171
Diagnosis
A diagnosis of Alzheimer’s disease is most commonly made by an individual’s primary
care physician. The physician obtains a medical and family history, including psychiatric
history and history of cognitive and behavioral changes. Ideally, a family member or other
individual close to the patient is available to provide input. The physician also conducts
cognitive tests and physical and neurologic examinations. In addition, the patient may
undergo magnetic resonance imaging (MRI) scans to identify brain changes that have
occurred so the physician can rule out other possible causes of cognitive decline. 9
Etiology
Although scientists do not know how the Alzheimer’s disease process begins, it appears
likely that damage to the brain starts a decade or more before problems become evident.
During the preclinical stage of the disease, people are symptom-free, but toxic changes
are taking place in the brain. Abnormal deposits of proteins form amyloid plaques and
neurofibrillary tangles (tauopathies) throughout the brain and once-healthy neurons begin
to work less efficiently. (The major component of the tangles is an abnormally hyperphos-
phorylated and aggregated form of tau.10) Over time, neurons lose their ability to function
and communicate with each other and eventually die. The damage begins in the entorhi-
nal cortex (a sliver of tissue behind the ears, toward the middle of the brain). It spreads
to a nearby structure in the brain, the hippocampus, which is essential in transforming
daily experiences into lasting memories. As more neurons die, affected brain regions
begin to shrink significantly.11 Many molecular lesions have been detected in patients
with Alzheimer’s disease, but the overarching theme to emerge from the data is that an
accumulation of misfolded proteins in the aging brain results in oxidative and inflam-
matory damage, which in turn leads to energy failure and synaptic dysfunction.12 The
molecular mechanisms of the disease are extremely complicated and many of the factors
leading to amyloid deposition and tauopathy in humans are unknown.13 It has, however,
become clear that Alzheimer’s disease develops because of a complex series of events that
take place over a long period of time. It is also likely that the causes include some mix of
genetic, environmental and lifestyle factors.
Treatment
Because Alzheimer’s disease is complex, current treatment and research approaches
focus on helping patients maintain mental function, managing behavioral symptoms and
attempting to slow or delay eventual memory loss. Four medications have been approved
for treatment. Donepezil, rivastigimine and galantamine are used to treat mild to moder-
ate conditions. Donepezil can also be used for severe cases. Memantine is used to treat
moderate to severe Alzheimer’s. These drugs work by regulating neurotransmitters. They
may help maintain thinking, memory and speaking skills, and address certain behavioral
problems. The drugs, however, do not change the underlying disease process and may help
for only a limited time.14 Drugs and other supportive treatment are used to manage other
common symptoms including sleeplessness, agitation, wandering, anger and depression.
Fortunately, there are methods, in addition to a physical examination, to detect
Alzheimer’s before other symptoms are apparent. The gold standard for detecting neu-
rofibrillary tangles and beta amyloid plaques is a radiotracer, 18 F-FDDNP, a molecule
that binds both lesions, and positron emission tomography. This technique developed by
researchers at the University of California at Los Angeles makes it possible not only to
detect but also to measure both types of lesions in the brains of living Alzheimer’s patients.15
The technique may be particularly useful in tracking the effectiveness of interventions
designed to delay the onset of dementia symptoms and eventually prevent the disease.16
Alzheimer’s—The Most Dreaded Age-related Disease
Diagnosis
A diagnosis of Alzheimer’s disease is most commonly made by an individual’s primary
care physician. The physician obtains a medical and family history, including psychiatric
history and history of cognitive and behavioral changes. Ideally, a family member or other
individual close to the patient is available to provide input. The physician also conducts
cognitive tests and physical and neurologic examinations. In addition, the patient may
undergo magnetic resonance imaging (MRI) scans to identify brain changes that have
occurred so the physician can rule out other possible causes of cognitive decline. 9
Etiology
Although scientists do not know how the Alzheimer’s disease process begins, it appears
likely that damage to the brain starts a decade or more before problems become evident.
During the preclinical stage of the disease, people are symptom-free, but toxic changes
are taking place in the brain. Abnormal deposits of proteins form amyloid plaques and
neurofibrillary tangles (tauopathies) throughout the brain and once-healthy neurons begin
to work less efficiently. (The major component of the tangles is an abnormally hyperphos-
phorylated and aggregated form of tau.10) Over time, neurons lose their ability to function
and communicate with each other and eventually die. The damage begins in the entorhi-
nal cortex (a sliver of tissue behind the ears, toward the middle of the brain). It spreads
to a nearby structure in the brain, the hippocampus, which is essential in transforming
daily experiences into lasting memories. As more neurons die, affected brain regions
begin to shrink significantly.11 Many molecular lesions have been detected in patients
with Alzheimer’s disease, but the overarching theme to emerge from the data is that an
accumulation of misfolded proteins in the aging brain results in oxidative and inflam-
matory damage, which in turn leads to energy failure and synaptic dysfunction.12 The
molecular mechanisms of the disease are extremely complicated and many of the factors
leading to amyloid deposition and tauopathy in humans are unknown.13 It has, however,
become clear that Alzheimer’s disease develops because of a complex series of events that
take place over a long period of time. It is also likely that the causes include some mix of
genetic, environmental and lifestyle factors.
Treatment
Because Alzheimer’s disease is complex, current treatment and research approaches
focus on helping patients maintain mental function, managing behavioral symptoms and
attempting to slow or delay eventual memory loss. Four medications have been approved
for treatment. Donepezil, rivastigimine and galantamine are used to treat mild to moder-
ate conditions. Donepezil can also be used for severe cases. Memantine is used to treat
moderate to severe Alzheimer’s. These drugs work by regulating neurotransmitters. They
may help maintain thinking, memory and speaking skills, and address certain behavioral
problems. The drugs, however, do not change the underlying disease process and may help
for only a limited time.14 Drugs and other supportive treatment are used to manage other
common symptoms including sleeplessness, agitation, wandering, anger and depression.
Fortunately, there are methods, in addition to a physical examination, to detect
Alzheimer’s before other symptoms are apparent. The gold standard for detecting neu-
rofibrillary tangles and beta amyloid plaques is a radiotracer, 18 F-FDDNP, a molecule
that binds both lesions, and positron emission tomography. This technique developed by
researchers at the University of California at Los Angeles makes it possible not only to
detect but also to measure both types of lesions in the brains of living Alzheimer’s patients.15
The technique may be particularly useful in tracking the effectiveness of interventions
designed to delay the onset of dementia symptoms and eventually prevent the disease.16
Alzheimer’s—The Most Dreaded Age-related Disease