Alzheimer’s and Parkinson’s Disease: Similarities and Differences

Swank Memory Care Center, Christiana Care Health System
Wednesday, May 24, 2017
Brain illustration

Explore the similarities and differences between two common degenerative brain disorders.

Ron brings his 78-year-old wife, Sara, to the Memory Clinic, with a pressing concern. Sara is forgetting things more often even though her Parkinson’s disease symptoms appear to be under good control with standard medications, healthy diet, and plenty of physical activity. She is losing her train of thought mid-sentence and she became very confused about where she was while driving the well-traveled route to her daughter’s home. Is she developing dementia? Is that a part of Parkinson’s disease? Or is she developing Alzheimer’s disease? And what are the differences between Alzheimer’s and Parkinson’s?

What is Parkinson’s Disease?

Parkinson’s disease (PD) was described by James Parkinson nearly 100 years before Dr. Alois Alzheimer described the dementia later named Alzheimer’s disease (AD). Called the “shaking palsy” by Parkinson, PD is diagnosed when a person shows at least two of these three symptoms: slowed movements (bradykinesia), muscle rigidity, and tremor (at rest). We recognize many other associated signs of PD, including expressionless face, quiet speech, cramped handwriting, shuffling gait, trouble getting out of a chair, and difficulty swallowing.

Most cases are called “idiopathic,” meaning the cause remains unknown, although a small number of cases are linked with reversible toxic medication effects (antipsychotics and some anti-vomiting medications), poisoning (certain pesticides, manganese, carbon monoxide), head trauma, or more complex PD-like neurological disorders (such as vascular parkinsonism, progressive supranuclear palsy, and multiple system atrophy).

Age of Onset

PD begins earlier than AD, typically between ages 50 and 65, with an average age of onset of around 62 years, and only a few cases begin before age 40. With a prevalence of around 3 cases per 1,000 people, PD is less common than AD but still an important cause of neurological illness among older adults.

Like the symptoms of AD, those of PD are caused by destruction of brain cells. Unlike AD, in which plaques and tangles are found, the microscopic finding in PD brains is loss of cells that produce dopamine, an important brain chemical involved in nerve cell communication, in a movement-related part of the brain called the substantia nigra. The cells in the substantia nigra can be seen to include abnormal collections of a protein, called “Lewy bodies.”

Cognitive Decline

Cognitive decline is common in both AD and PD, though significantly less common in PD. As many as half of people with PD develop cognitive difficulties, which can range from mild forgetfulness to full-blown dementia. The dementia of PD is called “subcortical” because of the location of affected brain areas, and subcortical dementias have somewhat different clinical symptoms than a “cortical” dementia like AD. In PD dementia, slowed physical activity can be accompanied by slowed thinking and by problems with memory that are more responsive to reminders than those of AD because the difficulty is with memory retrieval rather than, as in AD, with storage of new learning.

Behavioral Symptoms


Just like people with AD, people with PD can also develop behavioral problems. Apathy is a common development in both diseases, and so is depression. Sometimes it’s difficult to tell these syndromes apart but it’s important to try because they are managed differently. The depression of PD is often responsive to antidepressant treatment, maybe more than that of AD, and the opportunity for symptom-reducing treatment of PD should not be overlooked.


Anxiety is common to both PD and AD, and may require behavioral treatment, lowering of AD or PD medications, or addition of antidepressant or antianxiety medications—keeping in mind that both conditions leave patients vulnerable to medication side effects.

Psychotic Symptoms

Psychotic symptoms such as delusions and hallucinations, too, can occur in both AD and PD. In both disorders, these symptoms may indicate delirium caused by infection or other medical conditions. In PD patients, an additional risk for psychotic symptoms is added by the medications that treat movement disorder symptoms. At higher doses, these otherwise helpful medications can induce hallucinations and paranoid ideas.

Sleep Disturbances

Finally, the quality of sleep deteriorates in both AD and PD. AD patients often have fragmented sleep, while PD patients experience a different problem called REM (rapid eye movement) behavior disorder, in which physical activity occurs during the normally motionless period of REM sleep. REM behavior disorder can respond to treatment with clonazepam, a medication that would usually be avoided in AD because of concern about effects on memory and alertness.

Lewy Body Dementia

Some older adults develop movement symptoms similar to those of PD after, or only shortly before, developing cognitive difficulties that look like AD. This combination of movement and cognitive changes is characteristic of the disease considered by some to be the second most common dementia: Lewy Body Dementia (LBD). As its name suggests, LBD is a condition in which cognitive decline is very prominent, sometimes much more prominent than movement symptoms, yet the microscopic brain findings are those similar to PD.

Whether LBD is truly a different condition than PD with dementia or is a variant of the same disorder remains a topic under debate, although the finding of increased beta amyloid deposits (amyloid plaques) in the brains of people with LBD has suggested a difference between these conditions.  The symptoms of LBD can include dramatic fluctuations in cognitive functioning as well as falls and psychotic symptoms. Similar to patients with PD and even more than patients with AD, standard antipsychotic treatment is often complicated by severe toxic reactions. The cognitive enhancers used in AD, however, can play a useful role in treating LBD.


Distinguishing between different types of neurodegenerative conditions is important: it helps in determining the best treatment approach. Medications suitable for one of these conditions, for example, might create problems when given to a patient with the other condition. Sara’s further testing identified mild cognitive impairment symptoms that are probably related to her PD but exacerbated by one of the medications she has been taking. Her mental clarity improved a little with adjustment of that medication.  Although PD-related cognitive changes could get worse over time, there is no sign that she is developing AD and in fact at this point there is no diagnosis of dementia.


Further Reading:

Aarsland D, Larsen JP, Lim NG, et al. Range of neuropsychiatric disturbances in patients with Parkinson’s disease. J Neurol Neurosurg Psychiatry 1999;67:492-6.

Aarsland D, Cummings JL, Larsen JP. Neuropsychiatric differences between Parkinson’s disease with dementia and Alzheimer’s disease. Int J Geriatric Psychiatry 2001;16:184-91.

Borek LL, Amick MM, Friedman JH. Non-motor aspects of Parkinson’s Disease. CNS Spectr 2006;11(7):541-54.

Ferreri F, Agbokou C, Gauthier S. Recognition and management of neuropsychiatric complications in Parkinson’s disease. CMAJ 2006;175:1545-52.

Kirsch-Darrow L, Fernandez HF, Marsiske M, et al. Dissociating apathy and depression in Parkinson disease. Neurology 2006;67:33-8.

McDonald WM, Richard IH, DeLong MR. Prevalence, etiology, and treatment of depression in Parkinson’s disease. Biological Psychiatry 2003;54:363-75.

Menza M, Marsh L (Eds). Psychiatric Issues in Parkinson’s Disease. A Practical Guide. New York, Taylor & Francis, 2006.

Miyasaki JM, Shannon K, Voon V, et al. Practice parameter:  Evaluation and treatment of depression, psychosis, and dementia in Parkinson disease (an evidence-based review): Report of the quality standards subcommittee of the American Academy of Neurology. Neurology 2007;68:80-1.

Stacy M. Sleep disorders in Parkinson’s disease. Epidemiology and management . Drugs Aging 2002;19:733-9.

Weintraub D, Stern MB. Psychiatric complications in Parkinson Disease. Am J Geriatr Psychiatry 2005;13(10):844-51.

Gomperts SN, et al. Imaging amyloid deposition in Lewy body diseases. Neurology. 2008 Sep 16; 71(12): 903–910.

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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