Lewy body

Photomicrographs of regions of substantia nigra in this Parkinson's patient show Lewy bodies and Lewy neurites in various magnifications. Top panels show a 60-times magnification of the alpha-synuclein intraneuronal inclusions aggregated to form Lewy bodies. The bottom panels are 20x magnification images that show strand-like Lewy neurites and rounded Lewy bodies of various sizes. Neuromelanin-laden cells of the substantia nigra are visible in the background. Stains used: mouse monoclonal alpha-synuclein antibody; counterstained with Mayer's haematoxylin
Lewy bodies

Lewy bodies are abnormal aggregates of protein that develop inside nerve cells in Parkinson's disease (PD), Lewy body dementia, and some other disorders. They are identified under the microscope when histology is performed on the brain.

Lewy bodies appear as spherical masses that displace other cell components. Lewy bodies may be found in the brainstem (within the Substantia Nigra) or within the cortex. A classical Lewy body is an eosinophilic cytoplasmic inclusion consisting of a dense core surrounded by a halo of 10-nm-wide radiating fibrils, the primary structural component of which is alpha-synuclein. Cortical Lewy bodies are also composed of alpha-synuclein fibrils, but are less defined and lack halos. In histopathology, Cortical Lewy bodies are a distinguishing feature for dementia with Lewy bodies (DLB), but may occasionally be seen in ballooned neurons characteristic of Pick's disease and corticobasal degeneration,[1] as well as in patients with other tauopathies.[2] They are also seen in cases of multiple system atrophy, particularly the Parkinsonian variant.[3]


In 1910 Fritz Heinrich Lewy studied in Berlin to get his doctorate.[4] Fritz was the first doctor who noticed that there are some unusual proteins in the brain that make some people act and think differently. But, as of that time, scientists hadn't been able to figure out what the exact purpose of this protein actually is to the brain. Fritz's finding become known as Lewy bodies. This finding was published in the Handbook of Neurology in 1912.[5]

According to the Journal of the History of the Neurosciences, Dr. Lewy became interested in studying more about the brain (Neurology), because of the discovery that Alois Alzheimer made in 1906. In the article, it mentioned that the third reported case of Alzheimer's had histological structures that happened to be similar to Lewy body histology slides, but the contribution wasn't really given to Fritz's finding.[6]

Cell biology

Photomicrograph of the dorsal motor nucleus of the vagus nerve (DmX) in a transverse section along the upper medulla shown to be affected by the abnormally deposited alpha synuclein as part of intraneuronal Lewy bodies found (extreme right): DmX is one of the earliest sites affected by synuclein deposition in Parkinson's disease.[7]

A Lewy body is composed of the protein alpha-synuclein associated with other proteins, such as ubiquitin,[8] neurofilament protein, and alpha B crystallin. Tau proteins may also be present, and Lewy bodies may occasionally be surrounded by neurofibrillary tangles.[9][10] Lewy bodies and NFTs can occasionally exist in the same neuron, particularly in the amygdala.[11]

Lewy bodies are believed to represent an aggresome response in the cell.[12]

Lewy neurites

Lewy neurites are abnormal neurites in diseased neurons, containing granular material and abnormal α-synuclein filaments similar to those found in Lewy bodies.[13] Like Lewy bodies, lewy neurites are a feature of α-synucleinopathies such as dementia with Lewy bodies, Parkinson's disease, and multiple system atrophy.[14] They are also found in the CA2-3 region of the hippocampus in Alzheimer's disease.[14]

Cultural reference


Notable people who suffered from Lewy body dementia include:

