Role of the Lipid Membrane and Membrane Proteins in Tau Pathology
Open accessAbstract
Abnormal accumulation of misfolded tau aggregates is a pathological hallmark of various tauopathies including Alzheimer’s disease (AD). Although tau is a cytosolic microtubule-associated protein enriched in neurons, it is also found in extracellular milieu, such as interstitial fluid, cerebrospinal fluid, and blood. Accumulating evidence showed that pathological tau spreads along anatomically connected areas in the brain through intercellular transmission and templated misfolding, thereby inducing neurodegeneration and cognitive dysfunction. In line with this, the spatiotemporal spreading of tau pathology is closely correlated with cognitive decline in AD patients. Although the secretion and uptake of tau involve multiple different pathways depending on tau species and cell types, a growing body of evidence suggested that tau is largely secreted in a vesicle-free forms. In this regard, the interaction of vesicle-free tau with membrane is gaining growing attention due to its importance for both of tau secretion and uptake as well as aggregation. Here, we review the recent literature on the mechanisms of the tau-membrane interaction and highlights the roles of lipids and proteins at the membrane in the tau-membrane interaction as well as tau aggregation.
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Inflammaging impairs clearance of Aβ and tau aggregates, which can trigger activation of microglia and astrocytes and induce production of pro-inflammatory cytokines and ROS.
“One mechanism is that inflammaging impairs the clearance of Aβ and tau aggregates, which can trigger the activation of microglia and astrocytes, and induce the production of pro‐inflammatory cytokines and ROS.”
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 [97]
Inflammaging affects balance between pre- and post-synaptic tau levels and impairs interactions of tau with synaptic proteins such as Fyn kinase, PSD-95, and NMDA receptors.
“A third mechanism is that inflammaging affects the balance between pre‐ and post‐synaptic tau levels, and impairs the interactions of tau with other synaptic proteins, such as Fyn kinase, PSD‐95, and NMDA receptors. 97”
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 [97]
Inflammaging impairs BBB integrity, increasing entry of peripheral inflammatory factors into the brain.
“Another mechanism is that inflammaging impairs BBB integrity thereby increasing entry of peripheral inflammatory factors, such as cytokines, chemokines, and immune cells, into the brain.”
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 [97]
Inflammatory mediators can damage neurons and synapses and promote tau phosphorylation and aggregation that impair axonal transport, synaptic function, and neuronal viability.
“These inflammatory mediators can damage neurons and synapses, and also promote the tau phosphorylation and aggregation that ultimately impair axonal transport, synaptic function, and neuronal viability. 97”
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 [97]
These alterations can impair synaptic transmission and plasticity and lead to memory impairment.
“These alterations can impair synaptic transmission and plasticity, and lead to memory impairment. 97”
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 [97]
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References 149 · Cited by 61
- Authors
- Bok, E., Leem, E., Lee, B.-R., Lee, J. M., Yoo, C. J., Lee, E. M., & Kim, J.
- Affiliations
- Korea Brain Research Institute (KR)
- Kyungpook National University (KR)
- Daegu Gyeongbuk Institute of Science and Technology (KR)
- Corresponding author
- Kim, Jaekwang
- Venue
- Frontiers in Cell and Developmental Biology
- Publisher
- Frontiers Media SA
- Published
- 2021-04-30
- Volume
- 9
- Pages
- 653815-653815
- ISSN
- 2296-634X (ISSN-L)
- PMC
- PMC8119898
- OpenAlex
- W3158934081
- Cited by
- 61
- References
- 149
- Citations by year
- 2026: 11 · 2025: 12 · 2024: 12 · 2023: 12 · 2022: 10 · 2021: 4
- FWCI
- 1.27
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Cell and Developmental Biology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Ministry of Science and ICT, South Korea (2020R1F1A1075547, 21-BR-02-16)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Lipid Membrane Structure and Behavior
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- tau pathology, tauopathy, Alzheimer's disease, lipid membranes, membrane proteins, tau aggregation, tau secretion, neurodegeneration
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