The DOI matches its Crossref record; 302 of the 302 references it cites were found in a registry or an index.
Role of tau protein in Alzheimer’s disease: The prime pathological player
Abstract
Alzheimer's disease (AD) is a prevalently found tauopathy characterized by memory loss and cognitive insufficiency. AD is an age-related neurodegenerative disease with two major hallmarks which includes extracellular amyloid plaques made of amyloid-β (Aβ) and intracellular neurofibrillary tangles of hyperphosphorylated tau. With population aging worldwide, there is an indispensable need for treatment strategies that can potentially manage this developing dementia. Despite broad researches on targeting Aβ in the past two decades, research findings on Aβ targeted therapeutics failed to prove efficacy in the treatment of AD. Tau protein with its extensive pathological role in several neurodegenerative diseases can be considered as a promising target candidate for developing therapeutic interventions. The abnormal hyperphosphorylation of tau plays detrimental pathological functions which ultimately lead to neurodegeneration. This review will divulge the importance of tau in AD pathogenesis, the interplay of Aβ and tau, the pathological functions of tau, and potential therapeutic strategies for an effective management of neuronal disorders.
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“Besides, crosstalk with other proteins adds additional complexity; for example, α-synuclein, heat shock proteins, immunophilins, and the prolyl isomerase 1 (Pin1) have all been shown to regulate tau phosphorylation, aggregation, or degradation [48, 52].”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [52]
In the citing paper
“Additionally, tau pathology is associated with neuroinflammation, as pro-inflammatory cytokines can increase tau transcription and activate inflammatory pathways that further exacerbate tau-related neurodegeneration [13,14].”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [13]
In the citing paper
“This hyperphosphorylation promotes tau aggregation into paired helical filaments and NFTs, which correlate strongly with clinical symptoms of AD.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [13]
In the citing paper
“The tau protein hypothesis focuses on the hyperphosphorylation of tau protein leading to its detachment from microtubules, resulting in the formation of neurofibrillary tangles (NFTs) which are a hallmark of AD.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [13]
Citations
Cites
1 retracted
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RetractedTriple-Transgenic Model of Alzheimer’s Disease with Plaques and Tangles
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Cited by
Sorted by citations
Phosphorylated Tau in Alzheimer’s Disease and Other Tauopathies
Rawat, P., Sehar, U., Bisht, J., Selman, A., Culberson, J., & Reddy, P. H. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232112841 · Cited by 509
Alzheimer’s disease as type 3 diabetes: understanding the link and implications
Kciuk, M., Kruczkowska, W., Gałęziewska, J., Wanke, K., Kałuzińska-Kołat, Ż., Aleksandrowicz, M., & Kontek, R. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252211955 · Cited by 98
AmeliMojarad, M., & AmeliMojarad, M. (2024) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.14856 · Cited by 73
Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease
Thawabteh, A. M., Ghanem, A. W., AbuMadi, S., Thaher, D., Jaghama, W., Karaman, D., & Karaman, R. (2024) · Molecules · doi:10.3390/molecules29215131 · Cited by 56
“Additionally, tau pathology is associated with neuroinflammation, as pro-inflammatory cytokines can increase tau transcription and activate inflammatory pathways that further exacerbate tau-related neurodegeneration [13,14].”
BackgroundThe Interaction Between NF-κB and Estrogen in Alzheimer’s Disease
Mishra, P., Davies, D. A., & Albensi, B. C. (2023) · Molecular Neurobiology · doi:10.1007/s12035-022-03152-3 · Cited by 51
Metadata
- Authors
- Muralidar, S., Ambi, S. V., Sekaran, S., Thirumalai, D., & Palaniappan, B.
- Affiliations
- SASTRA University (IN)
- Corresponding author
- Ambi, Senthil Visaga
- Venue
- International Journal of Biological Macromolecules
- Publisher
- Elsevier BV
- Published
- 2020-11
- Volume
- 163
- Pages
- 1599-1617
- ISSN
- 0141-8130 (ISSN-L)
- OpenAlex
- W3047818817
- Semantic Scholar
- 470dc765eac307ea3b63b8c8b88e81d7cd112572
- Cited by
- 278
- References
- 302
- Citations by year
- 2026: 50 · 2025: 58 · 2024: 69 · 2023: 53 · 2022: 25 · 2021: 19 · 2020: 4
- FWCI
- 3.28
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- International Journal of Biological Macromolecules (publishedVersion)
- PubMed (publishedVersion)
- Funders
- SASTRA-Deemed-to-be-University
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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 protein, Alzheimer's disease, tau hyperphosphorylation, neurofibrillary tangles, amyloid-beta, amyloid plaques, tauopathy, neurodegeneration, dementia, therapeutic target
- MeSH terms
- Aging, Alzheimer Disease, Animals, Humans, Neurons, Phosphorylation, Amyloid beta-Peptides, tau Proteins
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