


A: Alzheimer's disease is not fatal, but the degradation of neurological function that is causes contributes to the development of certain infectious diseases, such as pneumonia, dehydration, malnutrition and/or other complications, and these can be fatal.

When an AD patient dies of one of these complications, AD is considered to be one of the causes of death. It is likely that the reporting of AD as the seventh leading cause of death in the U.S. is a significant underestimation of its true impact.

AD is the most common cause of dementia in the U.S., affecting 15 percent of Americans over age 65 –– about 20 percent of African Americans and Hispanics and 10 percent of Caucasians –– and over 40 percent of people over age 80, for a total of more than 5 million Americans. Many people with mild dementia have early AD but have not yet been diagnosed, so the true number of AD patients is even higher. As the baby boomers age, AD will become more prevalent and will affect over 8 million by 2030.

The early symptoms of AD include forgetfulness and mild confusion, and the severity of these may fluctuate from day to day. These patients may get lost easily, have trouble handling finances and may require more time to do normal tasks. Sometimes, early AD patients will avoid answering questions, answer questions in a roundabout way or change the subject to cover for their impaired memory.

Because of this, it is not uncommon for families to perceive the onset of AD as abrupt, even though it is a gradually progressive disease. An AD patient's cognitive function is evaluated by scoring a “mini mental status exam," a series of responses to a standardized set of questions. The overall score can be followed over time to assess disease progression.

Since other diseases can cause symptoms similar to those of AD, initial evaluation of a patient with dementia is focused on ruling out treatable conditions, such as thyroid dysfunction, vitamin deficiency –– like B12 or folate –– or central-nervous-system diseases, such as tumors, multi-infarct dementia or normal-pressure hydrocephalus.


Available AD treatments are medications called acetylcholinesterase inhibitors and N-methyl-D-aspartate receptor antagonists. Most studies conducted with these medications show some improvement –– or at least delay –– in the loss of cognition, functional ability and behavior, as well as delay in the need for nursing home placement.

In addition to medications to improve a patient's cognition and functional status, other treatments include medications to help minimize behavioral problems and interventions to ensure the patient's safety and to improve their living situation. This may include establishing a regular routine of daily activities, such as eating, hygiene, other personal care tasks and sleeping, as well as other interventions and activities to improve cognition and daily function. One key in all evaluations for patients with AD is to continually assess and re-assess their living situation to ensure their continued safety.

The mechanism behind which AD affects people is not clearly understood. Brain biopsy on autopsy usually shows senile plaques and neurofibrillary tangles thought to be from amyloid polypeptide deposition. Researchers have speculated that inflammatory changes from this condition destroy neighboring neurons. These changes start at least 10 to 20 years before symptoms become evident.

New advances in functional brain scanning with fluorodeoxyglucose positron emission tomography, functional MRI, perfusion MRI, perfusion single positron emission computed tomography and the development of amyloid tracers may allow identification of patients that are likely to develop symptomatic AD even before they have any symptoms.

Combining early patient identification with treatments now under development will slow or arrest the development of the underlying pathophysiologic brain anomalies that lead to AD. This is bringing new hope for improved outcomes for AD in the future.
