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Article: Association Between Axonopathy and Amyloid Plaques in the Spinal Cord of the Transgenic Mice of Alzheimer's Disease

TitleAssociation Between Axonopathy and Amyloid Plaques in the Spinal Cord of the Transgenic Mice of Alzheimer's Disease
Authors
KeywordsAxonopathy
Axonal transport
Electronic microscope
Aβ plaque pathogenesis
Spinal cord
Issue Date2019
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/neuroscience
Citation
Neuroscience, 2019, v. 409, p. 152-161 How to Cite?
AbstractAxonopathy manifested by axon swellings might constitute one of the earliest pathological features of Alzheimer's disease. It has been proposed that axonopathy might be associated with the origin of Aβ plaques. However, how axonopathy leads to Aβ plaque pathogenesis remains elusive. Our previous studies have shown that Aβ neuropathology (mainly diffuse plaques) selectively occurred in the regions of corticospinal tract (CST) pathway and its innervated region in the spinal cord of TgCRND8 mice. In this study, we investigated the occurrence and progression of axonopathy and the possible implication in Aβ plaque pathogenesis in the spinal cord of TgCRND8 mice. By anterograde labeling of CST system with a neuroanatomical tracer, we found that dilated corticospinal axons started to appear at 7 months, then exhibited an age-dependent increase. These abnormal structures appear before any plaque deposits are visible in the spinal cord of the mice. Importantly, they colocalized with Aβ plaques in either the white matter or gray matter of the spinal cord at later stages, suggesting that these axonal swellings might represent the initial stages of Aβ plaque formation, and could play a role in Aβ plaque pathogenesis. Furthermore, using ultrastructural analysis we demonstrated that intracellular contents in the axonal dystrophies such as various dense vesicles leaked out into the extracellular matrix under a condition of axon swelling rupture in CST pathways of spinal cord. This provided precise structural evidence that how the Aβ leaks out from the axonal dystrophies into extracellular matrix and how an axonal swelling might serve as a nidus of amyloid plaque formation.
Persistent Identifierhttp://hdl.handle.net/10722/276226
ISSN
2019 Impact Factor: 3.056
2015 SCImago Journal Rankings: 1.768
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYuan, Q-
dc.contributor.authorZhang, H-
dc.contributor.authorZhang, X-
dc.contributor.authorHuang, P-
dc.contributor.authorLiu, R-
dc.contributor.authorSong, Y-
dc.contributor.authorWu, W-
dc.contributor.authorLin, Z-
dc.date.accessioned2019-09-10T02:58:33Z-
dc.date.available2019-09-10T02:58:33Z-
dc.date.issued2019-
dc.identifier.citationNeuroscience, 2019, v. 409, p. 152-161-
dc.identifier.issn0306-4522-
dc.identifier.urihttp://hdl.handle.net/10722/276226-
dc.description.abstractAxonopathy manifested by axon swellings might constitute one of the earliest pathological features of Alzheimer's disease. It has been proposed that axonopathy might be associated with the origin of Aβ plaques. However, how axonopathy leads to Aβ plaque pathogenesis remains elusive. Our previous studies have shown that Aβ neuropathology (mainly diffuse plaques) selectively occurred in the regions of corticospinal tract (CST) pathway and its innervated region in the spinal cord of TgCRND8 mice. In this study, we investigated the occurrence and progression of axonopathy and the possible implication in Aβ plaque pathogenesis in the spinal cord of TgCRND8 mice. By anterograde labeling of CST system with a neuroanatomical tracer, we found that dilated corticospinal axons started to appear at 7 months, then exhibited an age-dependent increase. These abnormal structures appear before any plaque deposits are visible in the spinal cord of the mice. Importantly, they colocalized with Aβ plaques in either the white matter or gray matter of the spinal cord at later stages, suggesting that these axonal swellings might represent the initial stages of Aβ plaque formation, and could play a role in Aβ plaque pathogenesis. Furthermore, using ultrastructural analysis we demonstrated that intracellular contents in the axonal dystrophies such as various dense vesicles leaked out into the extracellular matrix under a condition of axon swelling rupture in CST pathways of spinal cord. This provided precise structural evidence that how the Aβ leaks out from the axonal dystrophies into extracellular matrix and how an axonal swelling might serve as a nidus of amyloid plaque formation.-
dc.languageeng-
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/neuroscience-
dc.relation.ispartofNeuroscience-
dc.subjectAxonopathy-
dc.subjectAxonal transport-
dc.subjectElectronic microscope-
dc.subjectAβ plaque pathogenesis-
dc.subjectSpinal cord-
dc.titleAssociation Between Axonopathy and Amyloid Plaques in the Spinal Cord of the Transgenic Mice of Alzheimer's Disease-
dc.typeArticle-
dc.identifier.emailSong, Y: songy@hku.hk-
dc.identifier.emailWu, W: wtwu@hku.hk-
dc.identifier.authoritySong, Y=rp00488-
dc.identifier.authorityWu, W=rp00419-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.neuroscience.2019.04.037-
dc.identifier.pmid31034974-
dc.identifier.scopuseid_2-s2.0-85065650448-
dc.identifier.hkuros303679-
dc.identifier.volume409-
dc.identifier.spage152-
dc.identifier.epage161-
dc.identifier.isiWOS:000470688200014-
dc.publisher.placeNetherlands-
dc.identifier.issnl0306-4522-

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