Increased levels of granular tau oligomers: An early sign of brain aging and Alzheimer's disease
Abstract
Development of neurofibrillary tangles (NFTs) is a pathological hallmark in various neurodegenerative disorders including Alzheimer's disease (AD). Recently, we identified a granular tau oligomer having a pre-filamentous structure. To determine the role of this oligomer in NFT formation, we quantified the amount of granular tau oligomer in 21 frontal cortex samples, each displaying varying degrees of Braak-staged NFT pathology. Here we report that granular tau oligomer levels in frontal cortex were significantly increased, even in brains displaying Braak-stage I neuropathology, a stage at which clinical symptoms of AD and NFTs in frontal cortex are believed to be absent. This suggests that increases in granular tau oligomer levels occur before NFTs form and before individuals manifest clinical symptoms of AD. Increased granular tau oligomer levels, therefore, may lead to NFT formation in frontal cortex, eventually leading to the development of AD. Thus, increases in granular tau oligomer levels may represent a very early sign of NFT formation and AD.
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Tau oligomers are the toxic agents responsible for synaptic dysfunction in AD and drive cognitive decline.
“Several groups have demonstrated that tau oligomers, which form prior to and independent of NFTs, are the toxic agents responsible for synaptic dysfunction in AD and drive cognitive decline [26, 49, 50, 58, 95].”
From Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer’s disease (2024) · cites this paper as [58]
Tau oligomers form prior to and independent of NFTs.
“Several groups have demonstrated that tau oligomers, which form prior to and independent of NFTs, are the toxic agents responsible for synaptic dysfunction in AD and drive cognitive decline [26, 49, 50, 58, 95].”
From Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer’s disease (2024) · cites this paper as [58]
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References 23 · Cited by 301
- Authors
- Maeda, S., Sahara, N., Saito, Y., Murayama, S., Ikai, A., & Takashima, A.
- Affiliations
- Tokyo Institute of Technology (JP)
- RIKEN Center for Brain Science (JP)
- Tokyo Metropolitan Institute of Gerontology (JP)
- Corresponding author
- Takashima, Akihiko
- Venue
- Neuroscience Research
- Publisher
- Elsevier BV
- Published
- 2006-03
- Volume
- 54
- Issue
- 3
- Pages
- 197-201
- ISSN
- 0168-0102 (ISSN-L)
- OpenAlex
- W2092704615
- Cited by
- 301
- References
- 23
- Citations by year
- 2026: 10 · 2025: 9 · 2024: 14 · 2023: 16 · 2022: 15 · 2021: 23 · 2020: 25 · 2019: 12 · 2018: 14 · 2017: 14 · 2016: 14 · 2015: 18 · 2014: 21 · 2013: 18 · 2012: 20
- FWCI
- 7.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Research (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
- neurofibrillary tangles, Alzheimer's disease, brain aging, Braak staging, frontal cortex, early biomarkers, neurodegeneration
- MeSH terms
- Aged, Aged, 80 and over, Aging, Alzheimer Disease, Brain, Female, Humans, Male, Middle Aged, Blotting, Western, Neurofibrillary Tangles, tau Proteins, Microscopy, Atomic Force
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