Vai ai contenuti. | Spostati sulla navigazione | Spostati sulla ricerca | Vai al menu | Contatti | Accessibilità

logo del sistema bibliotecario dell'ateneo di padova

Delegà, Monica (2010) Espressione del recettore per il fattore di crescita insulino-simile di tipo 1(IGF1-R) in neuroni corticali primari durante l'invecchiamento e implicazioni nella malattia di Alzheimer. [Laurea vecchio ordinamento]

Full text disponibile come:

[img]
Anteprima
Documento PDF
9Mb

Abstract

Lo studio oggetto di questa tesi è stato quello di definire il meccanismo di regolazione di IGF1-R nei neuroni durante l’invecchiamento, allo scopo di fornire nuovi approcci farmacologici in grado di ritardare l’insorgenza della malattia.

Tipologia del documento:Laurea vecchio ordinamento
Corsi di Laurea vecchio ordinamento:Facoltà di Scienze MM. FF. NN. > CL Scienze Biologiche
Parole chiave:IGF1-R, Invecchiamento, Alzheimer, Astrociti, Neuroni
Settori scientifico-disciplinari del MIUR:Area 05 - Scienze biologiche > BIO/09 Fisiologia
Codice ID:24291
Relatore:Irato, Paole
Data della tesi:2010
Biblioteca:Polo di Scienze > CIS "A. Vallisneri" - Biblioteca Biologico Medica
Tipo di fruizione per il documento:on-line per i full-text
Tesi sperimentale (Si) o compilativa (No)?:

Bibliografia

I riferimenti della bibliografia possono essere cercati con Cerca la citazione di AIRE, copiando il titolo dell'articolo (o del libro) e la rivista (se presente) nei campi appositi di "Cerca la Citazione di AIRE".
Le url contenute in alcuni riferimenti sono raggiungibili cliccando sul link alla fine della citazione (Vai!) e tramite Google (Ricerca con Google). Il risultato dipende dalla formattazione della citazione e non da noi.

Holtzman DM. 2001. Role of apoE/Aβ interactions in the pathogenesis of Alzheimer’s disease and cerebral amyloid angiopathy. J Mol Neurosci. 17:147-155. Cerca con Google

Selkoe DJ. 2001. Alzheimer’s disease: genes, proteins, and therapy. Physiol Rev. 81:741-766. Cerca con Google

Muresan Z, and Muresan V. 2005. c-Jun NH2-terminal kinase-interacting protein-3 facilitates phosphorylation and controls localization of amyloidbeta precursor protein. J Neurosci. 25:3741-3751. Cerca con Google

Hardy J, and Selkoe DJ. 2002. The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics. Science. 297:353-356. Cerca con Google

Zlokovic BV. 2004. Clearing amyloid through the blood-brain barrier. J Neurochem. 89:807-811. Cerca con Google

Guenette SJ. 2003. Mechanisms of Abeta clearance and catabolism. Neuromolecular Med. 4:147-160. Cerca con Google

Tanzi RE, Moir RD, and Wagner SL. 2004. Clearance of Alzheimer’s Aβ peptide : the many roads to perdition. Neuron. 43:605-608. Cerca con Google

Glabe C. 2001. Intracellular mechanisms of amyloid accumulation and phatogenesis in Alzheimer’s disease. J Mol Neurosci. 17:137-145. Cerca con Google

Klein WL, Stine WB, and Teplow DB. 2004. Small assemblies of unmodified amyloid β-protein are the proximate neurotoxin in Alzheimer’s disease. Neurobiol Aging. 25:569-580. Cerca con Google

Lorenzo A, and Yankner BA. 1994. β-amyloid neurotoxicity requires fibril formation and is inhibited by congo red. Proc Natl Acad Sci U S A. 91:12243-12247. Cerca con Google

Koh JY, Yang LL, and Cotman CW. 1990. β-amyloid protein increases the vulnerability of cultured cortical neurons to excitotoxic damage. Brain Res. 533:315-320. Cerca con Google

Meda L, Cassatella MA, Szendrei GI, Otvo L Jr, Baron P, Villalba M, Ferari D, and Rossi F. 1995. Activation of microglia cells by β-amyloid protein and interferon-γ. Nature. 374:647-650. Cerca con Google

Della Bianca V, Dusi S, Bianchini E, Dal Pra I, and Rossi F. 1999. Βamyloid activates O2-forming NADPH oxidase in microglia, monocytes and neutrphils. A possibile inflammatory mechanism of neuronal damage in Alzheimer’s disease. J Biol Chem. 274: 15493-15499. Cerca con Google

