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Is It Alzheimer's Disease or Lewy Body Dementia?

Swank Center for Memory Care and Geriatric Consultation, ChristianaCare
Photo showing Lewy bodies
National Library of Medicine | NIH
Learn about dementia with Lewy bodies and how it differs from Alzheimer's disease.

The most common cause of major neurocognitive disorder (the new term for what physicians had previously called dementia) is Alzheimer’s disease (AD); however, about one third of older adults with dementia have a different condition.

How Common is Lewy Body Dementia?

After AD, Lewy body dementia (LBD) or dementia with Lewy bodies is one of the most frequent causes of dementia, affecting some 1.3 million Americans. To put this in perspective, Alzheimer’s affects about four times as many older adults. LBD usually can begin between ages 50 and 85, and typically becomes clinically apparent during a person’s mid-to-late 70s. The disease usually runs its course over about 6 years. 

What Are Lewy Bodies?

The microscopic findings in brain tissue from LBD patients are different from those in people with AD. The important distinction is that in LBD there are small “Lewy bodies” inside the brain’s cells.  These Lewy bodies are neither plaques nor tangles, but rather synuclein, the same protein found in brains of people with Parkinson’s disease. The clinical disease of LBD reflects the widespread distribution of Lewy bodies, which are especially dense in parts of the brain most specialized for movements, memories, reasoning, and emotions.


Similar to people with AD, those affected by LBD develop cognitive difficulties that can include problems with memory and reasoning.  Executive function and visuospatial cognition are prominently affected as well. Social and occupational functioning are affected to such a degree that ultimately the patient must depend on others for basic care. Unlike AD, the LBD patient shows symptoms that resemble Parkinson’s disease:  muscle stiffness, rigidity, and tremor.  Other characteristics that differentiate LBD from AD include disturbances of autonomic function, resulting in changes in blood pressure, temperature, and digestion; fluctuation of cognitive status so that there are very good days and very bad days; fainting and falling; and intense visual hallucinations.  Depressed mood, too, is common among those affected by LBD, and may represent not only a psychological reaction to this devastating disease but also a neurochemical consequence of its pathology.

In some cases, the onset of LBD is preceded by a remarkable and potentially dangerous disturbance of sleep called REM Behavior Disorder (RBD). Unlike people who sleep normally and whose muscles remain quiet during dreams, those with RBD can act out their dreams because their muscles remain active like those of an awake person. This activity can have dangerous, even life-threatening consequences, when an affected person strikes a bed partner or hurls himself out of bed while still asleep.  This sleep disorder is not characteristic of AD.


LBD, as you can see, can produce some severe behavioral changes. In people with AD, behavioral symptoms that threaten a person’s safety or the safety of others, may be treated with antipsychotic medications (although this is controversial and only one of the available options). Perhaps because LBD shares pathological and clinical features with not only AD but also Parkinson’s disease, physicians see a response to the high-potency antipsychotic medications in LBD that is toxic and even dangerous, similar to the reaction that a person with Parkinson’s disease might have to these antipsychotic medications.  The person with LBD who receives even a small dose of a high-potency antipsychotic medication (such as haloperidol, aripiprazole, olanzapine, or risperidone) can become profoundly stiff, sedated, and more confused and agitated. Some lower-potency antipsychotic medications such as quetiapine or, in some cases, clozapine, may be safer. A new, non-dopamine-blocking antipsychotic named pimavanserin has recently been approved for treatment of Parkinson’s Disease Psychosis and is in testing for use with Lewy Body Dementia patients at this time. Other medications, such as serotonergic antidepressants, provide additional and perhaps safer alternatives for treating these patients’ non-cognitive symptoms.

Special Concerns for the Caregivers

Caregivers of patients with LBD are stressed in many of the same ways as caregivers of AD patients. The cognitive decline, decreasing functional capacity, and non-cognitive disturbances are every bit as stressful. In addition, though, LBD patients can present special concerns because their ability to function changes from day to day. Their falls and hallucinations add further stress and risk. Their response to cognitive enhancers such as the cholinesterase inhibitors or memantine can be as good as that of AD patients, so their use should be considered.  

A Clear Diagnosis Is Important

Cost-conscious observers of health care point out that our treatments for major neurocognitive disorders are limited in their scope and only modestly effective. Knowing the cause of a cognitive disorders will be of greatest value, they point out, once we have very specific treatment approaches for different diseases. In the case of LBD, knowing the diagnosis is of great value, because it may alert clinicians to the potentially hazardous effects that might be produced in LBD patients by high-potency antipsychotics, a class of medications still often used (despite recognition of their limited benefits and potential adverse effects) to treat behavioral disturbances in AD. For this reason, even if for no others, identifying LBD is already a very worthwhile endeavor. In time, diagnostic clarity should become even more valuable as future treatments are developed to target LBD specifically.

More Information

A specialized source of information and support is the LBD Association, and their online caregiver community is available through their website. Finally, the National Institute on Aging provides helpful information on LBD for patients, families, and caregivers.



This content was first posted on: October 10, 2017

The information provided here is a public service of the BrightFocus Foundation and should not in any way substitute for personalized advice of a qualified healthcare professional; it is not intended to constitute medical advice. Please consult your physician for personalized medical advice. BrightFocus Foundation does not endorse any medical product, therapy, or resources mentioned or listed in this article. All medications and supplements should only be taken under medical supervision. Also, although we make every effort to keep the medical information on our website updated, we cannot guarantee that the posted information reflects the most up-to-date research.

These articles do not imply an endorsement of BrightFocus by the author or their institution, nor do they imply an endorsement of the institution or author by BrightFocus.

Some of the content may be adapted from other sources, which will be clearly identified within the article.

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