Inflammation and α-Synuclein's Prion-like Behavior in Parkinson's Disease-Is There a Link?

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Inflammation and α-Synuclein's Prion-like Behavior in Parkinson's Disease-Is There a Link? / Lema Tomé, Carla; Tyson, Trevor; Rey, Nolwen; Grathwohl, Stefan; Britschgi, Markus; Brundin, Patrik.

I: Molecular Neurobiology, Vol. 47, Nr. 2, 2013, s. 561-574.

Forskningsoutput: TidskriftsbidragÖversiktsartikel

Harvard

Lema Tomé, C, Tyson, T, Rey, N, Grathwohl, S, Britschgi, M & Brundin, P 2013, 'Inflammation and α-Synuclein's Prion-like Behavior in Parkinson's Disease-Is There a Link?', Molecular Neurobiology, vol. 47, nr. 2, s. 561-574. https://doi.org/10.1007/s12035-012-8267-8

APA

Lema Tomé, C., Tyson, T., Rey, N., Grathwohl, S., Britschgi, M., & Brundin, P. (2013). Inflammation and α-Synuclein's Prion-like Behavior in Parkinson's Disease-Is There a Link? Molecular Neurobiology, 47(2), 561-574. https://doi.org/10.1007/s12035-012-8267-8

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MLA

Vancouver

Author

Lema Tomé, Carla ; Tyson, Trevor ; Rey, Nolwen ; Grathwohl, Stefan ; Britschgi, Markus ; Brundin, Patrik. / Inflammation and α-Synuclein's Prion-like Behavior in Parkinson's Disease-Is There a Link?. I: Molecular Neurobiology. 2013 ; Vol. 47, Nr. 2. s. 561-574.

RIS

TY - JOUR

T1 - Inflammation and α-Synuclein's Prion-like Behavior in Parkinson's Disease-Is There a Link?

AU - Lema Tomé, Carla

AU - Tyson, Trevor

AU - Rey, Nolwen

AU - Grathwohl, Stefan

AU - Britschgi, Markus

AU - Brundin, Patrik

N1 - The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Neuronal Survival (013212041)

PY - 2013

Y1 - 2013

N2 - Parkinson's disease patients exhibit progressive spreading of aggregated α-synuclein in the nervous system. This slow process follows a specific pattern in an inflamed tissue environment. Recent research suggests that prion-like mechanisms contribute to the propagation of α-synuclein pathology. Little is known about factors that might affect the prion-like behavior of misfolded α-synuclein. In this review, we suggest that neuroinflammation plays an important role. We discuss causes of inflammation in the olfactory bulb and gastrointestinal tract and how this may promote the initial misfolding and aggregation of α-synuclein, which might set in motion events that lead to Parkinson's disease neuropathology. We propose that neuroinflammation promotes the prion-like behavior of α-synuclein and that novel anti-inflammatory therapies targeting this mechanism could slow disease progression.

AB - Parkinson's disease patients exhibit progressive spreading of aggregated α-synuclein in the nervous system. This slow process follows a specific pattern in an inflamed tissue environment. Recent research suggests that prion-like mechanisms contribute to the propagation of α-synuclein pathology. Little is known about factors that might affect the prion-like behavior of misfolded α-synuclein. In this review, we suggest that neuroinflammation plays an important role. We discuss causes of inflammation in the olfactory bulb and gastrointestinal tract and how this may promote the initial misfolding and aggregation of α-synuclein, which might set in motion events that lead to Parkinson's disease neuropathology. We propose that neuroinflammation promotes the prion-like behavior of α-synuclein and that novel anti-inflammatory therapies targeting this mechanism could slow disease progression.

U2 - 10.1007/s12035-012-8267-8

DO - 10.1007/s12035-012-8267-8

M3 - Review article

C2 - 22544647

VL - 47

SP - 561

EP - 574

JO - Molecular Neurobiology

JF - Molecular Neurobiology

SN - 1559-1182

IS - 2

ER -