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当代阿耳茨海默病研究

Editor-in-Chief

ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

Review Article

阿尔茨海默病与其他神经退行性疾病的生物学途径,遗传学和细胞机制的共同点

卷 14, 期 11, 2017

页: [1190 - 1197] 页: 8

弟呕挨: 10.2174/1567205014666170203141151

价格: $65

摘要

背景:阿尔茨海默病(AD)是最常见和研究良好的神经变性疾病(ND)。 AD的生物学途径,病理生理学和遗传学显示与其他ND的共同点,帕金森氏病(PD),肌萎缩性侧索硬化(ALS),亨廷顿舞蹈病(HD),朊病毒病和牙髓 - 苍白球囊性萎缩症(DRPLA)。许多ND共享共同特征和分子机制表明,病理学可能是直接可比的,并且涉及疾病预防和发展高效疗法。 方法:在本综述中,对AD的病理生理学,临床症状和可用治疗情况进行了简要的介绍,特别强调AD。这些致命的ND中的共同点为治疗进展提供了支持,并增强了对疾病表现的理解。 结论:研究集中在生物学途径,细胞机制和遗传学上的共同之处,可能为研究人员提供了多种新型共同靶点,用于预防和发展多种神经退行性疾病的有效常用药物。

关键词: 神经变性疾病,阿尔茨海默病,帕金森病,亨廷顿病,肌萎缩性侧索硬化,生物学途径。

[1]
Silberberg D. The high impact of neurologic disorders in developing countries: the struggle for global recognition. Neurology 77(3): 307-8. (2011).
[2]
Pedro AV. Coping with Brain Disorders using Neurotechnology. Malays J Med Sci 19(1): 1-3. (2012).
[3]
Teplow DB. Molecular biology of neurodegenerative diseases. Preface. Prog Mol Biol Transl Sci 107: xiii-v. (2012).
[4]
Gao HM, Hong JS. Why neurodegenerative diseases are progressive: uncontrolled inflammation drives disease progression. Trends Immunol 29(8): 357-65. (2008).
[5]
Kruttgen A, Saxena S, Evangelopoulos ME, Weis J. Neurotrophins and neurodegenerative diseases: receptors stuck in traffic? J Neuropathol Exp Neurol 62(4): 340-50. (2003).
[6]
Ahmad K, Balaramnavar VM, Baig MH, Srivastava AK, Khan S, Kamal MA. Identification of potent caspase-3 inhibitors for treatment of multi- neurodegenerative diseases using pharmacophore modeling and docking approaches. CNS Neurol Disord Drug Targets 13(8): 1346-53. (2014).
[7]
Jellinger KA. Formation and development of Lewy pathology: a critical update. J Neurol 256(3): 270-9. (2009).
[8]
Brookmeyer R, Johnson E, Ziegler-Graham K, Arrighi HM. Forecasting the global burden of Alzheimer’s disease. Alzheimers Dement 3(3): 186-91. (2007).
[9]
Przedborski S, Vila M, Jackson-Lewis V. Neurodegeneration: what is it and where are we? J Clin Invest 111(1): 3-10. (2003).
[10]
Martin JB. Molecular basis of the neurodegenerative disorders. N Engl J Med 340(25): 1970-80. (1999).
[11]
Hebert LE, Beckett LA, Scherr PA, Evans DA. Annual incidence of Alzheimer disease in the United States projected to the years 2000 through 2050. Alzheimer Dis Assoc Disord 15(4): 169-73. (2001).
[12]
Hebert LE, Scherr PA, Bienias JL, Bennett DA, Evans DA. Alzheimer disease in the US population: prevalence estimates using the 2000 census. Arch Neurol 60(8): 1119-22. (2003).
[13]
Russell A, Drozdova A, Wang W, Thomas M. The impact of dementia development concurrent with Parkinson’s disease: a new perspective. CNS Neurol Disord Drug Targets 13(7): 1160-8. (2014).
[14]
Cavalli A, Bolognesi ML, Minarini A, Rosini M, Tumiatti V, Recanatini M, et al. Multi-target-directed ligands to combat neurodegenerative diseases. J Med Chem 51(3): 347-72. (2008).
[15]
Rizzi L, Rosset I, Roriz-Cruz M. Global epidemiology of dementia: Alzheimer’s and vascular types. Biomed Res Int 2014: 908915 (2014).
[16]
