ウィキペディア |
アルツハイマー型認知症の生化学
出典: フリー百科事典『ウィキペディア(Wikipedia)』 (2012/05/08 10:44 UTC 版)
アルツハイマー型認知症は、成人が発症する認知症の代表的な疾患であるが、その生化学的基盤は依然として未知な点が多い。タンパク質のミスフォールディング(折りたたみ異常)がもたらす疾患であることは判明しており、アルツハイマー型認知症の患者の脳からは異常に折りたたまれたアミロイドβタンパク質の蓄積が見られる[1]。また、アルツハイマー型認知症は、タウタンパク質の異常凝集が原因となるタウオパチーと呼ばれる疾患の一種であると考えられている。
- ^ a b Hashimoto M, Rockenstein E, Crews L, Masliah E (2003). “Role of protein aggregation in mitochondrial dysfunction and neurodegeneration in Alzheimer's and Parkinson's diseases”. Neuromolecular Med. 4 (1-2): 21–36. doi:10.1385/NMM:4:1-2:21. PMID 14528050.
- ^ Wenk GL (2003). “Neuropathologic changes in Alzheimer's disease”. J Clin Psychiatry 64 Suppl 9: 7–10. PMID 12934968.
- ^ Tiraboschi P, Hansen L, Thal L, Corey-Bloom J (2004). “The importance of neuritic plaques and tangles to the development and evolution of AD.”. Neurology 62 (11): 1984–9. PMID 15184601.
- ^ Bouras C, Hof PR, Giannakopoulos P, Michel JP, Morrison JH (1994). “Regional distribution of neurofibrillary tangles and senile plaques in the cerebral cortex of elderly patients: a quantitative evaluation of a one-year autopsy population from a geriatric hospital”. Cereb. Cortex 4 (2): 138–50. doi:10.1093/cercor/4.2.138. PMID 8038565.
- ^ Kerr ML, Small DH (2005). “Cytoplasmic domain of the beta-amyloid protein precursor of Alzheimer's disease: function, regulation of proteolysis, and implications for drug development”. J. Neurosci. Res. 80 (2): 151–9. doi:10.1002/jnr.20408. PMID 15672415.
- ^ Cai D, Netzer WJ, Zhong M, et al. (2006). “Presenilin-1 uses phospholipase D1 as a negative regulator of beta-amyloid formation”. Proc. Natl. Acad. Sci. U.S.A. 103 (6): 1941–6. doi:10.1073/pnas.0510708103. PMC 1413665. PMID 16449386.
- ^ Danielsson J, Andersson A, Jarvet J, Gräslund A (2006). “15N relaxation study of the amyloid beta-peptide: structural propensities and persistence length”. Magnetic resonance in chemistry : MRC 44 Spec No: S114–21. doi:10.1002/mrc.1814. PMID 16826550.
- ^ Tomaselli S, Esposito V, Vangone P, et al. (2006). “The alpha-to-beta conformational transition of Alzheimer's Abeta-(1-42) peptide in aqueous media is reversible: a step by step conformational analysis suggests the location of beta conformation seeding”. Chembiochem 7 (2): 257–67. doi:10.1002/cbic.200500223. PMID 16444756.
- ^ Ohnishi S, Takano K (2004). “Amyloid fibrils from the viewpoint of protein folding”. Cell. Mol. Life Sci. 61 (5): 511–24. doi:10.1007/s00018-003-3264-8. PMID 15004691.
- ^ Goedert M, Klug A, Crowther RA (2006). “Tau protein, the paired helical filament and Alzheimer's disease”. J. Alzheimers Dis. 9 (3 Suppl): 195–207. PMID 16914859.
- ^ Pastorino L, Sun A, Lu PJ, et al. (2006). “The prolyl isomerase Pin1 regulates amyloid precursor protein processing and amyloid-beta production”. Nature 440 (7083): 528–34. doi:10.1038/nature04543. PMID 16554819.
- ^ Lim J, Lu KP (2005). “Pinning down phosphorylated tau and tauopathies”. Biochim. Biophys. Acta 1739 (2-3): 311–22. doi:10.1016/j.bbadis.2004.10.003. PMID 15615648.
- ^ Baskys. “Receptor found that could lead to better treatments for stroke, alzheimer's disease”. UCI Medical Center. 2006年11月4日閲覧。
- ^ Shen ZX (2004). “Brain cholinesterases: II. The molecular and cellular basis of Alzheimer's disease”. Med. Hypotheses 63 (2): 308–21. doi:10.1016/j.mehy.2004.02.031. PMID 15236795.
- ^ Wenk GL (2003). “Neuropathologic changes in Alzheimer's disease”. The Journal of clinical psychiatry 64 Suppl 9: 7–10. PMID 12934968.
- ^ a b c Mudher A, Lovestone S (2002). “Alzheimer's disease-do tauists and baptists finally shake hands?”. Trends Neurosci. 25 (1): 22–6. doi:10.1016/S0166-2236(00)02031-2. PMID 11801334.
- ^ Schmitz C, Rutten BP, Pielen A, et al. (1 April 2004). “Hippocampal neuron loss exceeds amyloid plaque load in a transgenic mouse model of Alzheimer's disease”. Am. J. Pathol. 164 (4): 1495–502. PMC 1615337. PMID 15039236.
- ^ Gray EG, Paula-Barbosa M, Roher A (1987). “Alzheimer's disease: paired helical filaments and cytomembranes”. Neuropathol. Appl. Neurobiol. 13 (2): 91–110. doi:10.1111/j.1365-2990.1987.tb00174.x. PMID 3614544.
- ^ Williams DR (2006). “Tauopathies: classification and clinical update on neurodegenerative diseases associated with microtubule-associated protein tau”. Internal medicine journal 36 (10): 652–60. doi:10.1111/j.1445-5994.2006.01153.x. PMID 16958643.
