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Alzheimer Disease

Practice Essentials

Alzheimer disease (AD) is a neurodegenerative disorder marked by cognitive and behavioral impairment that significantly interferes with social and occupational functioning. It is an incurable disease with a long preclinical period and progressive course. In AD, plaques develop in the hippocampus, a structure deep in the brain that helps to encode memories, and in other areas of the cerebral cortex that are involved in thinking and making decisions. Whether plaques themselves cause AD or whether they are a by-product of the AD process remains unknown. The following image depicts one of the cardinal neuroimaging findings in AD – hippocampal atrophy.

Coronal T1-weighted magnetic resonance imaging (MR

Coronal T1-weighted magnetic resonance imaging (MRI) scan in a patient with moderate Alzheimer disease. Brain image reveals hippocampal atrophy, especially on the right side.

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Signs and symptoms

Preclinical Alzheimer disease

A patient with preclinical AD may appear completely normal on physical examination and mental status testing. Specific regions of the brain (eg, entorhinal cortex, hippocampus) are likely to be affected decades before any signs or symptoms appear.

Mild Alzheimer disease

Signs of mild AD can include the following:

Memory loss

Confusion about the location of familiar places

Taking longer to accomplish normal, daily tasks

Trouble handling money and paying bills

Compromised judgment, often leading to bad decisions

Loss of spontaneity and sense of initiative

Mood and personality changes; increased anxiety

Moderate Alzheimer disease

The symptoms of this stage can include the following:

Increasing memory loss and confusion

Shortened attention span

Problems recognizing friends and family members

Difficulty with language; problems with reading, writing, working with numbers

Difficulty organizing thoughts and thinking logically

Inability to learn new things or to cope with new or unexpected situations

Restlessness, agitation, anxiety, tearfulness, wandering, especially in the late afternoon or at night

Repetitive statements or movement; occasional muscle twitches

Hallucinations, delusions, suspiciousness or paranoia, irritability

Loss of impulse control: Shown through behavior such as undressing at inappropriate times or places or vulgar language

Perceptual-motor problems: Such as trouble getting out of a chair or setting the table

Severe Alzheimer disease

Patients with severe AD cannot recognize family or loved ones and cannot communicate effectively. They are completely dependent on others for care, and all sense of self seems to vanish.

Other symptoms of severe AD can include the following:

Weight loss

Seizures, skin infections, difficulty swallowing

Groaning, moaning, or grunting

Increased sleeping

Lack of bladder and bowel control

In end-stage AD, patients may be in bed much or all of the time. Death is often the result of other illnesses, frequently aspiration pneumonia.

See Clinical Presentation for more detail.


Means of diagnosing AD include the following:

Clinical examination: The clinical diagnosis of AD is usually made during the mild stage of the disease, using the above-listed signs

Lumbar puncture: levels of tau and phosphorylated tau in the cerebrospinal fluid are often elevated in AD, whereas amyloid levels are usually low; at present, however, routine measurement of CSF tau and amyloid is not recommended except in research settings

Imaging studies: Imaging studies are particularly important for ruling out potentially treatable causes of progressive cognitive decline, such as chronic subdural hematoma or normal-pressure hydrocephalus.
 Moreover, volumetric studies of the hippocampus and 2-[18F]fluoro-2-Deoxy-D-glucose positron emission tomography (FDG-PET) with or without amyloid imaging have been employed for early detection and differentiating dementia etiologies.

See Clinical Presentation and Workup for more detail.


All drugs approved by the US Food and Drug Administration (FDA) for the treatment of AD are symptomatic therapies that modulate neurotransmitters, either acetylcholine or glutamate. The standard medical treatment for AD includes cholinesterase inhibitors (ChEIs) and a partial N-methyl-D-aspartate (NMDA) antagonist.
 They do not treat the underlying cause of AD nor halt the rate of decline.

The following classes of psychotropic medications have been used to treat the secondary symptoms of AD, such as depression, agitation, aggression, hallucinations, delusions, and sleep disorders



Antiparkinsonian agents


Antiepileptic drugs


Amyloid-directed antibody


There are no proven modalities for preventing AD,
but evidence, largely epidemiologic, suggests that healthy lifestyles can reduce the risk of developing the disease; the following may be protective

Physical activity


Cardiorespiratory fitness

Diet: Although no definitive dietary recommendations can be made, in general, nutritional patterns that appear beneficial for AD prevention fit the Mediterranean diet

See Treatment and Medication for more detail.

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