アミロイドβとは? わかりやすく解説

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アミロイドβ

出典: フリー百科事典『ウィキペディア(Wikipedia)』 (2023/02/26 08:56 UTC 版)

アミロイドβアミロイドベータ: Amyloid beta、略称: )は、アルツハイマー病患者のに見られるアミロイド斑の主成分として、アルツハイマー病に重大な関与を行う36–43アミノ酸ペプチドである[2]。このペプチドはアミロイド前駆体タンパク質 (amyloid precursor protein, APP) に由来し、β-セクレターゼγ-セクレターゼによる切断によって産生される。Aβ分子は凝集し、いくつかの形態の柔軟な可溶性のオリゴマーを形成する。現在では、特定の誤ったフォールディング(ミスフォールディング)をしたオリゴマー(「シード」として知られる)が他のAβ分子のミスフォールドを誘導し、プリオンの感染と類似した連鎖反応が引き起こされると考えられている。このオリゴマーは神経細胞に対する毒性がある[3]。アルツハイマー病への関与が示唆される他のタンパク質であるタウタンパク質も同様にプリオン様のミスフォールドオリゴマーを形成し、ミスフォールドしたAβがタウのミスフォールドを誘導するという証拠も存在する[4][5]


  1. ^ “A partially folded structure of amyloid-beta(1-40) in an aqueous environment”. Biochemical and Biophysical Research Communications 411 (2): 312–6. (July 2011). doi:10.1016/j.bbrc.2011.06.133. PMC 3148408. PMID 21726530. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3148408/. 
  2. ^ “The Amyloid Beta Peptide: A Chemist's Perspective. Role in Alzheimer's and Fibrillization”. Chemical Reviews 112 (10): 5147–92. (October 2012). doi:10.1021/cr3000994. PMID 22813427. 
  3. ^ “Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid beta-peptide”. Nature Reviews. Molecular Cell Biology 8 (2): 101–12. (February 2007). doi:10.1038/nrm2101. PMID 17245412. 
  4. ^ “Alzheimer disease: a tale of two prions”. Prion 7 (1): 14–9. (Jan–Feb 2013). doi:10.4161/pri.22118. PMC 3609044. PMID 22965142. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3609044/. 
  5. ^ “Ubiquitous amyloids”. Applied Biochemistry and Biotechnology 166 (7): 1626–43. (April 2012). doi:10.1007/s12010-012-9549-3. PMC 3324686. PMID 22350870. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3324686/. 
  6. ^ “Origins of amyloid-β”. BMC Genomics 14 (1): 290. (April 2013). doi:10.1186/1471-2164-14-290. PMC 3660159. PMID 23627794. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3660159/. 
  7. ^ “Functional roles of amyloid-beta protein precursor and amyloid-beta peptides: evidence from experimental studies”. Journal of Alzheimer's Disease 18 (2): 401–12. (2009). doi:10.3233/JAD-2009-1154. PMID 19584429. 
  8. ^ “Beta-amyloid exhibits antagonistic effects on alpha 7 nicotinic acetylcholine receptors in orchestrated manner”. Journal of Medical Hypotheses and Ideas 8 (2): 48–52. (2014). doi:10.1016/j.jmhi.2014.01.001. 
  9. ^ “BACE1 (beta-secretase) knockout mice do not acquire compensatory gene expression changes or develop neural lesions over time”. Neurobiology of Disease 14 (1): 81–8. (October 2003). doi:10.1016/S0969-9961(03)00104-9. PMID 13678669. 
  10. ^ “Targeting the JNK MAPK cascade for inhibition: basic science and therapeutic potential”. Biochimica et Biophysica Acta 1697 (1–2): 89–101. (March 2004). doi:10.1016/j.bbapap.2003.11.016. PMID 15023353. 
  11. ^ “Signaling effect of amyloid-beta(42) on the processing of AβPP”. Experimental Neurology 221 (1): 18–25. (January 2010). doi:10.1016/j.expneurol.2009.09.002. PMC 2812589. PMID 19747481. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2812589/. 
