File:Neuron with mHtt inclusion.jpg

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Neuron_with_mHtt_inclusion.jpg(362 × 470 pixels, file size: 60 KB, MIME type: image/jpeg)

Summary

A montage of three images of single striatal neurons transfected with a disease-associated version of huntingtin, the protein that causes Huntington's disease. Nuclei of untransfected neurons are seen in the background (blue). The neuron in the center (yellow) contains an abnormal intracellular accumulation of huntingtin called an inclusion body (orange). Studies using an automated microscope and survival analysis demonstrated that neurons with disease-associated huntingtin that form inclusion bodies survive longer than those that do not, from press release <a rel="nofollow" class="external autonumber" href="http://www.ninds.nih.gov/news_and_events/press_releases/pressrelease_huntington%27s_inclusion_bodies_101304.htm">[1]</a>, Attribution 'Dr. Steven Finkbeiner, Gladstone Institute of Neurological Disease, The Taube-Koret Center for Huntington's Disease Research, and the University of California San Francisco'

Licensing

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File history

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Date/TimeThumbnailDimensionsUserComment
current09:52, 12 January 2017Thumbnail for version as of 09:52, 12 January 2017362 × 470 (60 KB)127.0.0.1 (talk)A montage of three images of single striatal neurons transfected with a disease-associated version of huntingtin, the protein that causes Huntington's disease. Nuclei of untransfected neurons are seen in the background (blue). The neuron in the center (yellow) contains an abnormal intracellular accumulation of huntingtin called an inclusion body (orange). Studies using an automated microscope and survival analysis demonstrated that neurons with disease-associated huntingtin that form inclusion bodies survive longer than those that do not, from press release <a rel="nofollow" class="external autonumber" href="http://www.ninds.nih.gov/news_and_events/press_releases/pressrelease_huntington%27s_inclusion_bodies_101304.htm">[1]</a>, Attribution 'Dr. Steven Finkbeiner, Gladstone Institute of Neurological Disease, The Taube-Koret Center for Huntington's Disease Research, and the University of California San Francisco'
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