Cited by 13Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Demonstration and distribution of tau-positive glial coiled body-like structures in white matter and white matter threads in early onset Alzheimer's disease

Umahara, Takahiko, Tsuchiya, Kuniaki, Ikeda, Kenzi, Kanaya, Kiyoshi, Iwamoto, Toshihiko, Takasaki, Masharu, Mukai, Kiyoshi, Shibata, Noriyuki +1 more·2002·Neuropathology

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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Crossref · 10.1046/j.0919-6544.2002.00422.x

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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.”

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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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