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000163370 037__ $$aDZNE-2022-00133
000163370 041__ $$aGerman
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000163370 1001_ $$0P:(DE-2719)2811659$$aLevin, Johannes$$b0$$eFirst author$$udzne
000163370 245__ $$aNeuroprotektive Therapien bei idiopathischen, genetischen und atypischen Parkinson-Syndromen mit α-Synuklein – Pathologie.
000163370 260__ $$aHeidelberg$$bSpringer$$c2021
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000163370 520__ $$aThe key aspect of the classification of neurodegenerative diseases is the histopathological detection of certain proteins in the brain. The various disease entities are distinguished with respect to the type of detected protein and with respect to the configuration and localization of the corresponding protein aggregates. Aggregates of alpha-synuclein (ASYN) are the defining hallmark of several neurodegenerative disorders termed synucleinopathies. The most well-known diseases in this spectrum are Parkinson's disease (PD) with neuronal detection of Lewy bodies, dementia with Lewy bodies (DLB), with additional detection of beta-amyloid and multiple system atrophy (MSA), where ASYN aggregates are found in glia cells in the form of Papp-Lantos inclusions. ASYN has been identified as a key target for the development of therapeutic approaches to synucleinopathies given its central role in the pathophysiology of these diseases. Current treatment strategies can be roughly classified into six groups: 1) lowering ASYN expression (antisense therapy), 2) inhibition of formation of toxic ASYN aggregates (aggregation inhibitors, chelators), 3) dissolving or removal of intracellular or extracellular toxic AYSN aggregates (active and passive immunotherapy, aggregation inhibitors), 4) enhancement of cellular clearance mechanisms (autophagy, lysosomal microphagy) for removal of toxic forms of alpha-synuclein, 5) modulation of neuroinflammatory processes and 6) neuroprotective strategies. This article summarizes the current therapeutic approaches and sheds light on promising future treatment approaches.
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000163370 650_7 $$2Other$$aDisease-modifying drugs
000163370 650_7 $$2Other$$aLewy body dementia
000163370 650_7 $$2Other$$aMultiple system atrophy
000163370 650_7 $$2Other$$aParkinson’s disease
000163370 650_7 $$2Other$$aSynucleinopathies
000163370 650_7 $$2NLM Chemicals$$aalpha-Synuclein
000163370 650_2 $$2MeSH$$aHumans
000163370 650_2 $$2MeSH$$aNeurodegenerative Diseases: diagnosis
000163370 650_2 $$2MeSH$$aNeurodegenerative Diseases: genetics
000163370 650_2 $$2MeSH$$aNeurodegenerative Diseases: therapy
000163370 650_2 $$2MeSH$$aNeurons
000163370 650_2 $$2MeSH$$aParkinson Disease: diagnosis
000163370 650_2 $$2MeSH$$aParkinson Disease: genetics
000163370 650_2 $$2MeSH$$aParkinson Disease: therapy
000163370 650_2 $$2MeSH$$aSynucleinopathies
000163370 650_2 $$2MeSH$$aalpha-Synuclein: genetics
000163370 7001_ $$aNübling, Georg$$b1
000163370 7001_ $$0P:(DE-2719)9000906$$aGiese, Armin$$b2$$udzne
000163370 7001_ $$aJanzen, Annette$$b3
000163370 7001_ $$0P:(DE-2719)9000908$$aOertel, Wolfgang H$$b4$$udzne
000163370 773__ $$0PERI:(DE-600)1462945-8$$a10.1007/s00115-021-01220-y$$gVol. 92, no. 12, p. 1249 - 1259$$n12$$p1249 - 1259$$tDer Nervenarzt$$v92$$x1433-0407$$y2021
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