The DOI matches its Crossref record; 188 of the 188 references it cites were found in a registry or an index.
Amyloid β, Tau, and α-Synuclein aggregates in the pathogenesis, prognosis, and therapeutics for neurodegenerative diseases
Open accessAbstract
Aggregation of specific proteins are histopathological hallmarks of several neurodegenerative diseases, such as, Amyloid β (Aβ) plaques and tau neurofibrillary tangles in Alzheimer's disease (AD); morphologically different inclusions of ratiometric 3 repeat (3 R) and 4 repeat (4 R) tau isoforms in progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and Pick's disease (PiD); α-Synuclein (α-Syn) containing Lewy bodies (LBs) and dystrophic Lewy neurites (LNs) in Parkinson's disease (PD) and dementia with Lewy bodies (DLB). However, mixed brain protein pathologies have been frequently observed in many of these diseases and in normal aging brains, among which Aβ/tau and tau/α-Syn crosstalks have received increased attention. Interestingly, studies have also shown synergistic interplay among Aβ, tau, and α-Syn in several neurodegenerative diseases, suggesting a protein triumvirate. In this review, we summarize the emerging evidence of Aβ, tau, and α-Syn aggregation in pathophysiology, and their overlap in a spectrum of neurodegenerative diseases including AD, PSP, PiD, CBD, PD and DLB. We discuss the prognostic advancements made in biomarker and imaging techniques in the triumvirate proteinopathies. Finally, we discuss the combined therapeutic modality involving biomarkers and imaging techniques for future combinatorial immunotherapeutic targeting more than one protein aggregates. We hope that such a multitarget therapeutic approach will have synergistic or additive effects to manage neurodegenerative diseases with two or more protein pathologies that might uncover a promising strategy for personalized combination therapies. Managing neurodegenerative diseases by optimizing the diagnostic criteria and the correct combination of immunotherapies will be a key factor in the success of future treatment.
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1 retracted
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RetractedNeuropathological stageing of Alzheimer-related changes.
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“While pure tauopathies embody a wide-ranging heterogeneity in clinical symptoms and morphology of tau aggregates, AD, a ‘secondary tauopathy’ is characterized by Aβ senile plaques and tau neurofibrillary tangles (NFTs) (Braak and Braak, 1991; DeTure and Dickson, 2019; Silva and Haggarty, 2020).”
BackgroundProtein Misfolding, Functional Amyloid, and Human Disease
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“recruitment of microglia to Aβ plaques, reversed amyloid-associated gene expression, and improved spatial learning and novel object recognition memory in 5XFAD mice developing Aβ plaques and gliosis (Oakley et al., 2006; Price et al., 2020).”
BackgroundThe neuropathological diagnosis of Alzheimer's disease
DeTure, M. A., & Dickson, D. W. (2019) · Molecular Neurodegeneration · doi:10.1186/s13024-019-0333-5 · Cited by 3,329 · cited 3×
“Nonetheless, overlapping late-stage clinical symptoms and postmortem protein pathologies stance a huge challenge to their accurate diagnosis (Das et al., 2020; DeTure and Dickson, 2019; Dugger and Dickson, 2017; Kovacs, 2019a).”
BackgroundAgeing as a risk factor for neurodegenerative disease
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TREM2 Variants in Alzheimer's Disease
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NLRP3 is activated in Alzheimer’s disease and contributes to pathology in APP/PS1 mice
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Variant of TREM2 Associated with the Risk of Alzheimer's Disease
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Cited by
Scheiblich, H., Eikens, F., Wischhof, L., Opitz, S., Jüngling, K., Cserép, C., Schmidt, S. V., Lambertz, J., Bellande, T., Pósfai, B., et al. (2024) · Neuron · doi:10.1016/j.neuron.2024.06.029 · Cited by 207
Gaikwad, S., Senapati, S., Haque, M. A., & Kayed, R. (2024) · Alzheimer's & Dementia · doi:10.1002/alz.13490 · Cited by 117
Self-citationWu, X., Yang, Z., Zou, J., Gao, H., Shao, Z., Li, C., & Lei, P. (2025) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-025-02179-x · Cited by 88
Recent advances in the study of Na+/K+-ATPase in neurodegenerative diseases
Zhang, X., Lee, W., & Bian, J.-S. (2022) · Cells · doi:10.3390/cells11244075 · Cited by 66
Nagori, K., Nakhate, K. T., Yadav, K., Ajazuddin, & Pradhan, M. (2023) · Future Pharmacology · doi:10.3390/futurepharmacol3040053 · Cited by 61
Metadata
- Authors
- Sengupta, U., & Kayed, R.
- Venue
- Progress in Neurobiology
- Publisher
- Elsevier BV
- Published
- 2022-07
- Volume
- 214
- Pages
- 102270
- ISSN
- 0301-0082 (ISSN-L)
- OpenAlex
- W4223942559
- Cited by
- 293
- References
- 188
- FWCI
- 28.49
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Sengupta, U., & Kayed, R. (2022). Amyloid β, Tau, and α-Synuclein aggregates in the pathogenesis, prognosis, and therapeutics for neurodegenerative diseases. Progress in Neurobiology. https://doi.org/10.1016/j.pneurobio.2022.102270
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