Tau Oligomers in Sera of Patients with Alzheimer’s Disease and Aged Controls
Abstract
Although tau protein was long regarded as an intracellular protein with several functions inside the cell, new evidence has shown tau secretion into the extracellular space. The active secretion of tau could be a physiological response of neurons to increased intracellular amounts of tau during the progression of tau pathology. We looked for potential differences in the serum levels of toxic tau oligomers in regards to cognitive impairment of subjects. We detected tau oligomers in the serum of Alzheimer’s disease (AD) patients, but they were also present to some extent in the serum of healthy older subjects where the levels positively correlated with aging (Spearman r = 0.26, p = 0.016). On the contrary, we found lower levels of tau oligomers in the serum of mild cognitive impairment (MCI) ( p = 0.033) and MCI-AD ( p = 0.006) patients. These results could suggest that clearance of extracellular tau proteins takes place, in part, in the periphery. In the case of MCI patients, the lower levels of tau oligomers could be the result of impaired clearance of tau protein from interstitium to blood and consequent accumulation of tau aggregates in the brain.
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Elevation of SASP components in AD patients correlates with CSF tau levels, inflammation, and cognitive impairment.
“This elevation of SASP components in AD patients correlates with CSF tau levels, inflammation, and cognitive impairment.”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [17]
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- Authors
- Kolarova, M., Sengupta, U., Bartos, A., Ricny, J., & Kayed, R.
- Affiliations
- Charles University (CZ)
- The University of Texas Medical Branch at Galveston (US)
- National Institute of Mental Health, Klecany, Czech Republic
- Corresponding author
- Kolarova, Michala
- Kayed, Rakez
- Venue
- Journal of Alzheimer’s Disease
- Publisher
- SAGE Publications
- Published
- 2017-04-28
- Volume
- 58
- Issue
- 2
- Pages
- 471-478
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- OpenAlex
- W2608194522
- Cited by
- 27
- References
- 53
- Citations by year
- 2025: 1 · 2024: 4 · 2023: 5 · 2022: 4 · 2021: 1 · 2020: 2 · 2019: 6 · 2018: 1 · 2017: 3
- FWCI
- 2.43
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Univerzita Karlova v Praze
- Ministerstvo Školství, Mládeže a Tělovýchovy
- National Institutes of Health
- Mitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch
- National Institute on Aging (R01AG054025)
- National Institute of Neurological Disorders and Stroke (R01NS094557)
- 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
- tau oligomers, Alzheimer's disease
- MeSH terms
- Aged, Aged, 80 and over, Aging, Alzheimer Disease, Enzyme-Linked Immunosorbent Assay, Female, Humans, Male, Mental Status Schedule, Middle Aged, Peptide Fragments, Amyloid beta-Peptides, tau Proteins, Cognitive Dysfunction
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