Amyloid-beta: a crucial factor in Alzheimer's disease - PubMed (original) (raw)
Review
Amyloid-beta: a crucial factor in Alzheimer's disease
Saeed Sadigh-Eteghad et al. Med Princ Pract. 2015.
Abstract
Alzheimer's disease (AD) is the most prevalent form of dementia which affects people older than 60 years of age. In AD, the dysregulation of the amyloid-beta (Aβ) level leads to the appearance of senile plaques which contain Aβ depositions. Aβ is a complex biological molecule which interacts with many types of receptors and/or forms insoluble assemblies and, eventually, its nonphysiological depositions alternate with the normal neuronal conditions. In this situation, AD signs appear and the patients experience marked cognitional disabilities. In general, intellect, social skills, personality, and memory are influenced by this disease and, in the long run, it leads to a reduction in quality of life and life expectancy. Due to the pivotal role of Aβ in the pathobiology of AD, a great deal of effort has been made to reveal its exact role in neuronal dysfunctions and to finding efficacious therapeutic strategies against its adverse neuronal outcomes. Hence, the determination of its different molecular assemblies and the mechanisms underlying its pathological effects are of interest. In the present paper, some of the well-established structural forms of Aβ, its interactions with various receptors and possible molecular and cellular mechanisms underlying its neurotoxicity are discussed. In addition, several Aβ-based rodent models of AD are reviewed.
© 2014 S. Karger AG, Basel.
Figures
Fig. 1
The 3 major features of AD within the neuronal system. a Cleavage of APP, and formation and accumulation of extraneuronal Aβ. b Formation and deposition of intraneuronal NFTs. c Synaptic dysfunction due to Aβ accumulation and its interaction with receptors. AICD = APP intracellular domain.
Fig. 2
Interrelationship between Aβ and NFT formation.
Similar articles
- Revisiting the role of brain and peripheral Aβ in the pathogenesis of Alzheimer's disease.
Uddin MS, Kabir MT, Tewari D, Mamun AA, Mathew B, Aleya L, Barreto GE, Bin-Jumah MN, Abdel-Daim MM, Ashraf GM. Uddin MS, et al. J Neurol Sci. 2020 Sep 15;416:116974. doi: 10.1016/j.jns.2020.116974. Epub 2020 Jun 7. J Neurol Sci. 2020. PMID: 32559516 Review. - Intracellular amyloid-β accumulation in calcium-binding protein-deficient neurons leads to amyloid-β plaque formation in animal model of Alzheimer's disease.
Moon M, Hong HS, Nam DW, Baik SH, Song H, Kook SY, Kim YS, Lee J, Mook-Jung I. Moon M, et al. J Alzheimers Dis. 2012;29(3):615-28. doi: 10.3233/JAD-2011-111778. J Alzheimers Dis. 2012. PMID: 22269161 - [The pathophysiology of Alzheimer's disease with special reference to "amyloid cascade hypothesis"].
Tamaoka A. Tamaoka A. Rinsho Byori. 2013 Nov;61(11):1060-9. Rinsho Byori. 2013. PMID: 24450113 Review. Japanese. - Neuronal Protein Tyrosine Phosphatase 1B Hastens Amyloid β-Associated Alzheimer's Disease in Mice.
Ricke KM, Cruz SA, Qin Z, Farrokhi K, Sharmin F, Zhang L, Zasloff MA, Stewart AFR, Chen HH. Ricke KM, et al. J Neurosci. 2020 Feb 12;40(7):1581-1593. doi: 10.1523/JNEUROSCI.2120-19.2019. Epub 2020 Jan 8. J Neurosci. 2020. PMID: 31915254 Free PMC article. - Alzheimer's disease.
De-Paula VJ, Radanovic M, Diniz BS, Forlenza OV. De-Paula VJ, et al. Subcell Biochem. 2012;65:329-52. doi: 10.1007/978-94-007-5416-4_14. Subcell Biochem. 2012. PMID: 23225010 Review.
Cited by
- Exploring the Benzazoles Derivatives as Pharmacophores for AChE, BACE1, and as Anti-Aβ Aggregation to Find Multitarget Compounds against Alzheimer's Disease.
Rosales Hernández MC, Olvera-Valdez M, Velazquez Toledano J, Mendieta Wejebe JE, Fragoso Morales LG, Cruz A. Rosales Hernández MC, et al. Molecules. 2024 Oct 9;29(19):4780. doi: 10.3390/molecules29194780. Molecules. 2024. PMID: 39407708 Free PMC article. Review. - WIMOAD: Weighted Integration of Multi-Omics data for Alzheimer's Disease (AD) Diagnosis.
Xiao H, Wang J, Wan S. Xiao H, et al. bioRxiv [Preprint]. 2024 Sep 27:2024.09.25.614862. doi: 10.1101/2024.09.25.614862. bioRxiv. 2024. PMID: 39386613 Free PMC article. Preprint. - Inhibition of cytotoxic self-assembly of HEWL through promoting fibrillation by new synthesized α-hydroxycarbamoylphosphinic acids.
Mahdavimehr M, Kaboudin B, Alaie S, Tondkar F, Eshkaftaki ZM, Ebrahim-Habibi MB, Ghashghaee M, Tahmasebi E, Zhang T, Gu Y, Meratan AA. Mahdavimehr M, et al. RSC Adv. 2024 Oct 1;14(42):31227-31242. doi: 10.1039/d4ra02969k. eCollection 2024 Sep 24. RSC Adv. 2024. PMID: 39355328 Free PMC article. - Levels of Amyloid Beta (Aβ) Expression in the Caenorhabditis elegans Neurons Influence the Onset and Severity of Neuronally Mediated Phenotypes.
Sirwani N, Hedtke SM, Grant K, McColl G, Grant WN. Sirwani N, et al. Cells. 2024 Sep 23;13(18):1598. doi: 10.3390/cells13181598. Cells. 2024. PMID: 39329779 Free PMC article. - Ellagic acid improves the symptoms of early-onset Alzheimer's disease: Behavioral and physiological correlates.
Jha AB, Chaube UJ, Jha AB. Jha AB, et al. Heliyon. 2024 Sep 7;10(18):e37372. doi: 10.1016/j.heliyon.2024.e37372. eCollection 2024 Sep 30. Heliyon. 2024. PMID: 39309887 Free PMC article.
References
- Koudinov AR, Berezov TT. Alzheimer's amyloid-beta (Aβ) is an essential synaptic protein, not neurotoxic junk. Acta Neurobiol Exp. 2004;64:71–79. - PubMed
- Nordberg A. Amyloid plaque imaging in vivo: current achievement and future prospects. Eur J Nucl Med Mol Imaging. 2007;35:46–50. - PubMed
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical