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

Swank Center for Memory Care and Geriatric Consultation, ChristianaCare
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 Dementia?

Dementia is a syndrome, not a specific disease. This means that the clinical features of dementia can result from any one of a large group of injuries, infections, or diseases. The symptoms of dementia can include one or more from a list that includes memory failure, diminished ability to keep multiple tasks in mind simultaneously and divide attention between them, problems with language comprehension or expression, trouble understanding spatial orientation, impaired executive function, and inaccurate decoding of others’ nonverbal cues.

What is Alzheimer's Disease?

Alzheimer's disease (AD), the most common form of dementia among older adults, is an irreversible degeneration of the brain that causes disruptions in memory, cognition, personality, and other functions that eventually lead to death from complete brain failure. Genetic and environmental factors including diet, activity, smoking, traumatic brain injury, diabetes, and other medical diseases contribute to the risk of developing this form of the disease. The hallmarks of Alzheimer's disease are the accumulation of beta-amyloid plaques between nerve cells (neurons) in the brain and neurofibrillary tangles, which are twisted fibers found inside the brain's cells). These tangles consist primarily of a protein called tau.

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. Many of the symptoms of idiopathic Parkinson's disease result when certain nerve cells that produce dopamine in the brain begin to malfunction and die.

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

Age of Onset

The majority of people with AD have the late-onset type—where symptoms first appear after the mid-60s. 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.

A small percentage of people with AD and PD have "early-onset" disease. In PD, symptoms can begin before age 50. The early-onset forms of PD are often, but not always inherited. In AD, the early-onset form begins before age 60. Many people with early-onset AD, although not all, have inherited specific gene mutations.

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.

The table below summarizes the similarities and differences between Alzheimer's and Parkinson's. On mobile devices, swipe left to see all of the table columns.


Comparion of Alzheimer's and Parkinson's Disease
 Alzheimer's Parkinson's
Typical Age of Onset

After the mid-60s (late-onset form)

Before age 60 (early-onset form)

50 - 65 (late-onset form)

Before age 50 (early-onset form)

Key Proteins Associated with the DiseaseBeta-amyloid and tauAlpha-synuclein
Movement and CoordinationDiminshed coordinationWill display at least two of these three symptoms: muscle rigidity, slowed movements, or tremor
Disruptions in Memory, Cognition, Personality, and other FunctionsTypcially presentOften present
MemoryDifficulty learning new memoriesDifficulty retrieving memories
Apathy and DepressionCommonCommon
Psychotic Symptoms
(delusions, paranoia, and hallucinations)
Can occurCan occur both as part of the disease process or as a side effect of dopaminergic medications
Sleep DisordersSleep continuity is disrupted and fragmented early in disease, resulting in naps during the day and wakeful episodes at night

REM behavior disorder (active bodily movements during dreams) is common

Quality of sleep deteriorates in general



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.

This content was first posted on: May 24, 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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