Tăng phosphoryl hóa protein trung gian đáp ứng collapsin-2 tại Thr514 tương quan với gánh nặng β-amyloid và khiếm khuyết synap trong chứng mất trí Lewy

Goshima Y, Nakamura F, Strittmatter P, Strittmatter SM. Collapsin-induced growth cone collapse mediated by an intracellular protein related to UNC-33. Nature. 1995;376:509–14. Charrier E, Reibel S, Rogemond V, Aguera M, Thomasset N, Honnorat J. Collapsin response mediator proteins (CRMPs): involvement in nervous system development and adult neurodegenerative disorders. Mol Neurobiol. 2003;28:51–64. Wang LH, Strittmatter SM. A family of rat CRMP genes is differentially expressed in the nervous system. J Neurosci. 1996;16:6197–207. Brittain JM, Piekarz AD, Wang Y, Kondo T, Cummins TR, Khanna R. An atypical role for collapsin response mediator protein 2 (CRMP-2) in neurotransmitter release via interaction with presynaptic voltage-gated calcium channels. J Biol Chem. 2009;284:31375–90. Ip JP, Shi L, Chen Y, Itoh Y, Fu W-Y, Betz A, Yung W-H, Gotoh Y, Fu AK, Ip NY. α2-chimaerin controls neuronal migration and functioning of the cerebral cortex through CRMP-2. Nat Neurosci. 2012;15:39–47. Kawano Y, Yoshimura T, Tsuboi D, Kawabata S, Kaneko-Kawano T, Shirataki H, Takenawa T, Kaibuchi K. CRMP-2 is involved in kinesin-1-dependent transport of the Sra-1/WAVE1 complex and axon formation. Mol Cell Biol. 2005;25:9920–35. Uchida Y, Ohshima T, Sasaki Y, Suzuki H, Yanai S, Yamashita N, Nakamura F, Takei K, Ihara Y, Mikoshiba K, et al. Semaphorin3A signalling is mediated via sequential Cdk5 and GSK3b phosphorylation of CRMP2: implication of common phosphorylating mechanism underlying axon guidance and Alzheimer’s disease. Genes Cells. 2005;10:165–79. Brittain JM, Wang Y, Eruvwetere O, Khanna R. Cdk5-mediated phosphorylation of CRMP-2 enhances its interaction with CaV2.2. FEBS Lett. 2012;586:3813–8. Li T, Hawkes C, Qureshi HY, Kar S, Paudel HK. Cyclin-dependent protein kinase 5 primes microtubule-associated protein tau site-specifically for glycogen synthase kinase 3β. Biochemistry. 2006;45:3134–45. Yoshimura T, Kawano Y, Arimura N, Kawabata S, Kikuchi A, Kaibuchi K. GSK-3b regulates phosphorylation of CRMP-2 and neuronal polarity. Cell. 2005;120:137–49. Patrick GN, Zukerberg L, Nikolic M, de la Monte S, Dikkes P, Tsai LH. Conversion of p35 to p25 deregulates Cdk5 activity and promotes neurodegeneration. Nature. 1999;402:615–22. Kaytor MD, Orr HT. The GSK3b signaling cascade and neurodegenerative disease. Curr Opin Neurobiol. 2002;12:275–8. Petratos S, Ozturk E, Azari MF, Kenny R, Lee JY, Magee KA, Harvey AR, McDonald C, Taghian K, Moussa L, et al. Limiting multiple sclerosis related axonopathy by blocking Nogo receptor and CRMP-2 phosphorylation. Brain. 2012;135:1794–818. Zhu LQ, Zheng HY, Peng CX, Liu D, Li HL, Wang Q, Wang JZ. Protein phosphatase 2A facilitates axonogenesis by dephosphorylating CRMP2. J Neurosci. 2010;30:3839–48. Stokin GB, Lillo C, Falzone TL, Brusch RG, Rockenstein E, Mount SL, Raman R, Davies P, Masliah E, Williams DS, Goldstein LS. Axonopathy and transport deficits early in the pathogenesis of Alzheimer’s disease. Science. 2005;307:1282–8. Cole AR, Noble W, van Aalten L, Plattner F, Meimaridou R, Hogan D, Taylor M, LaFrancois J, Gunn-Moore F, Verkhratsky A, et al. Collapsin response mediator protein-2 hyperphosphorylation is an early event in Alzheimer’s disease progression. J Neurochem. 