000169044 001__ 169044
000169044 005__ 20250127111029.0
000169044 0247_ $$2ISSN$$a1545-5343
000169044 0247_ $$2pmc$$apmc:PMC10119350
000169044 0247_ $$2doi$$a10.1007/s13311-022-01332-6
000169044 0247_ $$2pmid$$apmid:36512255
000169044 0247_ $$2ISSN$$a1933-7213
000169044 0247_ $$2ISSN$$a1878-7479
000169044 0247_ $$2altmetric$$aaltmetric:140247020
000169044 0247_ $$2ISSN$$a1545-5351
000169044 037__ $$aDZNE-2022-01766
000169044 041__ $$aEnglish
000169044 082__ $$a610
000169044 1001_ $$0P:(DE-2719)9001609$$aPinto-Costa, Rita$$b0$$eFirst author$$udzne
000169044 245__ $$aOverexpression-Induced α-Synuclein Brain Spreading.
000169044 260__ $$aNew York, NY$$bSpringer$$c2023
000169044 3367_ $$2DRIVER$$aarticle
000169044 3367_ $$2DataCite$$aOutput Types/Journal article
000169044 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1683032127_12618$$xReview Article
000169044 3367_ $$2BibTeX$$aARTICLE
000169044 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000169044 3367_ $$00$$2EndNote$$aJournal Article
000169044 520__ $$aInterneuronal transfer of pathological α-synuclein species is thought to play an important role in the progressive advancement of Lewy pathology and increasing severity of clinical manifestations in Parkinson's and other diseases commonly referred to as synucleinopathies. Pathophysiological conditions and mechanisms triggering this trans-synaptic spreading bear therefore significant pathogenetic implications but have yet to be fully elucidated. In vivo experimental models support the conclusion that increased expression of intraneuronal α-synuclein can itself induce protein spreading throughout the brain as well as from the brain to peripheral tissues. For example, overexpression of α-synuclein targeted to the rodent dorsal medulla oblongata results in its transfer and accumulation into recipient axons innervating this brain region; through these axons, α-synuclein can then travel caudo-rostrally and reach other brain sites in the pons, midbrain, and forebrain. When protein overexpression is induced in the rodent midbrain, long-distance α-synuclein spreading can be followed over time; spreading-induced α-synuclein accumulation affects lower brain regions, including the dorsal motor nucleus of the vagus, proceeds through efferent axons of the vagus nerve, and is ultimately detected within vagal motor nerve endings in the gastric wall. As discussed in this review, animal models featuring α-synuclein overexpression not only support a relationship between α-synuclein burden and protein spreading but have also provided important clues on conditions/mechanisms capable of promoting interneuronal α-synuclein transfer. Intriguing findings include the relationship between neuronal activity and protein spreading and the role of oxidant stress in trans-synaptic α-synuclein mobility.
000169044 536__ $$0G:(DE-HGF)POF4-352$$a352 - Disease Mechanisms (POF4-352)$$cPOF4-352$$fPOF IV$$x0
000169044 588__ $$aDataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
000169044 650_2 $$2MeSH$$aAnimals
000169044 650_2 $$2MeSH$$aalpha-Synuclein: metabolism
000169044 650_2 $$2MeSH$$aBrain: metabolism
000169044 650_2 $$2MeSH$$aNeurons: metabolism
000169044 650_2 $$2MeSH$$aParkinson Disease: metabolism
000169044 650_2 $$2MeSH$$aStomach: innervation
000169044 650_2 $$2MeSH$$aStomach: metabolism
000169044 650_2 $$2MeSH$$aSynaptic Transmission: physiology
000169044 650_2 $$2MeSH$$aSynucleinopathies: metabolism
000169044 650_2 $$2MeSH$$aVagus Nerve: metabolism
000169044 650_2 $$2MeSH$$aVagus Nerve: physiology
000169044 650_7 $$2NLM Chemicals$$aalpha-Synuclein
000169044 650_7 $$2Other$$aAnimal models
000169044 650_7 $$2Other$$aGut-brain axis
000169044 650_7 $$2Other$$aNeuronal activity
000169044 650_7 $$2Other$$aOxidative stress
000169044 650_7 $$2Other$$aParkinson
000169044 650_7 $$2Other$$aVagus nerve
000169044 7001_ $$0P:(DE-2719)9001593$$aHarbachova, Eugenia$$b1$$udzne
000169044 7001_ $$0P:(DE-2719)9001592$$aLa Vitola, Pietro$$b2$$udzne
000169044 7001_ $$0P:(DE-2719)2481741$$aDi Monte, Donato Antonio$$b3$$eLast author$$udzne
000169044 773__ $$0PERI:(DE-600)2279496-7$$a10.1007/s13311-022-01332-6$$n1$$p83-96$$tNeurotherapeutics$$v20$$x1933-7213$$y2023
000169044 8564_ $$uhttps://pub.dzne.de/record/169044/files/DZNE-2022-01766.pdf$$yOpenAccess
000169044 8564_ $$uhttps://pub.dzne.de/record/169044/files/DZNE-2022-01766.pdf?subformat=pdfa$$xpdfa$$yOpenAccess
000169044 909CO $$ooai:pub.dzne.de:169044$$pdnbdelivery$$pdriver$$pVDB$$popen_access$$popenaire
000169044 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9001609$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b0$$kDZNE
000169044 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9001593$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b1$$kDZNE
000169044 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9001592$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b2$$kDZNE
000169044 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2481741$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b3$$kDZNE
000169044 9131_ $$0G:(DE-HGF)POF4-352$$1G:(DE-HGF)POF4-350$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lNeurodegenerative Diseases$$vDisease Mechanisms$$x0
000169044 9141_ $$y2022
000169044 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2022-11-08
000169044 915__ $$0LIC:(DE-HGF)CCBY4$$2HGFVOC$$aCreative Commons Attribution CC BY 4.0
000169044 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2022-11-08
000169044 915__ $$0StatID:(DE-HGF)3002$$2StatID$$aDEAL Springer$$d2022-11-08$$wger
000169044 915__ $$0StatID:(DE-HGF)0510$$2StatID$$aOpenAccess
000169044 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2023-10-25
000169044 915__ $$0StatID:(DE-HGF)0320$$2StatID$$aDBCoverage$$bPubMed Central$$d2023-10-25
000169044 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2023-10-25
000169044 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2023-10-25
000169044 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences$$d2023-10-25
000169044 915__ $$0StatID:(DE-HGF)1110$$2StatID$$aDBCoverage$$bCurrent Contents - Clinical Medicine$$d2023-10-25
000169044 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bNEUROTHERAPEUTICS : 2022$$d2023-10-25
000169044 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2023-10-25
000169044 915__ $$0StatID:(DE-HGF)9905$$2StatID$$aIF >= 5$$bNEUROTHERAPEUTICS : 2022$$d2023-10-25
000169044 9201_ $$0I:(DE-2719)1013008$$kAG Di Monte$$lNeurodegeneration and Neuroprotection in Parkinson´s Disease$$x0
000169044 980__ $$ajournal
000169044 980__ $$aVDB
000169044 980__ $$aI:(DE-2719)1013008
000169044 980__ $$aUNRESTRICTED
000169044 9801_ $$aFullTexts