Both N-terminal and C-terminal fragments of Presenilin 1 colocalize with neurofibrillary tangles in neurons and dystrophic neurites of senile plaques in Alzheimer's disease
1998; Wiley; Volume: 53; Issue: 1 Linguagem: Inglês
10.1002/(sici)1097-4547(19980701)53
ISSN1097-4547
AutoresDehua Chui, Keiro Shirotani, Hiroshi Tanahashi, Haruhiko Akiyama, Kazuharu Ozawa, Tatsuhide Kunishita, Keikichi Takahashi, Takao Makifuchi, Takeshi Tabira,
Tópico(s)Parkinson's Disease Mechanisms and Treatments
ResumoJournal of Neuroscience ResearchVolume 53, Issue 1 p. 99-106 Both N-terminal and C-terminal fragments of Presenilin 1 colocalize with neurofibrillary tangles in neurons and dystrophic neurites of senile plaques in Alzheimer's disease De-Hua Chui, De-Hua Chui Division of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, JapanSearch for more papers by this authorKeiro Shirotani, Keiro Shirotani Division of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, JapanSearch for more papers by this authorHiroshi Tanahashi, Hiroshi Tanahashi Division of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, JapanSearch for more papers by this authorHaruhiko Akiyama, Haruhiko Akiyama Tokyo Institute of Psychiatry, Kamikitazawa, Setagaya, Tokyo, JapanSearch for more papers by this authorKazuharu Ozawa, Kazuharu Ozawa Division of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, JapanSearch for more papers by this authorTatsuhide Kunishita, Tatsuhide Kunishita Division of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, JapanSearch for more papers by this authorKeikichi Takahashi, Keikichi Takahashi Division of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, JapanSearch for more papers by this authorTakao Makifuchi, Takao Makifuchi National Saigata Hospital, Saigata, Nakakubikigun, Niigata, JapanSearch for more papers by this authorTakeshi Tabira, Corresponding Author Takeshi Tabira tabira@ncnaxp.ncnp.go.jp Division of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, JapanNational Institute of Neuroscience, NCNP, 4–1-1 Ogawahigashi, Kodaira, Tokyo 187–8502, Japan.Search for more papers by this author De-Hua Chui, De-Hua Chui Division of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, JapanSearch for more papers by this authorKeiro Shirotani, Keiro Shirotani Division of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, JapanSearch for more papers by this authorHiroshi Tanahashi, Hiroshi Tanahashi Division of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, JapanSearch for more papers by this authorHaruhiko Akiyama, Haruhiko Akiyama Tokyo Institute of Psychiatry, Kamikitazawa, Setagaya, Tokyo, JapanSearch for more papers by this authorKazuharu Ozawa, Kazuharu Ozawa Division of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, JapanSearch for more papers by this authorTatsuhide Kunishita, Tatsuhide Kunishita Division of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, JapanSearch for more papers by this authorKeikichi Takahashi, Keikichi Takahashi Division of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, JapanSearch for more papers by this authorTakao Makifuchi, Takao Makifuchi National Saigata Hospital, Saigata, Nakakubikigun, Niigata, JapanSearch for more papers by this authorTakeshi Tabira, Corresponding Author Takeshi Tabira tabira@ncnaxp.ncnp.go.jp Division of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, JapanNational Institute of Neuroscience, NCNP, 4–1-1 Ogawahigashi, Kodaira, Tokyo 187–8502, Japan.Search for more papers by this author First published: 07 December 1998 https://doi.org/10.1002/(SICI)1097-4547(19980701)53:1 3.0.CO;2-YCitations: 27AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Abstract Presenilin 1 (PS1) is a causative gene for chromosome 14-linked familial Alzheimer's disease. The gene product is known to be cleaved into N-terminal fragments (PS1-N) and C-terminal fragments (PS1-C). To understand the pathophysiological role of PS1, we conducted immunohistochemical studies using antibodies specific for PS1-N and PS1-C in sporadic Alzheimer's disease (AD). Both antibodies showed punctuate staining exclusively in neurons and their processes in both control and AD brains. PS1-N immunolabeling colocalized with neurofibrillary tangles (NFTs) in 36% of NFT-bearing neurons and with dystrophic neurites in 28% of senile plaques (SPs). PS1-C immunolabeling colocalized with dystrophic neurites in 70% of NFT-bearing SPs and with intraneuronal NFTs in 32% of NFT-bearing neurons. Both antibodies did not detect PHF-tau-positive neuropil threads and Aβ amyloid fibrils. The colocalization was also found in 33–38% of NFT-bearing neurons in progressive supranuclear palsy. These results indicate that both PS1-N and PS1-C fragments are deposited in part of NFT-bearing neurons and dystrophic neurites in SPs; both are the pathologic hallmarks of AD. J. Neurosci. Res. 53:99–106, 1998. © 1998 Wiley-Liss, Inc. Citing Literature Volume53, Issue11 July 1998Pages 99-106 RelatedInformation
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