Terry RD, Peck A, DeTeresa R, Schechter R, Horoupian DS. Some morphometric aspects of the brain in senile dementia of the Alzheimer type. Ann Neurol 10(2): 184-92. (1981).
[17]
Katzman R. Alzheimer’s disease. N Engl J Med 314(15): 964-73. (1986).
[18]
Masliah E, Mallory M, Alford M, DeTeresa R, Iwai A, Saitoh T. Molecular Mechanisms of Synaptic Disconnection in Alzheimer’s Disease. In: Connections, Cognition and Alzheimer’s Disease. (Eds: Hayman BT, Duyckaerts C, Christen Y). Berlin, Heidelberg: Springer Berlin Heidelberg; pp. 121-40 (1997).
[19]
Budson AE, Price BH. Memory dysfunction. N Engl J Med 352(7): 692-9. (2005).
[20]
LaFerla FM, Oddo S. Alzheimer’s disease: Abeta, tau and synaptic dysfunction. Trends Mol Med 11(4): 170-6. (2005).
[21]
Kang J, Lemaire HG, Unterbeck A, Salbaum JM, Masters CL, Grzeschik KH, et al. The precursor of Alzheimer’s disease amyloid A4 protein resembles a cell-surface receptor. Nature 325(6106): 733-6. (1987).
[22]
Chartier-Harlin MC, Crawford F, Houlden H, Warren A, Hughes D, Fidani L, et al. Early-onset Alzheimer’s disease caused by mutations at codon 717 of the beta-amyloid precursor protein gene. Nature 353(6347): 844-6. (1991).
[23]
Goate A, Chartier-Harlin MC, Mullan M, Brown J, Crawford F, Fidani L, et al. Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer’s disease. Nature 349(6311): 704-6. (1991).
[24]
Citron M, Oltersdorf T, Haass C, McConlogue L, Hung AY, Seubert P, et al. Mutation of the beta-amyloid precursor protein in familial Alzheimer’s disease increases beta-protein production. Nature 360(6405): 672-4. (1992).
[25]
Games D, Adams D, Alessandrini R, Barbour R, Berthelette P, Blackwell C, et al. Alzheimer-type neuropathology in transgenic mice overexpressing V717F beta-amyloid precursor protein. Nature 373(6514): 523-7. (1995).
[26]
Cole SL, Vassar R. The Alzheimer’s disease beta-secretase enzyme, BACE1. Mol Neurodegener 2: 22. (2007).
[27]
Suzuki N, Cheung TT, Cai XD, Odaka A, Otvos L Jr, Eckman C, et al. An increased percentage of long amyloid beta protein secreted by familial amyloid beta protein precursor (beta APP717) mutants. Science 264(5163): 1336-40. (1994).
[28]
Adlard PA, Cummings BJ. Alzheimer’s disease--a sum greater than its parts? Neurobiol Aging 25(6): 725-733; discussion 43-6. (2004).
[29]
Holscher C. Possible causes of Alzheimer’s disease: amyloid fragments, free radicals, and calcium homeostasis. Neurobiol Dis 5(3): 129-41. (1998).
[30]
Bolognesi ML, Banzi R, Bartolini M, Cavalli A, Tarozzi A, Andrisano V, et al. Novel class of quinone-bearing polyamines as multi-target-directed ligands to combat Alzheimer’s disease. J Med Chem 50(20): 4882-97. (2007).
[31]
Gotz J, Schild A, Hoerndli F, Pennanen L. Amyloid-induced neurofibrillary tangle formation in Alzheimer’s disease: insight from transgenic mouse and tissue-culture models. Int J Dev Neurosci 22(7): 453-65. (2004).
[32]
Waite LM. Treatment for Alzheimer’s disease: has anything changed? Aust Prescr 38(2): 60-3. (2015).
[33]
Lev N, Melamed E, Offen D. Apoptosis and Parkinson’s disease. Prog Neuropsychopharmacol Biol Psychiatry 27(2): 245-50. (2003).
[34]