2007;103:1132–44. Williamson R, van Aalten L, Mann DM, Platt B, Plattner F, Bedford L, Mayer J, Howlett D, Usardi A, Sutherland C, Cole AR. CRMP2 hyperphosphorylation is characteristic of Alzheimer’s disease and not a feature common to other neurodegenerative diseases. J Alzheimers Dis. 2011;27:615–25. Zaccai J, McCracken C, Brayne C. A systematic review of prevalence and incidence studies of dementia with Lewy bodies. Age Ageing. 2005;34:561–6. Tsuboi Y, Dickson DW. Dementia with Lewy bodies and Parkinson’s disease with dementia: are they different? Parkinsonism Relat Disord. 2005;11 Suppl 1:S47–51. McKeith IG, Dickson DW, Lowe J, Emre M, O’Brien JT, Feldman H, Cummings J, Duda JE, Lippa C, Perry EK, et al. Diagnosis and management of dementia with Lewy bodies: third report of the DLB Consortium. Neurology. 2005;65:1863–72. Edison P, Rowe CC, Rinne JO, Ng S, Ahmed I, Kemppainen N, Villemagne VL, O’Keefe G, Nagren K, Chaudhury KR, et al. Amyloid load in Parkinson’s disease dementia and Lewy body dementia measured with [11C] PIB positron emission tomography. J Neurol Neurosurg Psychiatry. 2008;79:1331–8. Gomperts SN, Locascio JJ, Marquie M, Santarlasci AL, Rentz DM, Maye J, Johnson KA, Growdon JH. Brain amyloid and cognition in lewy body diseases. Mov Disord. 2012;27:965–73. Howlett DR, Whitfield D, Johnson M, Attems J, O’Brien JT, Aarsland D, Lai MK, Lee JH, Chen C, Ballard C, et al. Regional multiple pathology scores are associated with cognitive decline in lewy body dementias. Brain Pathol. 2015;25:401–8. Lewis DA. The human brain revisited. Opportunities and challenges in postmortem studies of psychiatric disorders. Neuropsychopharmacology. 2002;26:143–54. Rahajeng J, Giridharan SS, Naslavsky N, Caplan S. Collapsin response mediator protein-2 (Crmp2) regulates trafficking by linking endocytic regulatory proteins to dynein motors. J Biol Chem. 2010;285:31918–22. Haq S, Kilter H, Michael A, Tao J, O’Leary E, Sun XM, Walters B, Bhattacharya K, Chen X, Cui L, et al. Deletion of cytosolic phospholipase A2 promotes striated muscle growth. Nat Med. 2003;9:944–51. Yu Z, Huang Z, Lung ML. Subcellular fractionation of cultured human cell lines. Bio-Protocol. 2013;3:e754. Yoshiike Y, Chui DH, Akagi T, Tanaka N, Takashima A. Specific compositions of amyloid-b peptides as the determinant of toxic b-aggregation. J Biol Chem. 2003;278:23648–55. Kuperstein I, Broersen K, Benilova I, Rozenski J, Jonckheere W, Debulpaep M, Vandersteen A, Segers-Nolten I, Van Der Werf K, Subramaniam V, et al. Neurotoxicity of Alzheimer’s disease Ab peptides is induced by small changes in the Ab42 to Ab40 ratio. EMBO J. 2010;29:3408–20. Blennow K, De Meyer G, Hansson O, Minthon L, Wallin A, Zetterberg H, Lewczuk P, Vanderstichele H, Vanmechelen E, Kornhuber J. Evolution of Aβ42 and Aβ40 levels and Aβ42/Aβ40 ratio in plasma during progression of Alzheimer’s disease: a multicenter assessment. J Nutr Health Aging. 2009;13:205–8. Blennow K, Mattsson N, Scholl M, Hansson O, Zetterberg H. Amyloid biomarkers in Alzheimer’s disease. Trends Pharmacol Sci. 2015;36:297–309. Augustinack JC, Schneider A, Mandelkow EM, Hyman BT. Specific tau phosphorylation sites correlate with severity of neuronal cytopathology in Alzheimer’s disease. Acta Neuropathol. 