Querfurth HW, MD, PhD, and La Ferla MD, PhD. 2010. Alzheimer’s disease. N Engl J Med. 362:329-344. Cerca con Google

Gong Y, Chang L, Viola KL, Lambert MP, Frinch CE, Krafft GA, and Klein WL. 2003. Alzheimer’s disease-affected brain: presence of oligomeric Aβ ligands (ADDLs) suggests a molecular basis for reversibile memory loss. Proc Natl Acad Sci U S A. 100:10417-10422. Cerca con Google

Walsh DM, Klyubin I, Fadeeva JV, Kulln WK, Anwyl R, wolfe MS, Rowan MJ, and Selkoe DJ. 2002. Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo. Nature. 416:535-539. Cerca con Google

Wang HW, Pasternak JF, Kuo H, Ristic H, Lambert MP, Chromy B, Viola KL, Klein WL, Stine WB, Krafft GA, and Trommer BL. 2002. Soluble oligomers of β-amyloid (1-42) inhibit long-term potentiation but not long-term depression in rat dentate gyrus. Brain Res. 924:133-140. Cerca con Google

Werner H, and Maor S. 2006. The insulin-like growth factor.1 receptor gene: a downstream target for oncogene and tumor suppressor action. Trends Endocrinol Metab. 17:236-242. Cerca con Google

Bondy CA, and Cheng CM. 2004. Signaling by insulin-like growth factor 1 in brain. Eur J Pharmacol. 490:25-31. Cerca con Google

Carro E, and Torres-Aleman I. 2004. The role of insulin and insulin like growth factor 1 in the molecular and cellular mechanism underlying the pathology of Alzheimer’s disease. Eur J Pharmacol. 490:127-133. Cerca con Google

Russo VC, Gluckman PD, Feldman EL, and Werther GA. 2005. The insulin-like growth factor system and its pleiotropic function in brain. Endocrine Reviews. 26(7):916-943. Cerca con Google

Carro L, Trejo JL, Gomez-Isla T, Le Roith D, and Torres-Aleman I. 2002. Serum insulin- like growth factor 1 regulates brain amyloid-β levels. Nature Med. 8(12):1390-1397. Cerca con Google

Gualco E, Wang JY, Del Valle L, Urbanska K, Peruzzi F, Khalili K, Amini S, and Reiss K. 2009. IGF-1R in neuroprotection and brain tumors. Biosci. 14:352-375. Cerca con Google

Federici M, Porzio O, Zucaro L, Fusco A, Borboni P, Lauro D, and Sesti G. 1997. Distributio of insulin/insulin-like growth factor-1 hybrid receptors in human tissues. Mol Cel Endocrinol. 129:121-126. Cerca con Google

Puglielli L. 2008. Aging of the brain, neurotrophin signaling, and Alzheimer’s disease: is IGF1-R the common culprit? Neurobiol Aging. 29:795-811. Cerca con Google

Lesort M, and Johnson GV. 2000. Insulin-like growth factor-1 and insulin mediate transient site-selective increases in tau phosphorylation in primary cortical neurons. Neuroscience. 99:305-316. Cerca con Google

Moloney AM, Griffin RJ, Timmons S, O’Connor R, Ravid R, and O’Neill C. 2008. Defects in IGF-1 receptor, insulin receptor and IRS-1/2 in Alzheimer’s disease indicate possible resistance to IGF-1 and insulin signaling. Neurobiol Aging. 31:224-243. Cerca con Google

Freude S, Schilbach K, and Schubert M. 2009. The role of IGF-1 receptor and insulin receptor signaling for the pathogenesis of Alzheimer’s disease: from model organism to human disease. Current Alzheimer Research. 1565:2050-2059. Cerca con Google

Cohen E, Paulsson JF, Blinder P, Burstyn-Cohen T, Du D, Estepa G, Adame A, Pham HM, Holzenberger M, Kelly JW, Masliah E, and Dilling A. 2009. Reduced IGF-1 Signaling Delays Age-Associated Proteotoxicity in Mice. Cell. 139:1157-1169. Cerca con Google

Longo VD, and Finch CE. 2003. Evolutionary medicine: from Dwarf model systems to healthy centenarians? Science. 299:1342-1346. Cerca con Google

Kenyon C. 2005. The plasticity of aging: insights from long-lived mutants. Cell. 120:449-460. Cerca con Google

Broughton S, and Partridge L. 2009. Insulin/IGF-like signalling, the central nervous system and aging. Biochem J. 418:1-12. Cerca con Google

Costantini C, Scrable H, and Puglielli L. 2006. An aging pathway controls the TrkA to p75NTR receptor switch and amyloid beta-peptide generation. EMBO J. 5:1997-2006. Cerca con Google

