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001007799 1001_ $$00000-0001-5443-8540$$aKuzkina, A.$$b0$$eCorresponding author
001007799 245__ $$aCombining skin and olfactory α-synuclein seed amplification assays (SAA)—towards biomarker-driven phenotyping in synucleinopathies
001007799 260__ $$aLondon [u.a.]$$bNature Publ. Group$$c2023
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001007799 520__ $$aSeed amplification assays (SAA) are becoming commonly used in synucleinopathies to detect α-synuclein aggregates. Studies in Parkinson's disease (PD) and isolated REM-sleep behavior disorder (iRBD) have shown a considerably lower sensitivity in the olfactory epithelium than in CSF or skin. To get an insight into α-synuclein (α-syn) distribution within the nervous system and reasons for low sensitivity, we compared SAA assessment of nasal brushings and skin biopsies in PD (n = 27) and iRBD patients (n = 18) and unaffected controls (n = 30). α-syn misfolding was overall found less commonly in the olfactory epithelium than in the skin, which could be partially explained by the nasal brushing matrix exerting an inhibitory effect on aggregation. Importantly, the α-syn distribution was not uniform: there was a higher deposition of misfolded α-syn across all sampled tissues in the iRBD cohort compared to PD (supporting the notion of RBD as a marker of a more malignant subtype of synucleinopathy) and in a subgroup of PD patients, misfolded α-syn was detectable only in the olfactory epithelium, suggestive of the recently proposed brain-first PD subtype. Assaying α-syn of diverse origins, such as olfactory (part of the central nervous system) and skin (peripheral nervous system), could increase diagnostic accuracy and allow better stratification of patients.
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001007799 7001_ $$0P:(DE-HGF)0$$aRößle, J.$$b1
001007799 7001_ $$0P:(DE-Juel1)184882$$aSeger, A.$$b2
001007799 7001_ $$0P:(DE-HGF)0$$aPanzer, C.$$b3
001007799 7001_ $$0P:(DE-Juel1)142225$$aKohl, A.$$b4
001007799 7001_ $$0P:(DE-HGF)0$$aMaltese, V.$$b5
001007799 7001_ $$0P:(DE-HGF)0$$aMusacchio, T.$$b6
001007799 7001_ $$0P:(DE-Juel1)186027$$aBlaschke, S. J.$$b7
001007799 7001_ $$0P:(DE-Juel1)177986$$aTamgüney, G.$$b8
001007799 7001_ $$0P:(DE-HGF)0$$aKaulitz, S.$$b9
001007799 7001_ $$00000-0003-2109-3536$$aRak, K.$$b10
001007799 7001_ $$0P:(DE-HGF)0$$aScherzad, A.$$b11
001007799 7001_ $$0P:(DE-HGF)0$$aZimmermann, P. H.$$b12
001007799 7001_ $$0P:(DE-HGF)0$$aKlussmann, J. P.$$b13
001007799 7001_ $$0P:(DE-HGF)0$$aHackenberg, S.$$b14
001007799 7001_ $$0P:(DE-HGF)0$$aVolkmann, J.$$b15
001007799 7001_ $$aSommer, C.$$b16
001007799 7001_ $$0P:(DE-Juel1)179044$$aSommerauer, Michael$$b17
001007799 7001_ $$0P:(DE-HGF)0$$aDoppler, K.$$b18$$eCorresponding author
001007799 773__ $$0PERI:(DE-600)2819218-7$$a10.1038/s41531-023-00519-8$$gVol. 9, no. 1, p. 79$$n1$$p79$$tnpj Parkinson's Disease$$v9$$x2373-8057$$y2023
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