2002;103:26–35. Oueslati A. Implication of a-synuclein phosphorylation at S129 in synucleinopathies: what have we learned in the last decade? J Parkinsons Dis. 2016;6:39–51. Conde C, Cáceres A. Microtubule assembly, organization and dynamics in axons and dendrites. Nat Rev Neurosci. 2009;10:319–32. Shen K, Cowan CW. Guidance molecules in synapse formation and plasticity. Cold Spring Harb Perspect Biol. 2010;2:a001842. Avwenagha O, Campbell G, Bird MM. Distribution of GAP-43, b-III tubulin and F-actin in developing and regenerating axons and their growth cones in vitro, following neurotrophin treatment. J Neurocytol. 2003;32:1077–89. Tischfield MA, Baris HN, Wu C, Rudolph G, Van Maldergem L, He W, Chan WM, Andrews C, Demer JL, Robertson RL, et al. Human TUBB3 mutations perturb microtubule dynamics, kinesin interactions, and axon guidance. Cell. 2010;140:74–87. Britschgi M, Takeda-Uchimura Y, Rockenstein E, Johns H, Masliah E, Wyss-Coray T. Deficiency of terminal complement pathway inhibitor promotes neuronal tau pathology and degeneration in mice. J Neuroinflammation. 2012;9:220. Hensley K, Kursula P. Collapsin Response Mediator Protein-2 (CRMP2) is a plausible etiological factor and potential therapeutic target in alzheimer’s disease: comparison and contrast with microtubule-associated protein Tau. J Alzheimers Dis. 2016;1–14. Selkoe DJ. Alzheimer’s disease is a synaptic failure. Science. 2002;298:789–91. Fukata Y, Itoh TJ, Kimura T, Menager C, Nishimura T, Shiromizu T, Watanabe H, Inagaki N, Iwamatsu A, Hotani H, Kaibuchi K. CRMP-2 binds to tubulin heterodimers to promote microtubule assembly. Nat Cell Biol. 2002;4:583–91. Gu Y, Ihara Y. Evidence that collapsin response mediator protein-2 is involved in the dynamics of microtubules. J Biol Chem. 2000;275:17917–20. Khanna R, Wilson SM, Brittain JM, Weimer J, Sultana R, Butterfield A, Hensley K. Opening Pandora’s jar: a primer on the putative roles of CRMP2 in a panoply of neurodegenerative, sensory and motor neuron, and central disorders. Future Neurol. 2012;7:749–71. Nishimura T, Fukata Y, Kato K, Yamaguchi T, Matsuura Y, Kamiguchi H, Kaibuchi K. CRMP-2 regulates polarized Numb-mediated endocytosis for axon growth. Nat Cell Biol. 2003;5:819–26. Aarsland D, Ballard CG, Halliday G. Are Parkinson’s disease with dementia and dementia with lewy bodies the same entity? J Geriatr Psychiatry Neurol. 2004;17:137–45. Aarsland D, Londos E, Ballard C. Parkinson’s disease dementia and dementia with lewy bodies: different aspects of one entity. Int Psychogeriatr. 2009;21:216–9. Lippa CF, Duda JE, Grossman M, Hurtig HI, Aarsland D, Boeve BF, Brooks DJ, Dickson DW, Dubois B, Emre M, et al. DLB and PDD boundary issues: diagnosis, treatment, molecular pathology, and biomarkers. Neurology. 2007;68:812–9. Quinn JG, Coulson DT, Brockbank S, Beyer N, Ravid R, Hellemans J, Irvine GB, Johnston JA. a-synuclein mRNA and soluble a-synuclein protein levels in post-mortem brain from patients with Parkinson’s disease, dementia with lewy bodies, and Alzheimer’s disease. Brain Res. 2012;1459:71–80. Vallortigara J, Whitfield D, Quelch W, Alghamdi A, Howlett D, Hortobagyi T, Johnson M, Attems J, O’Brien JT, Thomas A, et al. Decreased levels of VAMP2 and monomeric alpha-synuclein correlate with duration of dementia. J Alzheimers Dis. 2015;50:101–10. Abdelnour C, van Steenoven I, Londos E, Blanc F, Auestad B, Kramberger MG, Zetterberg H, Mollenhauer B, Boada M, Aarsland D. Alzheimer’s disease