Costantini C, Weindruch R, Della Valle G, and Puglielli L. 2005. A TrkA-to-p75NTR molecular switch activates amyloid beta-peptide generation during aging. Biochem J. 391:59-67. Cerca con Google

Saura J, Tusell JM, and Serratosa J. 2003. Haigh-yield isolation of murine microglia by mild trypsinization. Glia. 44:183-189. Cerca con Google

Burgess SK, Jacobs S, Cuatrecasas P, and Sahyoum N. 1987. Caracterization of a neuronal subtype of insulin-like growth factor 1 receptor. J Biol Chem. 262:1618-1622. Cerca con Google

Araque A. 2006. Astrocyte-neuron signaling in the brain implication for disease. Curr Opin Investig Drugs. 7:619-624. Cerca con Google

Bondy CA, and Cheng CM. 2004. Signaling by insulin-like growth factor 1 in brain. Eur J Pharmacol. 490:25-31. Cerca con Google

Chesik D, De Keyser J, and Wilczak N. 2004. Involvement of insulin-like growth factor binding protein-2 in activated microglia as assessed in post mortem human brain. Neurosci Lett. 362:14-16. Cerca con Google

Zeger M, Popken G, Zhang J, Xuan S, Lu QR, Schwab MH, Nave KA, Rowitch D, D’Eercole AJ, and Ye P. 2007. Insulin-like growth factor type 1 receptor signaling in the cells of oligodendrocyte lineage is required for normal in vivo oligodendrocyte development and myelination. Glia. 55:400-411. Cerca con Google

Mendez P, Wandosell F, and Garcia-Segura LM. 2006. Cross-talk between estrogen receptors and insulin-like growth factor-1 receptor in the brain: cellular and molecular mechanism. Front Neuroendocrinol. 27:391-403. Cerca con Google

Quesada A, and Romeo HE, Micevych P. 2007. Distribution of localization patterns of estrogens receptor-beta and insulin-like growth factor-1 receptors in neurons snd glial cells of the female rat substantia nigra: localization of Erbeta and IGF1-R in substantia nigra. J Comp Neurol. 503:198-208. Cerca con Google

Gomes FC, Spohr TC, Martinez R, and Moura Neto V. 2001. Cross-talk between neuron and glia: highlights on soluble factors. Braz J Med Biol Res. 34:611-620. Cerca con Google

Wilhelmsson U, Bushong EA, Price DL, Smarr BL, Phung V, Terada M, Ellisman MH, and Pekny M. 2006. Redefining the concept of reactive astrcyts as cells that remain within their unique domains upon reaction to injury. Proc Natl Acad Sci U S A. 103:17513-17518. Cerca con Google

Blasco I, Stampfer-Kountchev M, Robatscher P, Veerhuis R, Eikelenboom P, and Grubeck-Loebenstein B. 2004. How chronic inflammation can affect the brain and support the development of Alzheimer disease in old age: the role of microglia and astrocytes. Aging Cell. 3:169-176. Cerca con Google

Cotrina ML, and Nedergaard M. 2002. Astrocytes in the aging brain. J Neurosci Res. 67:1-10. Cerca con Google

Hayakawa N, Kato H, and Araki T. 2007. Age-related changes of astrocytes, oligodendrocytes and microglia in the mouse hippocampal CA1 sector. Mech Ageing Dev. 128:311-316. Cerca con Google

Godbout JP, and Johnson RW. 2006. Age and neuroinflammation: a lifetime of psychoneuroimmune consequences. Neurol Clin. 24:521-538. Cerca con Google

Yankner BA, Lu T, and Loerch P. 2008. The aging brain. Annu Rev Pathol. 3:41-66. Cerca con Google

Farina C, Aloisi F, and Meinl E. 2007. Astrocytes are active players in cerebral innate immunità. Trends Immunol. 28:138-145. Cerca con Google

Steven B. 2008. Neuron-astrocyte signaling in the development and plasticity of neural circuits. Neurosignals. 16:278-88. Cerca con Google

Di Giorgio FP, Carrasco MA, Siao MC, Maniatis T, and Eggan K. 2007. Non-cell autonomous effect foglia on motor neurons in an embryonic stem cell-based ALS model. Nat Neurosci. 10:608-614. Cerca con Google

Nagai M, Re DB, Nagata T, Chalazonitis A, Jessel TM, Wichterle H, and Przedborski S. 2007. Astrcytes expressing ALS-linked mutated SOD1 release factors selectively toxic to motor neurons. Nat Neurosci. 10:615-622. Cerca con Google

Solo per lo Staff dell Archivio: Modifica questo record