  12. ^ “A novel function of monomeric amyloid beta-protein serving as an antioxidant molecule against metal-induced oxidative damage”. The Journal of Neuroscience 22 (12): 4833–41. (June 2002). doi:10.1523/JNEUROSCI.22-12-04833.2002. PMID 12077180. 
  13. ^ “Aβ40, either soluble or aggregated, is a remarkably potent antioxidant in cell-free oxidative systems”. Biochemistry 48 (20): 4354–70. (May 2009). doi:10.1021/bi802361k. PMID 19320465. 
  14. ^ “Function of beta-amyloid in cholesterol transport: a lead to neurotoxicity”. FASEB Journal 16 (12): 1677–9. (October 2002). doi:10.1096/fj.02-0285fje. PMID 12206998. 
  15. ^ “Amyloid beta-protein stimulates trafficking of cholesterol and caveolin-1 from the plasma membrane to the Golgi complex in mouse primary astrocytes”. Neuroscience 162 (2): 328–38. (August 2009). doi:10.1016/j.neuroscience.2009.04.049. PMC 3083247. PMID 19401218. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3083247/. 
  16. ^ “The Alzheimer's amyloid β-peptide (Aβ) binds a specific DNA Aβ-interacting domain (AβID) in the APP, BACE1, and APOE promoters in a sequence-specific manner: characterizing a new regulatory motif”. Gene 488 (1–2): 1–12. (November 2011). doi:10.1016/j.gene.2011.06.004. PMC 3381326. PMID 21699964. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3381326/. 
  17. ^ “Functional activity of the novel Alzheimer's amyloid β-peptide interacting domain (AβID) in the APP and BACE1 promoter sequences and implications in activating apoptotic genes and in amyloidogenesis”. Gene 488 (1–2): 13–22. (November 2011). doi:10.1016/j.gene.2011.06.017. PMC 3372404. PMID 21708232. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3372404/. 
  18. ^ “Antimicrobial properties of amyloid peptides”. Molecular Pharmaceutics 9 (4): 708–17. (April 2012). doi:10.1021/mp200419b. PMC 3297685. PMID 22081976. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3297685/. 
  19. ^ “Antimicrobial peptides in the brain: neuropeptides and amyloid”. Frontiers in Bioscience (Scholar Edition) 4: 1375–80. (June 2012). doi:10.2741/339. PMID 22652879. 
  20. ^ “Amyloid, tau, pathogen infection and antimicrobial protection in Alzheimer's disease -conformist, nonconformist, and realistic prospects for AD pathogenesis”. Translational Neurodegeneration 7: 34. (2018). doi:10.1186/s40035-018-0139-3. PMC 6306008. PMID 30603085. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6306008/. 
  21. ^ “A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid β”. Science Translational Medicine 4 (147): 147ra111. (August 2012). doi:10.1126/scitranslmed.3003748. PMC 3551275. PMID 22896675. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3551275/. 
  22. ^ “Sleep drives metabolite clearance from the adult brain”. Science 342 (6156): 373–7. (October 2013). Bibcode2013Sci...342..373X. doi:10.1126/science.1241224. PMC 3880190. PMID 24136970. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3880190/. 
  23. ^ “Clearance systems in the brain-implications for Alzheimer disease”. Nature Reviews. Neurology 11 (8): 457–70. (August 2015). doi:10.1038/nrneurol.2015.119. PMC 4694579. PMID 26195256. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4694579/. 
  24. ^ “Amyloid-beta: a crucial factor in Alzheimer's disease”. Medical Principles and Practice 24 (1): 1–10. (2014). doi:10.1159/000369101. PMC 5588216. PMID 25471398. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5588216/. 
  25. ^ “Assembly of β-Amyloid Aggregates at the Molecular Level”. Chemtracts-Organic Chemistry 13 (1): 51–56. (2000). 