Corti O, Hampe C, Darios F, Ibanez P, Ruberg M, Brice A. Parkinson’s disease: from causes to mechanisms. C R Biol 328(2): 131-42. (2005).
[35]
Booth TC, Nathan M, Waldman AD, Quigley AM, Schapira AH, Buscombe J. The role of functional dopamine-transporter SPECT imaging in parkinsonian syndromes, part 1. AJNR Am J Neuroradiol 36(2): 229-35. (2015).
[36]
Shastry BS. Parkinson disease: etiology, pathogenesis and future of gene therapy. Neurosci Res 41(1): 5-12. (2001).
[37]
Samii A, Nutt JG, Ransom BR. Parkinson’s disease. Lancet 363(9423): 1783-93. (2004).
[38]
Payami H, Factor SA. Promise of pharmacogenomics for drug discovery, treatment and prevention of Parkinson’s disease. A perspective. Neurotherapeutics 11(1): 111-6. (2014).
[39]
Goodman AO, Murgatroyd PR, Medina-Gomez G, Wood NI, Finer N, Vidal-Puig AJ, et al. The metabolic profile of early Huntington’s disease--a combined human and transgenic mouse study. Exp Neurol 210(2): 691-8. (2008).
[40]
Kim HS, Lyoo CH, Lee PH, Kim SJ, Park MY, Ma HI, et al. Current Status of Huntington’s Disease in Korea: A Nationwide Survey and National Registry Analysis. J Mov Disord 8(1): 14-20. (2015).
[41]
Block RC, Dorsey ER, Beck CA, Brenna JT, Shoulson I. Altered cholesterol and fatty acid metabolism in Huntington disease. J Clin Lipidol 4(1): 17-23. (2010).
[42]
Fink KD, Deng P, Torrest A, Stewart H, Pollock K, Gruenloh W, et al. Developing stem cell therapies for juvenile and adult-onset Huntington’s disease. Regen Med 10(5): 623-46. (2015).
[43]
Patzke H, Tsai LH. Cdk5 sinks into ALS. Trends Neurosci 25(1): 8-10. (2002).
[44]
Hayashi Y, Kakita A, Yamada M, Egawa S, Oyanagi S, Naito H, et al. Hereditary dentatorubral-pallidoluysian atrophy: ubiquitinated filamentous inclusions in the cerebellar dentate nucleus neurons. Acta Neuropathol 95(5): 479-82. (1998).
[45]
Igarashi S, Koide R, Shimohata T, Yamada M, Hayashi Y, Takano H, et al. Suppression of aggregate formation and apoptosis by transglutaminase inhibitors in cells expressing truncated DRPLA protein with an expanded polyglutamine stretch. Nat Genet 18(2): 111-7. (1998).
[46]
Simpson CL, Al-Chalabi A. Amyotrophic lateral sclerosis as a complex genetic disease. Biochim Biophys Acta 1762(11-12): 973-85. (2006).
[47]
Mitchell JD, Borasio GD. Amyotrophic lateral sclerosis. Lancet 369(9578): 2031-41. (2007).
[48]
Phukan J, Pender NP, Hardiman O. Cognitive impairment in amyotrophic lateral sclerosis. Lancet Neurol 6(11): 994-1003. (2007).
[49]
Mohan RD, Abmayr SM, Workman JL. The expanding role for chromatin and transcription in polyglutamine disease. Curr Opin Genet Dev 26: 96-104. (2014).
[50]
Takada LT, Geschwind MD. Prion diseases. Semin Neurol 33(4): 348-56. (2013).
[51]
Karapetyan YE, Sferrazza GF, Zhou M, Ottenberg G, Spicer T, Chase P, et al. Unique drug screening approach for prion diseases identifies tacrolimus and astemizole as antiprion agents. Proc Natl Acad Sci USA 110(17): 7044-9. (2013).
[52]
Kayed R, Head E, Thompson JL, McIntire TM, Milton SC, Cotman CW, et al. Common structure of soluble amyloid oligomers implies common mechanism of pathogenesis. Science 300(5618): 486-9. (2003).
