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brain that prevents signals from beingsent between neurons (Dean 34). The amount of beta amyloid allowed toenter the brain is normally
limited by the blood-brain barrier, but if largeamounts of the protein
are being produced, this barrier cannot keep up(Wisniewski & Sadowski
23). Tangles are a buildup of tau, another protein,inside nerve cells.
Tangles prevent the cell from transmitting signals andeventually cause
it to die. Plaques and tangles both occur in healthy brains,but they are
far less frequent (Dean 4). The most prevalent cause of the
development of plaques and tanglesis aging. However, many factors
contribute to the production of excess betaamyloid and tau proteins
(Dean 10). Some of the other major contributorsare head injury,
strokes, a fatty diet (Dean 11), high blood pressure, anddiabetes
(Wisniewski & Sadowski 38). Even stress can be a
contributor,especially when combined with other health problems
(Dean 12). Anyonewho has Down syndrome will eventually develop
Alzheimers disease if helives long enough (Wisniewski & Sadowski
33).Although the disorder is not considered to be genetic, a single
genethat creates a protein called apolipoprotein E (or ApoE) has been
isolated asa factor that increases the risk of Alzheimers disease. ApoE
normally aidesin delivering cholesterol throughout the body, but a
mutated form of thisgene exists in about 15% of the worlds
population. It is, however, assumedthat there are other genes which
increase the risk of developing Alzheimersdisease that have not yet
been isolated (Fact Sheet).
Coyle 7 There are many ways to reduce the risk of Alzheimers
disease. Anyuse of the mind has some effect in decreasing the
chances, but certainactivities are more effective than others. Reading,
studying a foreignlanguage, and traveling are activities that are
considered to be highlyeffective. Activities such as watching television,
Coyle 9violent, but for those who do, there exist preventative
medications.Sedatives can help the patient overcome insomnia, but the side
effects of sedatives are often confused with worsening symptoms of
Alzheimersdisease (Dean 107).Medications can be combined for a stronger
overall effect on thedisease. Certain combinations work better than others,
and medications donot have the exact same effects in all patients. Care must
be taken to avoidharmful drug interactions and side effects, however
(Wisniewski 106). Aphysician will recommend a trial period of any drug
prescribed to make surethey are not detrimental to the patients health (Dean
103).While options seem fairly grim at present, there is always some hopefor
the future with constant advances in the medical field. Scientists,supported
by the federal government and the National Institute on Aging aswell as
private organizations, are hard at work researching new Alzheimerstools and
treatments that may soon become available (Petersen 89).MRI scans of the
brain have shown that the brains of people who willeventually develop
Alzheimers disease lose volume (or shrink) morequickly than those of
people who will remain healthy (Petersen 88). PETscans can show the activity
of different parts of the brain during stimulatingactivity. SPECT is another
scan similar to PET which measures blood flow inselect regions of the brain
(Petersen 89). In the future, these scans maybecome useful in predicting the
eventual onset of Alzheimers disease andbeginning preventative measures
as early as possible.
Coyle 10Neurotrophic agents and nerve growth factor, chemicals that
helpneurons grow and remain healthy, could repair or prevent damage
toneurons (Petersen 85). Research is currently being conducted to find out
thebest way to deliver these chemicals to the correct parts of the brain for
thehighest success rates. Leteprinim potassium, a chemical that appears
toimprove memory, is being tested as a treatment or preventative
forAlzheimers disease (Petersen 86).A vaccine for Alzheimers disease called
AN-1792 was created in labswhich caused the bodys immune system to
actively find and remove betaamyloid in the brain (Petersen 86-87). At first
this vaccine seemed to be amiracle in the field of Alzheimers disease
research, but then problems beganto occur in trial patients. After about a
year of using the vaccine, the over-stimulated immune system began to
attack healthy brain tissue as well. Thisbegan to cause dangerous
inflammation of the brain, and one patient died. Testing was immediately
stopped, and so far the vaccine has not been testedagain in humans
(Wisniewski & Sadowski 113).As with most modern diseases, our methods of
treatment becomemore and more diverse by the day. With the aid of funding,