β-Amyloids and Immune Responses Associated with Alzheimer’s Disease
Abstract
:1. Introduction
2. The Role of β-Amyloid and Its Forms in the Pathogenesis of AD
Mutation in Aβ | Effects |
---|---|
A2V | Increased Aβ production [63,64] Acceleration of Aβ aggregation [64,65,66] |
English (H6R) | Increased Zn2+-dependent oligomerization of Aβ [23] Increased neurotoxicity of Aβ oligomers [24,25] Acceleration of Aβ fibril formation [26] |
Tottori (D7N) | Acceleration of Aβ aggregation [27] Increased oligomerization of Aβ [24] Increased neurotoxicity of Aβ oligomers [24] Acceleration of Aβ fibril formation [26] |
Taiwan (D7H) | Increased Aβ production [28,29] Increased Aβ42/40 ratio [28] Increased Zn2+/Cu2+-dependent oligomerization of Aβ [28,29] Increased neurotoxicity of Aβ oligomers [28,29] |
Post-translational modification of Aβ | Effects |
Iso-D7-Aβ (isomerized Asp7 residue) | Increased Zn2+-dependent oligomerization of Aβ [34,36,38,43,48,49] Increased neurotoxicity of Aβ oligomers [43] Age-related accumulation [44] |
3pE-Aβ(pyroglutamate modified glutamic acid residue) | Acceleration of Aβ aggregation [31,46] Increased oligomerization of Aβ [31,45,47] Increased neurotoxicity of Aβ oligomers [31,35,45,46] Age-related accumulation [32] |
pS8-Aβ(phosphorylated Ser8 residue) | Acceleration of Aβ aggregation [39,40,41] Increased oligomerization of Aβ [39,40,41] Increased neurotoxicity of Aβ oligomers [39,40,41] Age-related accumulation in APP-PS1 tg mice [39,40] |
Inhibition of Zn2+-dependent oligomerization of Aβ [30] Prevention of Na+/K+ ATPase inhibition [30] Reduction of amyloid plaques in APP-PS1 tg mice [30,37] |
2.1. Possible Mechanisms of Aβ Oligomer Toxicity
2.1.1. Disruption of Cellular Membranes
2.1.2. Dysregulation of Ion Flows
2.1.3. Pathological Engagement of Membrane Receptors
2.1.4. Induction of Oxidative Stress
2.1.5. AD-Related Target Protein Phosphorylation
2.2. Scenarios of Aβ Oligomerization and Post-Translational Modifications
3. The Interaction of Aβ with the Innate Immune System and the Pathogenesis of Alzheimer’s Disease
4. The Interaction of Aβ with the Adaptive Immune System and the Pathogenesis of Alzheimer’s Disease
4.1. Aβ-Specific T Cells in AD
4.2. Aβ-Specific and Other B Cells in AD
4.2.1. Aβ-Specific Antibodies
4.2.2. B Cells
5. Concluding Notes
Author Contributions
Funding
Acknowledgments
Conflicts of Interest
Abbreviations
References
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Mouse Model NR2B-Containing NMDA Receptor | Gene (Mutation) | Aβ Pathology | Tau Pathology | Neuronal Loss | Cognitive Impairment | First Described |
---|---|---|---|---|---|---|
PDAPP | APP (V717F) | 6 mo. + | - | - | 3 mo. + | 1995 [140] |
APP-Tg J20 | APP (K670/671NL, V717F) | 8 mo. + | - | 3 mo. + | 4 mo. + | [141] |
APP/PS1 | APP (KM670/671NL) | 6 mo. + | - | 8 mo. + | 12 mo. + | 2006 [142] |
PSEN1 (delta9) | ||||||
5xFAD | APP (KM670/671NL, I716V, V717I) | 8 mo. + | - | 6 mo. + | 4 mo. + | 2006 [143] |
PSEN1 (M146L, L286V) | ||||||
3xTgAD | APP (KM670/671NL) | 6 mo. + | 12 mo. + | unknown | 4 mo. + | 2003 [144] |
MAPT 0N4R (P301L) | ||||||
Psen (M146V knock-in) | ||||||
SJL mice | expressing IFN-γ under the MBP promoter | [145] | ||||
APP/IFN-γ Tg | homozygous IFN-γ-Tg mice were bred with APP-Tg J20 mice | [146] |
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Kolobova, E.; Petrushanko, I.; Mitkevich, V.; Makarov, A.A.; Grigorova, I.L. β-Amyloids and Immune Responses Associated with Alzheimer’s Disease. Cells 2024, 13, 1624. https://doi.org/10.3390/cells13191624
Kolobova E, Petrushanko I, Mitkevich V, Makarov AA, Grigorova IL. β-Amyloids and Immune Responses Associated with Alzheimer’s Disease. Cells. 2024; 13(19):1624. https://doi.org/10.3390/cells13191624
Chicago/Turabian StyleKolobova, Elizaveta, Irina Petrushanko, Vladimir Mitkevich, Alexander A Makarov, and Irina L Grigorova. 2024. "β-Amyloids and Immune Responses Associated with Alzheimer’s Disease" Cells 13, no. 19: 1624. https://doi.org/10.3390/cells13191624
APA StyleKolobova, E., Petrushanko, I., Mitkevich, V., Makarov, A. A., & Grigorova, I. L. (2024). β-Amyloids and Immune Responses Associated with Alzheimer’s Disease. Cells, 13(19), 1624. https://doi.org/10.3390/cells13191624