[53]
Bossy-Wetzel E, Schwarzenbacher R, Lipton SA. Molecular pathways to neurodegeneration. Nat Med 10: S2-9. (2004).
[54]
Ross CA, Poirier MA. Protein aggregation and neurodegenerative disease. Nat Med 10: S10-7. (2004).
[55]
Kamal MA, Mushtaq G, Greig NH. Current Update on Synopsis of miRNA Dysregulation in Neurological Disorders. CNS Neurol Disord Drug Targets 14(4): 492-501. (2015).
[56]
Carrell RW, Lomas DA. Conformational disease. Lancet 350(9071): 134-8. (1997).
[57]
Dobson CM. Protein misfolding, evolution and disease. Trends Biochem Sci 24(9): 329-32. (1999).
[58]
Soto C. Protein misfolding and disease; protein refolding and therapy. FEBS Lett 498(2-3): 204-7. (2001).
[59]
Orr HT, Zoghbi HY. Trinucleotide repeat disorders. Annu Rev Neurosci 30: 575-621. (2007).
[60]
Selkoe DJ. Alzheimer’s disease: genes, proteins, and therapy. Physiol Rev 81(2): 741-66. (2001).
[61]
Thomas B, Beal MF. Parkinson's disease. Hum Mol Genet 16 Spec No. 2: R183-94 (2007).
[62]
Ince PG, Highley JR, Kirby J, Wharton SB, Takahashi H, Strong MJ, et al. Molecular pathology and genetic advances in amyotrophic lateral sclerosis: an emerging molecular pathway and the significance of glial pathology. Acta Neuropathol 122(6): 657-71. (2011).
[63]
Grunblatt E. Commonalities in the genetics of Alzheimer’s disease and Parkinson’s disease. Expert Rev Neurother 8(12): 1865-77. (2008).
[64]
Giau VV, Bagyinszky E, An SS, Kim SY. Role of apolipoprotein E in neurodegenerative diseases. Neuropsychiatr Dis Treat 11: 1723-37. (2015).
[65]
Mathisen PM. Gene discovery and validation for neurodegenerative diseases. Drug Discov Today 8(1): 39-46. (2003).
[66]
Goehler H, Lalowski M, Stelzl U, Waelter S, Stroedicke M, Worm U, et al. A protein interaction network links GIT1, an enhancer of huntingtin aggregation, to Huntington’s disease. Mol Cell 15(6): 853-65. (2004).
[67]
Giorgini F, Muchowski PJ. Connecting the dots in Huntington’s disease with protein interaction networks. Genome Biol 6(3): 210. (2005).
[68]
Hiesinger PR, Hassan BA. Genetics in the age of systems biology. Cell 123(7): 1173-4. (2005).
[69]
Rhodes DR, Chinnaiyan AM. Integrative analysis of the cancer transcriptome. Nat Genet 37: S31-7. (2005).
[70]
Gunsalus KC, Ge H, Schetter AJ, Goldberg DS, Han JD, Hao T, et al. Predictive models of molecular machines involved in Caenorhabditis elegans early embryogenesis. Nature 436(7052): 861-5. (2005).
[71]
Goh KI, Cusick ME, Valle D, Childs B, Vidal M, Barabasi AL. The human disease network. Proc Natl Acad Sci USA 104(21): 8685-90. (2007).
[72]
Jin L, Zuo XY, Su WY, Zhao XL, Yuan MQ, Han LZ, et al. Pathway-based analysis tools for complex diseases: a review. Genomics Proteomics Bioinformatics 12(5): 210-20. (2014).
[73]
Kann MG. Protein interactions and disease: computational approaches to uncover the etiology of diseases. Brief Bioinform 8(5): 333-46. (2007).
[74]
Rao VS, Srinivas K, Sujini GN, Kumar GN. Protein-protein interaction detection: methods and analysis. Int J Proteomics 2014147648 (2014).

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