Lewy bodies are abnormal clumps of a protein called alpha‑synuclein that build up inside nerve cells in the brain.

These clumps interfere with how brain cells work and survive, particularly in areas that control movement, thinking, sleep, mood and behaviour.

What are Lewy bodies?

Lewy bodies are abnormal clumps of a protein called alpha‑synuclein that build up inside nerve cells in the brain. These clumps interfere with how brain cells work and survive, particularly in areas that control movement, thinking, sleep, mood and behaviour.

Alpha‑synuclein is found in healthy brains, but in Parkinson’s it folds the wrong way and sticks together. Over time, these protein clumps can spread to more parts of the brain. As this happens, symptoms can change and may become more complex.

How do Lewy bodies form?

Lewy bodies form when alpha‑synuclein proteins misfold and aggregate. The brain’s normal waste‑removal systems then struggle to clear them. Several factors influence this process:

  • Genetics: Variants in genes such as SNCA, LRRK2 and GBA can increase the risk of alpha‑synuclein build‑up.
  • Ageing: The brain becomes less efficient at clearing damaged proteins with age.
  • Cell stress: Inflammation, oxidative stress and mitochondrial problems make protein misfolding more likely.
  • Spread between cells: Misfolded alpha‑synuclein can move from one nerve cell to another, allowing Lewy bodies to spread through brain networks.

These processes do not happen suddenly. Lewy bodies usually develop over many years before symptoms appear.

Why are Lewy bodies a problem in Parkinson’s?

In Parkinson’s, Lewy bodies are closely linked to the loss of dopamine‑producing nerve cells. Dopamine is essential for smooth, coordinated movement. As these cells are damaged or die, movement symptoms appear, including:

  • Slowness of movement (bradykinesia)
  • Muscle stiffness (rigidity)
  • Tremor (in around 70% of PwP)
  • Changes in posture and balance

Lewy bodies are also found in brain areas involved in thinking, emotion and sleep. This explains why Parkinson’s includes non‑movement symptoms such as:

The number and location of Lewy bodies help explain why symptoms differ from person to person and why Parkinson’s changes over time.

How are Lewy body conditions diagnosed?

There is no single test that can confirm Lewy bodies during life. Diagnosis relies on clinical assessment and history, supported by tests that rule out other causes.

Assessment may include:

  • Detailed medical and symptom history
  • Neurological and cognitive examinations
  • Brain imaging, such as MRI or specialised nuclear scans
  • Sleep assessments if REM sleep behaviour disorder is suspected

A diagnosis is usually made by a neurologist or geriatrician with experience in Parkinson’s and dementia.

What is Lewy body dementia?

Lewy body dementia is an umbrella term for dementias caused by Lewy bodies in the brain. It describes a group of conditions where problems with thinking, attention, perception and daily function are significant.

Lewy body dementia includes two related conditions:

Both conditions involve the same underlying brain changes. The main difference lies in the timing of dementia symptoms in relation to movement symptoms.

What is dementia with Lewy bodies?

Dementia with Lewy bodies is diagnosed when problems with thinking and daily function appear before or at the same time as movement symptoms. Core features often include:

  • Fluctuating attention and alertness
  • Visual hallucinations that are detailed and recurrent
  • Parkinson‑like movement symptoms
  • REM sleep behaviour disorder

People with DLB may also experience sensitivity to certain medications, particularly antipsychotics. This sensitivity can lead to severe side effects and must be managed carefully.

What is Parkinson’s disease dementia?

Parkinson’s dementia develops after a person has lived with Parkinson’s for some time, usually many years. Movement symptoms such as tremor and stiffness come first, followed later by gradual changes in thinking.

Features of Parkinson’s dementia may include:

  • Slowed thinking and problem‑solving
  • Difficulties with planning and attention
  • Visual hallucinations
  • Changes in mood and motivation

Not everyone with Parkinson’s will develop dementia. Risk increases with age, longer duration of Parkinson’s, and the presence of certain non‑movement symptoms.

What is the difference between dementia with Lewy bodies and Parkinson’s dementia?

The key difference is timing:

  • Dementia with Lewy bodies: Thinking problems appear before or within one year of movement symptoms.
  • Parkinson’s dementia: Dementia develops after Parkinson’s has been present for more than one year.

The symptoms can be very similar. Both conditions involve Lewy bodies and are managed in similar ways. Many experts see them as part of the same spectrum rather than completely separate conditions.

Key Statistics

  • Lewy body dementia comprises both dementia with Lewy bodies and Parkinson’s disease dementia, and is the second most common cause of neurodegenerative dementia.
  • Dementia with Lewy bodies accounts for around 10–15% of all dementias.
  • Visual hallucinations affect up to 70% of people with Parkinson’s dementia or dementia with Lewy bodies.
  • Long‑term studies show that dementia risk rises with age and duration of Parkinson’s, reflecting the spread of Lewy bodies through the brain.

How are Lewy bodies treated?

There is currently no treatment that removes Lewy bodies from the brain. Management focuses on treating symptoms, supporting function and improving quality of life.

Movement symptoms

  • Levodopa is the main treatment for movement symptoms in Parkinson’s and Parkinson’s dementia.
  • Benefits must be balanced against side effects, including hallucinations in some people.