- ^ Nistor M, Don M, Parekh M, et al. (2007). “Alpha- and beta-secretase activity as a function of age and beta-amyloid in Down syndrome and normal brain”. Neurobiol. Aging 28 (10): 1493–506. doi:10.1016/j.neurobiolaging.2006.06.023. PMID 16904243.
- ^ Lott IT, Head E (2005). “Alzheimer disease and Down syndrome: factors in pathogenesis”. Neurobiol. Aging 26 (3): 383–9. doi:10.1016/j.neurobiolaging.2004.08.005. PMID 15639317.
- ^ Yankner BA, Duffy LK, Kirschner DA (1990). “Neurotrophic and neurotoxic effects of amyloid beta protein: reversal by tachykinin neuropeptides”. Science 250 (4978): 279–82. doi:10.1126/science.2218531. PMID 2218531.
- ^ Iijima K, Liu HP, Chiang AS, Hearn SA, Konsolaki M, Zhong Y (2004). “Dissecting the pathological effects of human Abeta40 and Abeta42 in Drosophila: a potential model for Alzheimer's disease”. Proc. Natl. Acad. Sci. U.S.A. 101 (17): 6623–8. doi:10.1073/pnas.0400895101. PMC 404095. PMID 15069204.
- ^ Gregory GC, Halliday GM (2005). “What is the dominant Abeta species in human brain tissue? A review”. Neurotoxicity research 7 (1-2): 29–41. doi:10.1007/BF03033774. PMID 15639796.
- ^ Blanchard BJ, Hiniker AE, Lu CC, Margolin Y, Yu AS, Ingram VM (2000). “Elimination of Amyloid beta Neurotoxicity”. J Alzheimers Dis 2 (2): 137–149. PMID 12214104.
- ^ Abramov AY, Canevari L, Duchen MR (2004). “Calcium signals induced by amyloid beta peptide and their consequences in neurons and astrocytes in culture”. Biochim. Biophys. Acta 1742 (1-3): 81–7. doi:10.1016/j.bbamcr.2004.09.006. PMID 15590058.
- ^ Barghorn S, Nimmrich V, Striebinger A, et al. (2005). “Globular amyloid beta-peptide oligomer - a homogenous and stable neuropathological protein in Alzheimer's disease”. J. Neurochem. 95 (3): 834–47. doi:10.1111/j.1471-4159.2005.03407.x. PMID 16135089.
- ^ Kokubo H, Kayed R, Glabe CG, Yamaguchi H (2005). “Soluble Abeta oligomers ultrastructurally localize to cell processes and might be related to synaptic dysfunction in Alzheimer's disease brain”. Brain Res. 1031 (2): 222–8. doi:10.1016/j.brainres.2004.10.041. PMID 15649447.
- ^ Blanchard BJ, Chen A, Rozeboom LM, Stafford KA, Weigele P, Ingram VM (2004). “Efficient reversal of Alzheimer's disease fibril formation and elimination of neurotoxicity by a small molecule”. Proc. Natl. Acad. Sci. U.S.A. 101 (40): 14326–32. doi:10.1073/pnas.0405941101. PMC 521943. PMID 15388848.
- ^ Porat Y, Abramowitz A, Gazit E. (2006). Inhibition of amyloid fibril formation by polyphenols: structural similarity and aromatic interactions as a common inhibition mechanism. Chem Biol Drug Des 67(1):27-37.
- ^ Kanapathipillai M, Lentzen G, Sierks M, Park CB (2005). “Ectoine and hydroxyectoine inhibit aggregation and neurotoxicity of Alzheimer's beta-amyloid”. FEBS Lett. 579 (21): 4775–80. doi:10.1016/j.febslet.2005.07.057. PMID 16098972.
- ^ Lee KH, Shin BH, Shin KJ, Kim DJ, Yu J (2005). “A hybrid molecule that prohibits amyloid fibrils and alleviates neuronal toxicity induced by beta-amyloid (1-42)”. Biochem. Biophys. Res. Commun. 328 (4): 816–23. doi:10.1016/j.bbrc.2005.01.030. PMID 15707952.
- ^ Espeseth AS, Xu M, Huang Q, et al. (2005). “Compounds that bind APP and inhibit Abeta processing in vitro suggest a novel approach to Alzheimer disease therapeutics”. J. Biol. Chem. 280 (18): 17792–7. doi:10.1074/jbc.M414331200. PMID 15737955.
- ^ Moreno, H.; Yu, E.; Pigino, G.; Hernandez, I.; Kim, N.; Moreira, E.; Sugimori, M.; Llinás, R. (Mar 2009), “Synaptic transmission block by presynaptic injection of oligomeric amyloid beta” (Free full text), Proceedings of the National Academy of Sciences of the United States of America 106 (14): 5901, doi:10.1073/pnas.0900944106, ISSN 0027-8424, PMC 2659170, PMID 19304802
- ^ Pigino, G.; Morfini, G.; Atagi, Y.; Deshpande, A.; Yu, C.; Jungbauer, L.; Ladu, M.; Busciglio, J. et al. (Mar 2009), “Disruption of fast axonal transport is a pathogenic mechanism for intraneuronal amyloid beta”, Proceedings of the National Academy of Sciences of the United States of America 106 (14): 5907, doi:10.1073/pnas.0901229106, ISSN 0027-8424, PMC 2667037, PMID 19321417
- ^ "Edlund C, Söderberg M, Kristensson K. Neurochem Int, 1994 Jul,25(1), 35-8."
- 1 アルツハイマー型認知症の生化学とは
- 2 アルツハイマー型認知症の生化学の概要
固有名詞の分類