyloid activates cell-death enzymes called caspases
that alter the tau protein in a way that causes it to form tangles. Researchers
believe these tangles may contribute to the neuron death in AD.
Vascular dementia can be caused by cerebrovascular disease or any other
condition that prevents normal blood flow to the brain. Without a normal supply
of blood, brain cells cannot obtain the oxygen they need to work correctly, and
they often become so deprived that they die.
The causes of other types of dementias vary. Some, such
as CJD and GSS, have been tied to abnormal forms of specific proteins. Others,
including Huntington's disease and FTDP-17, have been linked to defects in a
single gene. Post-traumatic dementia is directly related to brain cell death
after injury. HIV-associated dementia is clearly tied to infection by the HIV
virus, although
the exact way the virus causes damage is not yet certain. For other dementias,
such as corticobasal degeneration and most types of frontotemporal dementia, the
underlying causes have not yet been identified.
Next: What Are the Risk Factors for Dementia? »
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