Thinking & hallucinations

  • Cholinesterase inhibitors (such as rivastigmine or donepezil) can improve attention, thinking and hallucinations in Lewy body dementia.
  • These medicines are commonly used and supported by evidence.

Mental health & behaviour

  • Depression and anxiety can be treated with psychological support and selected medications.
  • Antipsychotic medicines should be used with extreme caution. Some can cause severe reactions in people with Lewy body dementia.

Sleep & other symptoms

  • REM sleep behaviour disorder may respond to melatonin or clonazepam.
  • Blood pressure changes, constipation and pain should be managed as part of routine Parkinson’s care.

Treatment plans should be individualised and reviewed regularly.

Non‑medication approaches

Non‑drug strategies are essential and often as important as medication.

These include:

Simple environmental changes, such as good lighting and clear routines, can reduce hallucinations and confusion.

Upcoming research & future directions

Research into Lewy bodies is advancing, although no disease‑modifying treatment is yet available.

Key areas of research include:

  • Alpha‑synuclein therapies: Studies are testing antibodies and vaccines designed to reduce or block alpha‑synuclein build‑up. Early trials have had mixed results, but research continues.
  • Genetic‑targeted treatments: Therapies aimed at LRRK2 and GBA pathways are under development for people with relevant genetic variants.
  • Biomarkers: New tests using spinal fluid, blood and imaging aim to detect Lewy body changes earlier and more accurately.
  • Personalised medicine: Researchers are working to tailor treatments based on symptoms, genetics and disease pattern rather than a one‑size‑fits‑all approach.

Clinical trials are essential to this progress. Participation may be an option for some people living with Parkinson’s and Lewy body dementia.

Key points to remember

  • Lewy bodies are abnormal protein clumps that damage brain cells.
  • They are central to Parkinson’s, Parkinson’s dementia and dementia with Lewy bodies.
  • Symptoms depend on where Lewy bodies build up and how widely they spread.
  • There is no cure yet, but many symptoms can be treated.
  • Ongoing research aims to slow or stop Lewy body formation in the future.

If you or the person you support has changes in thinking, hallucinations or behaviour, raise this early with your care team. Early assessment and treatment make a meaningful difference.

How do I access supports?

It’s advisable to explore all available pathways to find the support that best suits your individual needs. Look to:

  • getting a GP referral to someone with Parkinson‘s experience
  • your state-based Parkinson’s organisation for advice
  • Advance Care Planning Australia to help ensure health care wishes are met
  • Palliative Care Australia
  • Ask Izzy https://askizzy.org.au/ to search for local services to access
  • private health to see what is covered in relation to consultations and expenses
  • DVA, NDIS or My Aged Care plan supports.

Infosheet under review

References

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Braak, H., Del Tredici, K., Rüb, U., de Vos, R. A. I., Jansen Steur, E. N. H., & Braak, E. (2003). Staging of brain pathology related to sporadic Parkinson’s. Neurobiology of Aging, 24(2), 197–211. https://doi.org/10.1016/S0197-4580(02)00065-9

Dickson D. W. (2025). Neuropathology of Parkinson’s Disease and Parkinsonism. Cold Spring Harbor perspectives in medicine, a041610. Advance online publication. https://doi.org/10.1101/cshperspect.a041610

Fenelon, G., Mahieux, F., Huon, R., & Ziegler, M. (2000). Hallucinations in Parkinson’s: Prevalence, phenomenology and risk factors. Brain, 123(4), 733–745. https://doi.org/10.1093/brain/123.4.733

McKeith, I. G., Boeve, B. F., Dickson, D. W., Halliday, G., Taylor, J. P., Weintraub, D., Aarsland, D., Galvin, J., Attems, J., Ballard, C. G., Bayston, A., Beach, T. G., Blanc, F., Bohnen, N., Bonanni, L., Bras, J., Brundin, P., Burn, D., Chen-Plotkin, A., Duda, J. E., … Kosaka, K. (2017). Diagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium. Neurology, 89(1), 88–100. https://doi.org/10.1212/WNL.0000000000004058

Ross, G.W., Abbott, R.D., Petrovitch, H., Tanner, C.M., Davis, D.G., Nelson, J., Markesbery, W.R., Hardman, J., Masaki, K., Launer, L. and White, L.R. (2006), Association of olfactory dysfunction with incidental Lewy bodies. Mov. Disord., 21: 2062-2067. https://doi.org/10.1002/mds.21076

Science Direct Topic Summary: Lewy Bodies. https://www.sciencedirect.com/topics/neuroscience/lewy-body

Spillantini, M. G., Schmidt, M. L., Lee, V. M., Trojanowski, J. Q., Jakes, R., & Goedert, M. (1997). Alpha-synuclein in Lewy bodies. Nature, 388(6645), 839–840. https://doi.org/10.1038/42166

Taylor, J. P., McKeith, I. G., Burn, D. J., Boeve, B. F., Weintraub, D., Bamford, C., Allan, L. M., Thomas, A. J., & O’Brien, J. T. (2020). New evidence on the management of Lewy body dementia. The Lancet. Neurology, 19(2), 157–169. https://doi.org/10.1016/S1474-4422(19)30153-X

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