Lewy body

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Lewy bodies are abnormal aggregates of protein that develop inside nerve cells. They are identified under the microscope when histology is performed on the brain.

Lewy bodies appear as spherical masses that displace other cell components. There are two morphological types: classical (brain stem) Lewy bodies and cortical Lewy bodies. A classical Lewy body is an eosinophilic cytoplasmic inclusion that consists of a dense core surrounded by a halo of 10-nm wide radiating fibrils, the primary structural component of which is alpha-synucleinL. In contrast, a cortical Lewy body is less well-defined and lacks the halo. Nonetheless, it is still made up of alpha-synuclein fibrils.

Cell biology[edit | edit source]

A Lewy body is composed of the protein alpha-synuclein associated with other proteins such as ubiquitin, neurofilament protein, and alpha B crystallin. It is believed that Lewy bodies represent an aggresome response in the cell.

Associated diseases[edit | edit source]

The main disease associated with the presence of Lewy bodies is Parkinson's disease. Lewy bodies are also present in neurons in dementia with Lewy bodies and the Lewy body variant of Alzheimer's disease, as well as Hallervorden-Spatz syndrome.

Inclusions composed of alpha synuclein, different to Lewy bodies, can be found in glial cells in multiple system atrophy. These are termed glial cytoplasmic inclusions. Multiple system atrophy can be clinically confused with Parkinson's disease.

History[edit | edit source]

Lewy bodies were first seen and linked to Parkinson's disease ("paralysis agitans") in 1912 by the neurologist Frederic Lewy (1885-1950).

References[edit | edit source]

  • E. Forster and F. H. Lewy. "Paralysis agitans". In Pathologische Anatomie. Handbuch der Neurologie (edited by M. Lewandowsky). Berlin: Springer Verlag 1912, 920-933.
  • P. Duffy and V. Tennyson. Phase and electron microscopic observations of Lewy bodies and melanin granules in the substantia nigra and locus coeruleus in Parkinson's disease. J. Neuropathol. Exp. Neurol. 24: 398-414, 1965

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