  26. ^ “Amyloid-beta protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory”. Nature Medicine 14 (8): 837–42. (August 2008). doi:10.1038/nm1782. PMC 2772133. PMID 18568035. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2772133/. 非専門家向けの内容要旨 – Fox News. 
  27. ^ “Differences between vascular and plaque core amyloid in Alzheimer's disease”. Journal of Neurochemistry 51 (2): 648–51. (August 1988). doi:10.1111/j.1471-4159.1988.tb01087.x. PMID 3292706. 
  28. ^ a b “The toxicity of amyloid β oligomers”. International Journal of Molecular Sciences 13 (6): 7303–27. (2012). doi:10.3390/ijms13067303. PMC 3397527. PMID 22837695. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3397527/. 
  29. ^ “Alzheimer disease amyloid beta protein forms calcium channels in bilayer membranes: blockade by tromethamine and aluminum”. Proceedings of the National Academy of Sciences of the United States of America 90 (2): 567–71. (January 1993). Bibcode1993PNAS...90..567A. doi:10.1073/pnas.90.2.567. PMC 45704. PMID 8380642. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC45704/. 
  30. ^ “Calcium signals induced by amyloid beta peptide and their consequences in neurons and astrocytes in culture”. Biochimica et Biophysica Acta. 8th European Symposium on Calcium 1742 (1–3): 81–7. (December 2004). doi:10.1016/j.bbamcr.2004.09.006. PMID 15590058. 
  31. ^ “Beta-amyloid-induced calcium influx induces apoptosis in culture by oxidative stress rather than tau phosphorylation”. Brain Research. Molecular Brain Research 76 (2): 389–95. (March 2000). doi:10.1016/S0169-328X(00)00025-5. PMID 10762716. 
  32. ^ “Analytical model and multiscale simulations of Aβ peptide aggregation in lipid membranes: towards a unifying description of conformational transitions, oligomerization and membrane damage”. Physical Chemistry Chemical Physics 15 (23): 8940–51. (June 2013). Bibcode2013PCCP...15.8940P. doi:10.1039/c3cp44539a. PMID 23588697. 
  33. ^ “On the physiological/pathological link between Aβ peptide, cholesterol, calcium ions and membrane deformation: A molecular dynamics study”. Biochimica et Biophysica Acta 1858 (6): 1380–9. (June 2016). doi:10.1016/j.bbamem.2016.03.018. PMID 27003127. 
  34. ^ a b c “Amyloidosis and Alzheimer's disease”. Advanced Drug Delivery Reviews 54 (12): 1539–51. (December 2002). doi:10.1016/S0169-409X(02)00149-7. PMID 12453671. 
  35. ^ a b “Clearing the brain's amyloid cobwebs”. Neuron 32 (2): 177–80. (October 2001). doi:10.1016/S0896-6273(01)00475-5. PMID 11683988. 
  36. ^ “Genetic dissection of Alzheimer's disease and related dementias: amyloid and its relationship to tau”. Nature Neuroscience 1 (5): 355–8. (September 1998). doi:10.1038/1565. PMID 10196523. 
  37. ^ “Alzheimer diseases: a model of gene mutations and susceptibility polymorphisms for complex psychiatric diseases”. American Journal of Medical Genetics 81 (1): 49–57. (February 1998). doi:10.1002/(SICI)1096-8628(19980207)81:1<49::AID-AJMG10>3.0.CO;2-W. PMID 9514588. 
  38. ^ “Alzheimer's beta-amyloid peptides compete for insulin binding to the insulin receptor”. The Journal of Neuroscience 22 (10): RC221. (May 2002). doi:10.1523/JNEUROSCI.22-10-j0001.2002. PMID 12006603. 
  39. ^ “Cell surface presenilin-1 participates in the gamma-secretase-like proteolysis of Notch”. The Journal of Biological Chemistry 274 (51): 36801–7. (December 1999). doi:10.1074/jbc.274.51.36801. PMID 10593990. 
