General Description
Alzheimer's disease (AD), named after German physician Alois Alzheimer,
is the most common cause of dementia in elderly people. Affecting
the parts of the brain that control thought, memory, and language,
AD is characterized by insoluble deposits (plaques) of protein and
cellular material outside and around brain cells, and by the build-up
of twisted fibers inside brain cells. At first, AD destroys cells
in the hippocampus (the part of the brain that helps encode memories)
and related structures, causing deterioration of short-term memory
and loss of the ability to do simple, familiar tasks. AD also attacks
the cerebral cortex (the part of the brain responsible for language
and reasoning), causing loss of language skills and the inability
to make judgements. Emotional outbursts and disturbing behavior,
such as wandering and agitation, become more and more frequent as
the disease progresses. Depression (sometimes severe) is common
in AD patients. Eventually, many other areas of the brain deteriorate,
and the AD patient becomes bedridden, incontinent, and unresponsive
to the outside world. Uncommon in younger people, the disease usually
begins after age 65, and the risk of AD increases with age. About
3 percent of men and women ages 65 to 74 and nearly half of all
people over age 85 have AD. However, it is important to note that
the disease is not a normal part of aging. The cause of Alzheimer's
disease is still under debate, and there is no known cure.1
Genetic Factors
Conventional Treatments
Nutritional Considerations
Genetic factors
Scientists do not yet fully understand what causes Alzheimer's
disease, but it appears to result from many interrelated factors
including genetic, environmental, and other influences. Two types
of AD exist: familial AD (FAD), which follows a certain inheritance
pattern, and sporadic AD, where no obvious inheritance pattern
is seen. Because of variances in patients' ages at onset of the
disease, AD is further defined as early-onset (occurring in people
under age 65) or late-onset (occurring in people 65 and older).
All FAD observed so far has an early onset, and roughly half of
FAD cases are known to be caused by defects in three specific
genes located on three different chromosomes. However, there is
presently no evidence that any of these mutations is linked to
the sporadic form of AD. Nevertheless, genetics play a role in
the development of late-onset AD as well as FAD.2
Oxidative damage
Another factor believed to contribute to the development of Alzheimer's
disease is oxidative damage caused by free radicals. Scientists
believe that highly reactive free-radical molecules may play a
role in several diseases, including cancer, heart disease, and
AD. Oxidative damage caused by free radicals can contribute to
AD in several ways, including altering the structure of certain
proteins and damaging the cellular membranes that regulate the
flow of materials in and out of brain cells.
Inflammation
It is possible that inflammation in the brain may play a role
in the development of AD. Brain inflammation generally increases
with age, but this increase is more pronounced in AD patients.
Compounds involved in inflammatory processes can be found in AD
plaques, and many studies suggest ways in which inflammatory processes
could destroy brain cells.3 Investigations into the
potential for anti-inflammatory drugs in the treatment of AD are
currently in progress.
Conventional
treatments
The FDA has approved two medications for AD, tacrine (Cognex)
and donepezil hydrochloride (Aricept). Both act by inhibiting
an enzyme that breaks down acetylcholine, a key chemical "messenger"
required for normal brain function. Donepezil has fewer side effects
than tacrine,4 and is now commonly used to treat mild
to moderate symptoms of AD. However, the drug does not stop or
reverse the progression of AD, and it appears to help only some
AD patients for a period ranging from months to two years, so
its usefulness is limited. In Europe, an extract of Ginkgo biloba
leaf is commonly used to treat mild to moderate dementia, and
one study indicates it may be more effective than tacrine in treating
AD symptoms.5 In the U.S., ginkgo is sold as a dietary
supplement and has not been approved by the FDA for treatment
of AD.
Nutritional
considerations
Because oxidative damage is believed to contribute to the development
of Alzheimer's disease, dietary antioxidants may play an important
role in fighting the disease. Levels of antioxidant vitamins C
and E are often low in AD patients,6,7 and some studies
indicate that increasing intake of these vitamins can delay the
disease's progression.8 Ginkgo biloba extract also
has powerful antioxidant capabilities, and appears to provide
specific protection for brain tissues.9-11 The B-complex
vitamins may also be helpful in the fight against AD because they
are required for the formation of vital brain chemicals like acetylcholine
and they help control blood levels of homocysteine. High homocysteine
levels are common in AD patients, and may play a role in development
of the disease.12 Folic
acid, vitamin B-12, and vitamin B-6 help keep homocysteine
in check by converting it into methionine, a beneficial amino
acid. |
