Demonstration and distribution of tau-positive glial coiled body-like structures in white matter and white matter threads in early onset Alzheimer's disease
Abstract
The present report concerns the demonstration and distribution of tau-positive structures in the frontal and temporal white matter of five autopsy cases of early onset Alzheimer's disease (AD). The relationship between white matter lesions and tau positive structures was also investigated. Five early onset AD brains, which had not only unambiguous white matter lesions, but also no or rare atherosclerosis and minimal amyloid angiopathy, were examined. There were several tau-positive coiled body-like structures and many thread-like structures in the white matter, although previous reports showed only a few coiled bodies in the white matter in the AD brain. No relationship was found between the degree of each white matter lesion and number or distribution of tau-positive structures in the white matter. The results suggest that the AD brain has tau-positive structures in the white matter similar to some neurodegenarative brain diseases such as progressive supranuclear palsy, corticobasal degeneration, and dementia with grains. However, tau abnormalities may have fewer effects when they are located in white matter lesions in AD.
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Overexpression of NMNAT1 & 2, which delays axonal disruption propagating from a transaction site, is neuroprotective in tauopathy models.
“Notably, overexpression of nicotinamide mononucleotide adenylyl transferase 1 & 2 (NMNAT1 & 2), which delays the process of axonal disruption propagating from a transaction site, was found to be neuroprotective in tauopathy models 6465.”
From Amyloid-beta induced retrograde axonal degeneration in a mouse tauopathy model (2019) · cites this paper as [64]
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Neuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123 · see citing works
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Age-related myelin breakdown: a developmental model of cognitive decline and Alzheimer’s disease
Bartzokis, G. (2004) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2003.03.001 · Cited by 968 · see citing works
Bartzokis, G., Sultzer, D., Lu, P. H., Nuechterlein, K. H., Mintz, J., & Cummings, J. L. (2004) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2003.09.005 · Cited by 363 · see citing works
Bendlin, B. B., Carlsson, C. M., Johnson, S. C., Zetterberg, H., Blennow, K., Willette, A. A., Okonkwo, O. C., Sodhi, A., Ries, M. L., Birdsill, A. C., et al. (2012) · PLoS ONE · doi:10.1371/journal.pone.0037720 · Cited by 91 · see citing works
Amyloid-beta induced retrograde axonal degeneration in a mouse tauopathy model
Nishioka, C., Liang, H.-F., Barsamian, B., & Sun, S.-W. (2019) · NeuroImage · doi:10.1016/j.neuroimage.2019.01.007 · Cited by 30 · see citing works
- Authors
- Umahara, T., Tsuchiya, K., Ikeda, K., Kanaya, K., Iwamoto, T., Takasaki, M., Mukai, K., Shibata, N., & Kato, S.
- Affiliations
- Tokyo Medical University (JP)
- Tokyo Metropolitan Matsuzawa Hospital (JP)
- Tokyo Institute of Psychiatry (JP)
- Tokyo Women's Medical University (JP)
- Tottori University (JP)
- Corresponding author
- Umahara, Takahiko
- Venue
- Neuropathology
- Publisher
- Wiley
- Published
- 2002-03
- Volume
- 22
- Issue
- 1
- Pages
- 9-12
- ISSN
- 0919-6544 (ISSN-L)
- 1440-1789
- OpenAlex
- W2028113589
- Cited by
- 13
- References
- 1
- Citations by year
- 2019: 1 · 2014: 1 · 2013: 1 · 2012: 3
- FWCI
- 0.80
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuropathology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- white matter lesions, early-onset Alzheimer's disease, tau pathology, frontal lobe, temporal lobe, progressive supranuclear palsy, corticobasal degeneration, dementia with Lewy bodies, neurodegeneration
- MeSH terms
- Alzheimer Disease, Brain, Inclusion Bodies, Humans, Middle Aged, Neuroglia, Neurofibrillary Tangles, tau Proteins, Age of Onset
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