  40. ^ “Gamma-secretase inhibitors and Alzheimer's disease”. Advanced Drug Delivery Reviews 54 (12): 1579–88. (December 2002). doi:10.1016/S0169-409X(02)00155-2. PMID 12453675. 
  41. ^ “Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE”. Science 286 (5440): 735–41. (October 1999). doi:10.1126/science.286.5440.735. PMID 10531052. 
  42. ^ “Beta-secretase (BACE) as a drug target for Alzheimer's disease”. Advanced Drug Delivery Reviews 54 (12): 1589–602. (December 2002). doi:10.1016/S0169-409X(02)00157-6. PMID 12453676. 
  43. ^ Transport-clearance hypothesis for Alzheimer's disease and potential therapeutic implications. Landes Bioscience. (2003). pp. 114–122. https://www.ncbi.nlm.nih.gov/books/NBK5975/ 
  44. ^ “Amyloid plaque core protein in Alzheimer disease and Down syndrome”. Proceedings of the National Academy of Sciences of the United States of America 82 (12): 4245–9. (June 1985). Bibcode1985PNAS...82.4245M. doi:10.1073/pnas.82.12.4245. PMC 397973. PMID 3159021. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC397973/. 
  45. ^ “The length of amyloid-beta in hereditary cerebral hemorrhage with amyloidosis, Dutch type. Implications for the role of amyloid-beta 1-42 in Alzheimer's disease”. The Journal of Biological Chemistry 271 (50): 32185–91. (December 1996). doi:10.1074/jbc.271.50.32185. PMID 8943274. 
  46. ^ “beta-Amyloid-(1-42) is a major component of cerebrovascular amyloid deposits: implications for the pathology of Alzheimer disease”. Proceedings of the National Academy of Sciences of the United States of America 90 (22): 10836–40. (November 1993). Bibcode1993PNAS...9010836R. doi:10.1073/pnas.90.22.10836. PMC 47873. PMID 8248178. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC47873/. 
  47. ^ “Amyloid beta-proteins 1-40 and 1-42(43) in the soluble fraction of extra- and intracranial blood vessels”. Annals of Neurology 38 (3): 421–8. (September 1995). doi:10.1002/ana.410380312. PMID 7668828. 
  48. ^ “Kinesin-mediated axonal transport of a membrane compartment containing beta-secretase and presenilin-1 requires APP”. Nature 414 (6864): 643–8. (December 2001). doi:10.1038/414643a. PMID 11740561. 
  49. ^ “Soluble amyloid beta peptide concentration as a predictor of synaptic change in Alzheimer's disease”. The American Journal of Pathology 155 (3): 853–62. (September 1999). doi:10.1016/S0002-9440(10)65184-X. PMC 1866907. PMID 10487842. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1866907/. 
  50. ^ Tao, Kai; Wang, Jiqian; Zhou, Peng; Wang, Chengdong; Xu, Hai; Zhao, Xiubo; Lu, Jian R. (2011-03-15). “Self-assembly of short aβ(16-22) peptides: effect of terminal capping and the role of electrostatic interaction”. Langmuir: the ACS journal of surfaces and colloids 27 (6): 2723–2730. doi:10.1021/la1034273. ISSN 1520-5827. PMID 21309606. https://www.ncbi.nlm.nih.gov/pubmed/21309606. 
  51. ^ “Levels of amyloid-beta-42 and CSF pressure are directly related in patients with Alzheimer's disease”. Journal of Neural Transmission 124 (12): 1621–1625. (December 2017). doi:10.1007/s00702-017-1786-8. PMID 28866757. 
  52. ^ “Common structure of soluble amyloid oligomers implies common mechanism of pathogenesis”. Science 300 (5618): 486–9. (April 2003). Bibcode2003Sci...300..486K. doi:10.1126/science.1079469. PMID 12702875. 
