Alzheimer’s Symptoms | Causes
of Alzheimer’s | Alzheimer’s
Originally described by Alois Alzheimer in 1907, Alzheimer's disease
(AD) has emerged as the most common type of dementia in the elderly today.
Although the definitive diagnosis of AD requires histologic confirmation,
in the absence of a readily discernible cause, the clinician may establish
the diagnosis antemortem, with a fair degree of certainty, based on the
clinical findings of a gradually progressive cognitive decline that results
in the loss of memory, language skills, and a progressive decline in
the ability to do activities of daily living, and executive function.
the aging population continues to grow at a vigorous pace, it becomes
increasingly important to recognize the clinical spectrum of AD because
of the possible benefit of medical intervention. In recent years, research
studies have made major advances in our understanding of the histopathogenesis,
genetic risk factors, and treatment options for this devastating neurodegenerative
AD is a progressive dementia with memory loss as the major clinical
manifestation. Although short-term memory impairment is often the manifesting
symptom, remote memory loss also appears to be affected over time. Another
important feature of AD is the disturbance of language. The language
difficulties evolve into a communication breakdown as the patient struggles
with a markedly limited vocabulary, word finding problems, and defects
in verbal comprehension.
Other cortical signs and symptoms such as apraxia,
acalculia, and visuospatial dysfunction may become apparent over the
course of the disease. With the development of apraxia, patients lose
the ability to carry out such simple tasks as combing their hair or using
the shower. Acalculia may become evident when the patient is no longer
able to maintain a checkbook or household accounts. Visuospatial abnormalities
can also be seen as patients become disoriented with their body position
in space and frequently may become lost.
Behavioral problems emerge throughout
the various stages of the disease. Mood disturbances such as depression,
anxiety, or apathy may be present early on in AD, whereas delusions,
hallucinations, and psychosis can be prominent in later stages. In advanced
stages of AD, patients may exhibit tremor and gait disturbance, , urinary
incontinence, and myoclonus. Seizures can also be seen in some patients
with late-stage disease. Patients with end-stage AD may end up in a vegetative
state when all cognitive activity ceases
Scientists are still trying to fully understand the cause or causes
disease; however, plaques and tangles and the risk factors
that affect a person’s likelihood of developing the disease should be
Plaques and Tangles
Alzheimer's disease is characterized by a build-up of proteins in the
brain. Though this cannot be measured in a living person, extensive autopsy
studies have revealed this phenomenon. The build-up manifests in two
- Plaques –
deposits of the protein beta-amyloid that accumulate in the spaces
between nerve cells
- Tangles –
deposits of the protein tau that accumulate inside of nerve cells
Scientists are still studying how plaques and
related to Alzheimer’s disease. One theory is that they block the nerve
cells’ ability to communicate with each other, making it difficult for
the cells to survive.
Autopsies have shown that most people develop some plaques
and tangles as they age, but people with Alzheimer’s develop far more
than those who do not develop the disease. Scientists still don’t know
why some people develop so many compared to others. However, several
risk factors for Alzheimer’s disease have been uncovered.
Advancing age is the number one risk factor for developing Alzheimer’s
disease. One out of eight people over the age of 65 has Alzheimer’s disease,
and almost one out of every two people over the age of 85 has Alzheimer’s.
The probability of being diagnosed with Alzheimer’s nearly doubles every
five years after age 65.
People who have a parent or sibling that developed Alzheimer’s disease
are two to three times more likely to develop the disease than those
with no family history of Alzheimer’s. If more than one close relative
has been affected, the risk increases even more.
Scientists have identified
two kinds of genes that are associated with this familial risk factor.
The first is thought to be a “risk gene,” ApoE
4, which increases the
likelihood of developing Alzheimer’s, but does not guarantee it. In
addition to ApoE 4, scientists think there could be up to a dozen more
risk genes yet to be discovered.
The second kind of gene is a “deterministic
gene” and is much rarer than risk genes. Deterministic genes are only
found in a few hundred extended families around the world. If a deterministic
gene is inherited, the person will undoubtedly develop Alzheimer’s, probably
at a much earlier age.
Although age and family history are out of our control, scientists have
also identified several lifestyle
factors that can influence a person’s
risk of developing Alzheimer’s disease. A connection has been found between
injury and future development of Alzheimer’s, so those who
practice safety measures such as wearing helmets and seat belts and not
engaging in activities where there is a high risk of falling are at an
Scientific research is also providing valuable information about how
drug and non-drug approaches to treatment can improve day-to-day functioning
and maximize quality of life. Drug treatments currently available are
used to manage the cognitive symptoms of Alzheimer's, such as changes
in thinking, memory and perception. Several prescription drugs are currently
approved by the U.S. Food and Drug Administration (FDA) to treat people
who have been diagnosed with Alzheimer’s disease (AD). Treating the symptoms
of AD can provide patients with comfort, dignity, and independence for
a longer period of time and can encourage and assist their caregivers
It is important to understand that none of these medications
stops the disease itself.
Treatment for Mild to Moderate AD
Medications called cholinesterase inhibitors are prescribed for mild
to moderate AD. These drugs may help delay or prevent symptoms from
becoming worse for a limited time and may help control some behavioral
symptoms. The medications include: Razadyne® (galantamine, formerly
known as Reminyl® and now available as a generic drug), Exelon® (rivastigmine),
and Aricept® (donepezil). Another drug, Cognex® (tacrine), was the
first approved cholinesterase inhibitor but is rarely prescribed today
due to safety concerns.
Scientists do not yet fully understand how cholinesterase
inhibitors work to treat AD, but research indicates that they prevent
the breakdown of acetylcholine, a brain chemical believed to be important
for memory and thinking. As AD progresses, the brain produces less
and less acetylcholine; therefore, cholinesterase inhibitors may eventually
lose their effect.
No published study directly compares these drugs.
Because they work in a similar way, switching from one of these drugs
to another probably will not produce significantly different results.
However, an AD patient may respond better to one drug than another.
for Moderate to Severe AD
A medication known as Namenda® (memantine), an N-methyl D-aspartate (NMDA)
antagonist, is prescribed to treat moderate to severe AD. This drug’s
main effect is to delay progression of some of the symptoms of moderate
to severe AD. It may allow patients to maintain certain daily functions
a little longer than they would without the medication. For example,
Namenda® may help a patient in the later stages of AD maintain his or
her ability to use the bathroom independently for several more months,
a benefit for both patients and caregivers.
Namenda® is believed to work
by regulating glutamate, an important brain chemical. When produced in
excessive amounts, glutamate may lead to brain cell death. Because NMDA
antagonists work very differently from cholinesterase inhibitors, the
two types of drugs can be prescribed in combination.
The FDA has also
approved Aricept® for the treatment of moderate to severe AD.