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Article: Amyloid pathology in spinal cord of the transgenic Alzheimer's disease mice is correlated to the corticospinal tract pathway

TitleAmyloid pathology in spinal cord of the transgenic Alzheimer's disease mice is correlated to the corticospinal tract pathway
Authors
Issue Date2013
PublisherIOS Press. The Journal's web site is located at http://www.iospress.nl/html/13872877.php
Citation
Journal of Alzheimer's Disease, 2013, v. 35 n. 4, p. 675-685 How to Cite?
AbstractThe transgenic TgCRND8 mouse is widely used as an animal model of Alzheimer's disease (AD) and exhibits an early onset of senile plaque pathogenesis in the brain. Here we report that TgCRND8 mice also have amyloid-beta (Abeta) neuropathology in spinal cord. TgCRND8 mice began to show obvious Abeta deposition in both gray matter of dorsal horn and white matter in the central part of dorsal column of the spinal cord at 10 months of age onward. Further experiments showed that the distribution of Abeta deposition in the spinal cord corresponds to the corticospinal tract pathway and its projection regions in TgCRND8 mice. We hypothesized that neurons in the sensorimotor cortex is the source of the Abeta peptide deposited in the spinal cord of these mice. To test the hypothesis, we ablated the sensorimotor cortex to interrupt connections between the sensorimotor cortex and spinal cord. We found that Abeta burden was significantly reduced in the denervated side compared to the contralateral side. Our results suggest that the sensorimotor cortex might be the primary source of Abeta in spinal cord of TgCRND8 mice. This is consistent with the observation that the sensorimotor cortex is one region particularly vulnerable during the progression of AD. The characteristics of Abeta distribution in TgCRND8 mice suggest that there are other ways related to the formation of Abeta plaques in addition to the terminal and synaptic release of Abeta.
Persistent Identifierhttp://hdl.handle.net/10722/188848
ISSN
2015 Impact Factor: 3.92
2015 SCImago Journal Rankings: 1.774
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYuan, QJen_US
dc.contributor.authorSu, HXen_US
dc.contributor.authorZhang, Yen_US
dc.contributor.authorChau, WHen_US
dc.contributor.authorNg, GCTen_US
dc.contributor.authorSong, Yen_US
dc.contributor.authorHuang, Jen_US
dc.contributor.authorWu, Wen_US
dc.contributor.authorLin, ZXen_US
dc.date.accessioned2013-09-17T14:17:34Z-
dc.date.available2013-09-17T14:17:34Z-
dc.date.issued2013en_US
dc.identifier.citationJournal of Alzheimer's Disease, 2013, v. 35 n. 4, p. 675-685en_US
dc.identifier.issn1387-2877en_US
dc.identifier.urihttp://hdl.handle.net/10722/188848-
dc.description.abstractThe transgenic TgCRND8 mouse is widely used as an animal model of Alzheimer's disease (AD) and exhibits an early onset of senile plaque pathogenesis in the brain. Here we report that TgCRND8 mice also have amyloid-beta (Abeta) neuropathology in spinal cord. TgCRND8 mice began to show obvious Abeta deposition in both gray matter of dorsal horn and white matter in the central part of dorsal column of the spinal cord at 10 months of age onward. Further experiments showed that the distribution of Abeta deposition in the spinal cord corresponds to the corticospinal tract pathway and its projection regions in TgCRND8 mice. We hypothesized that neurons in the sensorimotor cortex is the source of the Abeta peptide deposited in the spinal cord of these mice. To test the hypothesis, we ablated the sensorimotor cortex to interrupt connections between the sensorimotor cortex and spinal cord. We found that Abeta burden was significantly reduced in the denervated side compared to the contralateral side. Our results suggest that the sensorimotor cortex might be the primary source of Abeta in spinal cord of TgCRND8 mice. This is consistent with the observation that the sensorimotor cortex is one region particularly vulnerable during the progression of AD. The characteristics of Abeta distribution in TgCRND8 mice suggest that there are other ways related to the formation of Abeta plaques in addition to the terminal and synaptic release of Abeta.en_US
dc.languageengen_US
dc.publisherIOS Press. The Journal's web site is located at http://www.iospress.nl/html/13872877.phpen_US
dc.relation.ispartofJournal of Alzheimer's Diseaseen_US
dc.titleAmyloid pathology in spinal cord of the transgenic Alzheimer's disease mice is correlated to the corticospinal tract pathwayen_US
dc.typeArticleen_US
dc.identifier.emailNg, GCT: gordng@hku.hken_US
dc.identifier.emailSong, Y: songy@hku.hken_US
dc.identifier.emailHuang, J: jdhuang@hkucc.hku.hken_US
dc.identifier.emailWu, W: wtwu@hkucc.hku.hken_US
dc.identifier.authoritySong, Y=rp00488en_US
dc.identifier.authorityHuang, J=rp00451en_US
dc.identifier.authorityWu, W=rp00419en_US
dc.identifier.doi10.3233/JAD-122323en_US
dc.identifier.pmid23478304en_US
dc.identifier.hkuros222731en_US
dc.identifier.volume35en_US
dc.identifier.issue4en_US
dc.identifier.spage675en_US
dc.identifier.epage685en_US
dc.identifier.isiWOS:000319345300003-
dc.publisher.placeNetherlandsen_US

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