  53. ^ “Days to criterion as an indicator of toxicity associated with human Alzheimer amyloid-beta oligomers”. Annals of Neurology 68 (2): 220–30. (August 2010). doi:10.1002/ana.22052. PMC 3094694. PMID 20641005. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3094694/. 非専門家向けの内容要旨 – Drug Discovery and Development. 
  54. ^ “Plasma Amyloid-Beta Levels in Patients with Different Types of Cancer”. Neurotoxicity Research 31 (2): 283–288. (February 2017). doi:10.1007/s12640-016-9682-9. PMID 27913965. 
  55. ^ “Amyloid-β precursor protein promotes cell proliferation and motility of advanced breast cancer”. BMC Cancer 14: 928. (December 2014). doi:10.1186/1471-2407-14-928. PMC 4295427. PMID 25491510. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4295427/. 
  56. ^ “Cognitive decline and brain amyloid-β accumulation across 3 years in adults with Down syndrome”. Neurobiology of Aging 58: 68–76. (October 2017). doi:10.1016/j.neurobiolaging.2017.05.019. PMC 5581712. PMID 28715661. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5581712/. 
  57. ^ “Characterization of intermediate steps in amyloid beta (Aβ) production under near-native conditions”. The Journal of Biological Chemistry 289 (3): 1540–50. (January 2014). doi:10.1074/jbc.M113.498246. PMC 3894335. PMID 24225948. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3894335/. 
  58. ^ “Distinct sites of intracellular production for Alzheimer's disease A beta40/42 amyloid peptides”. Nature Medicine 3 (9): 1016–20. (September 1997). doi:10.1038/nm0997-1016. PMID 9288729. 
  59. ^ “{gamma}-Secretase Substrate Concentration Modulates the Abeta42/Aβ40 Ratio: IMPLICATIONS FOR ALZHEIMER DISEASE”. The Journal of Biological Chemistry 282 (32): 23639–44. (August 2007). doi:10.1074/jbc.M704601200. PMID 17556361. 
  60. ^ “Dysregulated Metabolism of the Amyloid-β Protein and Therapeutic Approaches in Alzheimer Disease”. Journal of Cellular Biochemistry 118 (12): 4183–4190. (December 2017). doi:10.1002/jcb.26129. PMID 28488760. 
  61. ^ “The Alzheimer's amyloid-degrading peptidase, neprilysin: can we control it?”. International Journal of Alzheimer's Disease 2012: 1–12. (2012). doi:10.1155/2012/383796. PMC 3412116. PMID 22900228. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3412116/. 
  62. ^ “2008 Alzheimer's disease facts and figures”. Alzheimer's & Dementia 4 (2): 110–33. (March 2008). doi:10.1016/j.jalz.2008.02.005. PMID 18631956. 
  63. ^ “Alzheimer's disease and Down's syndrome: sharing of a unique cerebrovascular amyloid fibril protein”. Biochemical and Biophysical Research Communications 122 (3): 1131–5. (August 1984). doi:10.1016/0006-291X(84)91209-9. PMID 6236805. 
  64. ^ “The Alzheimer's peptide a beta adopts a collapsed coil structure in water”. Journal of Structural Biology 130 (2–3): 130–41. (June 2000). doi:10.1006/jsbi.2000.4288. PMID 10940221. 
  65. ^ “A partially folded structure of amyloid-beta(1-40) in an aqueous environment”. Biochemical and Biophysical Research Communications 411 (2): 312–6. (July 2011). doi:10.1016/j.bbrc.2011.06.133. PMC 3148408. PMID 21726530. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3148408/. 
  66. ^ “Amyloid beta-protein monomer folding: free-energy surfaces reveal alloform-specific differences”. Journal of Molecular Biology 384 (2): 450–64. (December 2008). doi:10.1016/j.jmb.2008.09.039. PMC 2673916. PMID 18835397. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2673916/. 
  67. ^ “Atomic-level characterization of the ensemble of the Aβ(1-42) monomer in water using unbiased molecular dynamics simulations and spectral algorithms”. Journal of Molecular Biology 405 (2): 570–83. (January 2011). doi:10.1016/j.jmb.2010.10.015. PMC 3060569. PMID 21056574. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060569/. 