cerebrospinal fluid biomarkers predict cognitive decline in Lewy body dementia. Mov Disord 2016, In Press Wang Y, Yin H, Li J, Zhang Y, Han B, Zeng Z, Qiao N, Cui X, Lou J, Li J. Amelioration of β-amyloid-induced cognitive dysfunction and hippocampal axon degeneration by curcumin is associated with suppression of CRMP-2 hyperphosphorylation. Neurosci Lett. 2013;557:112–7. Halliday GM, Holton JL, Revesz T, Dickson DW. Neuropathology underlying clinical variability in patients with synucleinopathies. Acta Neuropathol. 2011;122:187–204. Katsuse O, Iseki E, Marui W, Kosaka K. Developmental stages of cortical lewy bodies and their relation to axonal transport blockage in brains of patients with dementia with lewy bodies. J Neurol Sci. 2003;211:29–35. Mohamed NE, Zhao Y, Lee JH, Tan MG, Esiri MM, Wilcock GK, Smith AD, Wong PT, Chen CP, Lai MK. Upregulation of AMPA receptor GluR2 (GluA2) subunits in subcortical ischemic vascular dementia is repressed in the presence of Alzheimer’s disease. Neurochem Int. 2011;58:820–5. Yoshida H, Watanabe A, Ihara Y. Collapsin response mediator protein-2 is associated with neurofibrillary tangles in Alzheimer’s disease. J Biol Chem. 1998;273:9761–8. Anderson JP, Walker DE, Goldstein JM, de Laat R, Banducci K, Caccavello RJ, Barbour R, Huang J, Kling K, Lee M, et al. Phosphorylation of Ser-129 is the dominant pathological modification of a-synuclein in familial and sporadic Lewy body disease. J Biol Chem. 2006;281:29739–52. Fujiwara H, Hasegawa M, Dohmae N, Kawashima A, Masliah E, Goldberg MS, Shen J, Takio K, Iwatsubo T. a-Synuclein is phosphorylated in synucleinopathy lesions. Nat Cell Biol. 2002;4:160–4. Swirksi M, Miners S, de Silva R, Lashley Y, Ling H, Holton T, Revesz T, Love S. Evaluating the relationship between amyloid-β and α-synuclein phosphorylated at Ser129 in dementia with lewy bodies and Parkinson’s disease. Alzheimers Res Ther. 2014;6:77. Baum L, Hansen L, Masliah E, Saitoh T. Glycogen synthase kinase 3 alteration in Alzheimer disease is related to neurofibrillary tangle formation. Mol Chem Neuropathol. 1996;29:253–61. Lim NK, Hung LW, Pang TY, McLean CA, Liddell JR, Hilton JB, Li QX, White AR, Hannan AJ, Crouch PJ. Localized changes to glycogen synthase kinase-3 and collapsin response mediator protein-2 in the Huntington’s disease affected brain. Hum Mol Genet. 2014;23:4051–63. Yoo BC, Lubec G. Neurobiology: p25 protein in neurodegeneration. Nature. 2001;411:763–4. Taniguchi S, Fujita Y, Hayashi S, Kakita A, Takahashi H, Murayama S, Saido TC, Hisanaga S, Iwatsubo T, Hasegawa M. Calpain-mediated degradation of p35 to p25 in postmortem human and rat brains. FEBS Lett. 2001;489:46–50. Jacobs EH, Williams RJ, Francis PT. Cyclin-dependent kinase 5, Munc18a and Munc18-interacting protein 1/X11a protein up-regulation in Alzheimer’s disease. Neuroscience. 2006;138:511–22. Kerokoski P, Suuronen T, Salminen A, Soininen H, Pirttila T. The levels of cdk5 and p35 proteins and tau phosphorylation are reduced during neuronal apoptosis. Biochem Biophys Res Commun. 2001;280:998–1002. Emre M, Aarsland D, Brown R, Burn DJ, Duyckaerts C, Mizuno Y, Broe GA, Cummings J, Dickson DW, Gauthier S, et al. Clinical diagnostic criteria for dementia associated with Parkinson’s disease. Mov Disord. 2007;22:1689–707. quiz 1837. Braak H, Braak E. Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol. 1991;82:239–59.