LEADER 04236nam 2200493 450 001 9910688240803321 005 20231214145408.0 035 $a(CKB)3710000000631111 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/54519 035 $a(EXLCZ)993710000000631111 100 $a20160411d2016 c0 0 101 0 $aeng 135 $aur||#---uu||| 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 00$aNeuronal self-defense $ecompensatory mechanisms in neurodegenerative disorders /$fedited by: Rosanna Parlato and Pier Giorgio Mastroberardino 210 $cFrontiers Media SA$d2016 210 1$a[Lausanne, Switzerland] :$cFrontiers Media SA,$d2016. 210 4$d©2016 215 $a1 online resource (190 pages) $cillustrations; digital file(s) 225 1 $aFrontiers Research Topics 225 0 $aFrontiers in Cellular Neuroscience. 311 $a2-88919-759-X 320 $aIncludes bibliographical references. 330 3 $aNeurodegenerative disorders are characterized by the progressive loss of specific populations of neurons with consequent deterioration of brain?s function and dramatic impact on human behavior. At present, there are no effective cures for neurodegenerative diseases. Because unambiguous diagnosis is possible only after manifestation of symptoms, when a large proportion of neurons has been already lost, therapies are necessarily confined to alleviation of symptoms. Development of cures halting the disease course is hampered by our rudimentary understanding of the etiopathology. Most neurodegenerative disorders are sporadic and age-related and - even for those of known genetic origin - the mechanisms influencing disease onset and progression have not been fully characterized. The different diseases, however, share important similarities in the mechanisms responsible for neuronal loss, which is caused by a combination of endogenous and exogenous challenges. Trophic deprivation, oxidative stress, accumulation of abnormal protein aggregates, and bioenergetics defects have been described in most, if not all, neurodegenerative disease.To counterbalance these noxious stimuli cells deploy, at least during the initial pathogenic states, intrinsic neuroprotective responses. These are general compensatory mechanisms, common to several neurodegenerative conditions, which reprogram cellular physiology to overcome stress. Adaptation includes strategies to optimize energetic resources, for instance reduction of rRNA synthesis to repress translation, suppression of transcription, and bioenergetics and metabolic redesign. Additional mechanisms include potentiation of antioxidant capacity, induction of endoplasmic reticulum (ER) stress, and activation of protein quality control systems and autophagy. Ineffective execution of these compensatory strategies severely threatens cellular homeostasis and favors onset of pathology. Therefore, a better understanding of these ?buffering? mechanisms and of their interconnections may help to devise more effective therapeutic tools to prolong neuronal survival and activity, independently of the original genetic mutations and stress insults.This Research Topic focuses on the initial compensatory responses protecting against failure of those mechanisms that sustaining neuronal survival and activity. The collection intends to summarize the state-of-the-art in this field and to propose novel research contributes, with the ultimate goal of inspiring novel studies aimed to contrast progression of neurodegenerative diseases. 410 0$aFrontiers research topics. 606 $aNervous system$xDegeneration$xResearch 606 $aNeuropsychiatry 610 $amodels 610 $astress response 610 $aCompensation 610 $amechanisms 610 $atran 610 $aNeurodegenerative disorders 615 0$aNervous system$xDegeneration$xResearch. 615 0$aNeuropsychiatry. 702 $aParlato$b Rosanna 702 $aMastroberardino$b Pier Giorgio 712 02$aFrontiers Research Foundation, 906 $aBOOK 912 $a9910688240803321 996 $aNeuronal self-defense$93122485 997 $aUNINA LEADER 01764nas 2200397 n 450 001 990008951090403321 005 20240229084445.0 011 $a1720-4453 035 $a000895109 035 $aFED01000895109 035 $a(Aleph)000895109FED01 035 $a000895109 091 $2CNR$aP 00151331 100 $a20090724a19949999km-y0itaa50------ba 101 0 $aita 102 $aIT 110 $aauu-------- 200 1 $a<>Diritto industriale 207 1$a1994-2016 210 $aMilano$cIPSOA 326 $aBimestrale 452 0$12001$a<>Diritto industriale 452 0$12001$a<>Diritto industriale$eMarchi, brevetti, diritto d'autore, pubblicità, concorrenza e antitrust [banca dati su cd-rom] 530 0 $a<>Diritto industriale 675 $a351.82 712 02$aIstituto post-universitario per lo studio dell'organizzazione aziendale 801 0$aIT$bACNP$c20090723 859 4 $uhttp://acnp.cib.unibo.it/cgi-ser/start/it/cnr/dc-p1.tcl?catno=1092433&person=false&language=ITALIANO&libr=&libr_th=unina1$zBiblioteche che possiedono il periodico 901 $aSE 912 $a990008951090403321 958 $aBiblioteca Centrale della Facoltà di Giurisprudenza dell'Università di Napoli Federico II$b1994-2016.$ePer. it. 140$fFGBC 959 $aFGBC 996 $aDiritto industriale$960244 997 $aUNINA AP1 8 $6866-01$aNA073 Biblioteca Centrale della Facoltà di Giurisprudenza dell'Università di Napoli Federico II$bPer. it. 140$eCorso Umberto I, 80138 Napoli (NA)$m0812537531/33$m0812537532$nit AP2 40$aacnp.cib.unibo.it$nACNP Italian Union Catalogue of Serials$uhttp://acnp.cib.unibo.it/cgi-ser/start/it/cnr/df-p.tcl?catno=1092433&language=ITALIANO&libr=&person=&B=1&libr_th=unina&proposto=NO