  68. ^ “The Alzheimer's peptides Aβ40 and 42 adopt distinct conformations in water: a combined MD / NMR study”. Journal of Molecular Biology 368 (5): 1448–57. (May 2007). doi:10.1016/j.jmb.2007.02.093. PMC 1978067. PMID 17397862. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1978067/. 
  69. ^ “Structural conversion of neurotoxic amyloid-beta(1-42) oligomers to fibrils”. Nature Structural & Molecular Biology 17 (5): 561–7. (May 2010). doi:10.1038/nsmb.1799. PMC 2922021. PMID 20383142. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2922021/. 
  70. ^ “Structural characterization of a soluble amyloid beta-peptide oligomer”. Biochemistry 48 (9): 1870–7. (March 2009). doi:10.1021/bi802046n. PMID 19216516. 
  71. ^ “Transmembrane structures for Alzheimer's Aβ(1-42) oligomers”. Journal of the American Chemical Society 132 (38): 13300–12. (September 2010). doi:10.1021/ja103725c. PMID 20822103. 
  72. ^ “Pathways towards and away from Alzheimer's disease”. Nature 430 (7000): 631–9. (August 2004). Bibcode2004Natur.430..631M. doi:10.1038/nature02621. PMC 3091392. PMID 15295589. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3091392/. 
  73. ^ “2+ Influx into Lipid Vesicles Induced by Protein Aggregates”. Angewandte Chemie 56 (27): 7750–7754. (June 2017). doi:10.1002/anie.201700966. PMC 5615231. PMID 28474754. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5615231/. 
  74. ^ “Strategies for disease modification in Alzheimer's disease”. Nature Reviews. Neuroscience 5 (9): 677–85. (September 2004). doi:10.1038/nrn1495. PMID 15322526. 
  75. ^ a b “Alzheimer's disease drug development pipeline: 2017”. Alzheimer's & Dementia 3 (3): 367–384. (September 2017). doi:10.1016/j.trci.2017.05.002. PMC 5651419. PMID 29067343. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5651419/. 
  76. ^ “Passive Aβ Immunotherapy: Current Achievements and Future Perspectives”. Molecules 23 (5): 1068. (May 2018). doi:10.3390/molecules23051068. PMC 6099643. PMID 29751505. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6099643/. 
  77. ^ エーザイ、製品化目前の認知症薬を開発中止”. 日本経済新聞 (2019年3月21日). 2019年6月3日閲覧。
  78. ^ アデュカヌマブ中止も「知見を将来に」バイオジェン・スレイク社長 SMA、今後もスピンラザが基礎”. 日刊薬業 (2019年6月3日). 2019年6月3日閲覧。
  79. ^ “Lessons from Anti-Amyloid-β Immunotherapies in Alzheimer Disease: Aiming at a Moving Target”. Neuro-Degenerative Diseases 17 (6): 242–250. (2017). doi:10.1159/000478741. PMID 28787714. 
  80. ^ “New class of inhibitors of amyloid-beta fibril formation. Implications for the mechanism of pathogenesis in Alzheimer's disease”. The Journal of Biological Chemistry 277 (45): 42881–90. (November 2002). doi:10.1074/jbc.M206593200. PMID 12167652. 
  81. ^ “Inhibition of Alzheimer's amyloid-beta aggregation in-vitro by carbenoxolone: Insight into mechanism of action”. Neurochemistry International 108: 481–493. (September 2017). doi:10.1016/j.neuint.2017.06.011. PMID 28652220. 
  82. ^ “Synthesis of (-)-5,8-dihydroxy-3R-methyl-2R-(dipropylamino)-1,2,3,4-tetrahydronaphthalene: an inhibitor of beta-amyloid(1-42) aggregation”. Bioorganic & Medicinal Chemistry 10 (11): 3565–9. (November 2002). doi:10.1016/S0968-0896(02)00251-1. PMID 12213471. 