In fiction

See also


  1. Dickson DW, Feany MB, Yen SH, Mattiace LA, Davies P (1996). "Cytoskeletal pathology in non-Alzheimer degenerative dementia: new lesions in diffuse Lewy body disease, Pick's disease, and corticobasal degeneration". Journal of Neural Transmission. Supplementum. 47: 31–46. doi:10.1007/978-3-7091-6892-9_2. PMID 8841955.
  2. Popescu, A; Lippa, CF; Lee, VM; Trojanowski, JQ (2004). "Lewy Bodies in the Amygdala: Increase of -Synuclein Aggregates in Neurodegenerative Diseases With Tau-Based Inclusions". Archives of Neurology. 61 (12): 1915–1919. doi:10.1001/archneur.61.12.1915. PMID 15596612.
  3. Jellinger KA (2007). "More frequent Lewy bodies but less frequent Alzheimer-type lesions in multiple system atrophy as compared to age-matched control brains". Acta Neuropathologica. 114 (3): 299–303. doi:10.1007/s00401-007-0227-4. PMID 17476513.
  4. Lewy, Friedrich. "Whonamedit?".
  5. Hake MD, Ann Marie. "Dementia with Lewy bodies". MEDMERITS TM.
  6. García-Albea, E., Albea, E.; Trullen, J. M. Pérez2, J. M. Pérez (July 30, 2016). "The Spanish School of Neurology and the First American Cases of Alzheimer's Disease.". Journal of the History of the Neurosciences. December 1, 2003. 12 (4) via Database. Check date values in: |access-date= (help);
  7. Braak H, Del Tredici K, Rüb U, de Vos RA, Jansen Steur EN, Braak E (March–April 2003). "Staging of brain pathology related to sporadic Parkinson's disease.". Neurobiol Aging. 24 (2): 197–211. doi:10.1016/S0197-4580(02)00065-9. PMID 12498954.
  8. Engelender S (April 2008). "Ubiquitination of alpha-synuclein and autophagy in Parkinson's disease". Autophagy. 4 (3): 372–4. doi:10.4161/auto.5604. PMID 18216494.
  9. Ishizawa, Takashi MD; Matilla, Petri MD; Davies, Peter; Wang, Dengshun MD; Dickson, Dennis W. MD (April 2003). "Colocalization of tau and alpha-synuclein epitopes in Lewy bodies.". Journal of Neuropathology & Experimental Neurology. 62 (4): 389–397. PMID 12722831.
  10. Arima, K; Hirai, S; Sunohara, N; Aoto, K; Izumiyama, Y; Uéda, K; Ikeda, K; Kawai, M; Arima K, Hirai S, Sunohara N, Aoto K, Izumiyama Y, Uéda K, Ikeda K, Kawai M. (1999). "Cellular co-localization of phosphorylated tau- and NACP/alpha-synuclein-epitopes in Lewy bodies in sporadic Parkinson's disease and in dementia with Lewy bodies". Brain Research. 843 (1–2): 53–61. doi:10.1016/S0006-8993(99)01848-X. PMID 10528110.
  11. Marie Luise Schmidt; John A. Martin; Virginia M.-Y. Lee; John Q. Trojanowski (1996). "Convergence of Lewy bodies and neurofibrillary tangles in amygdala neurons of Alzheimer's disease and Lewy body disorders". Acta Neuropathol. 91 (5): 475–81. doi:10.1007/s004010050454. PMID 8740227.
  12. Tanaka M, Kim YM, Lee G, Junn E, Iwatsubo T, Mouradian MM (February 2004). "Aggresomes formed by alpha-synuclein and synphilin-1 are cytoprotective". J. Biol. Chem. 279 (6): 4625–31. doi:10.1074/jbc.M310994200. PMID 14627698.
  13. Maria Grazia Spillantini; R. Anthony Crowther; Ross Jakes; Masato Hasegawa; Michel Goedert (26 May 1998). "α-Synuclein in filamentous inclusions of Lewy bodies from Parkinson's disease and dementia with Lewy bodies". PNAS. 95 (11): 6469–73. doi:10.1073/pnas.95.11.6469. PMC 27806Freely accessible. PMID 9600990.
  14. 1 2 Wami Marui; Eizo Iskei; Masanori Kato; Hiroyasu Akatsu; Kenji Kosaka (2004). "Pathological entity of dementia with Lewy bodies and its differentiation from Alzheimer's disease". Acta Neuropathologica. 108 (2): 121–8. doi:10.1007/s00401-004-0869-4. PMID 15235805.
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