  83. ^ “A cholesterol-lowering drug reduces beta-amyloid pathology in a transgenic mouse model of Alzheimer's disease”. Neurobiology of Disease 8 (5): 890–9. (October 2001). doi:10.1006/nbdi.2001.0422. PMID 11592856. 
  84. ^ “Contribution by synaptic zinc to the gender-disparate plaque formation in human Swedish mutant APP transgenic mice”. Proceedings of the National Academy of Sciences of the United States of America 99 (11): 7705–10. (May 2002). Bibcode2002PNAS...99.7705L. doi:10.1073/pnas.092034699. PMC 124328. PMID 12032347. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC124328/. 
  85. ^ “L-Norvaline Reverses Cognitive Decline and Synaptic Loss in a Murine Model of Alzheimer's Disease”. Neurotherapeutics : the Journal of the American Society for Experimental NeuroTherapeutics 15 (4): 1036–1054. (October 2018). doi:10.1007/s13311-018-0669-5. PMC 6277292. PMID 30288668. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6277292/. 
  86. ^ “Inhibition of amyloid-induced toxicity by ergothioneine in a transgenic Caenorhabditis elegans model”. FEBS Lett . 593 (16): 2139–2150. (August 2019). doi:10.1002/1873-3468.13497. PMID 31211853. 
  87. ^ “Imaging β-amyloid using [(18)F]flutemetamol positron emission tomography: from dosimetry to clinical diagnosis”. European Journal of Nuclear Medicine and Molecular Imaging 43 (2): 362–73. (February 2016). doi:10.1007/s00259-015-3208-1. PMID 26440450. 
  88. ^ “Quantitative Analysis of Amyloid Deposition in Alzheimer Disease Using PET and the Radiotracer ¹¹C-AZD2184”. Journal of Nuclear Medicine 55 (6): 932–8. (June 2014). doi:10.2967/jnumed.113.133793. PMID 24732152. 
  89. ^ Tissue processing prior to analysis of Alzheimer's disease associated proteins and metabolites, including Aβ. Methods in Molecular Biology. 849. (2012). pp. 493–506. doi:10.1007/978-1-61779-551-0_33. ISBN 978-1-61779-550-3. PMID 22528111 
  90. ^ Aβ measurement by enzyme-linked immunosorbent assay. Methods in Molecular Biology. 849. (2012). pp. 507–27. doi:10.1007/978-1-61779-551-0_34. ISBN 978-1-61779-550-3. PMID 22528112 
  91. ^ “In vitro characterization of conditions for amyloid-beta peptide oligomerization and fibrillogenesis”. The Journal of Biological Chemistry 278 (13): 11612–22. (March 2003). doi:10.1074/jbc.M210207200. PMID 12499373. 
  92. ^ “Impairments of hippocampal synaptic plasticity induced by aggregated beta-amyloid (25-35) are dependent on stimulation-protocol and genetic background”. Experimental Brain Research 179 (4): 621–30. (June 2007). doi:10.1007/s00221-006-0819-6. PMID 17171334. 
  93. ^ “Monitoring the prevention of amyloid fibril formation by alpha-crystallin. Temperature dependence and the nature of the aggregating species”. The FEBS Journal 274 (24): 6290–304. (December 2007). doi:10.1111/j.1742-4658.2007.06144.x. PMID 18005258. 
  94. ^ “Insight into early events in the aggregation of the prion protein on lipid membranes”. Biochimica et Biophysica Acta 1788 (10): 2245–51. (October 2009). doi:10.1016/j.bbamem.2009.08.005. PMID 19703409. 
  95. ^ “A highly sensitive plasma-based amyloid-β detection system through medium-changing and noise cancellation system for early diagnosis of the Alzheimer's disease” (英語). Scientific Reports 7 (1): 8882. (August 2017). doi:10.1038/s41598-017-09370-3. PMC 5567090. PMID 28827785. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5567090/. 


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