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  •   University of Thessaly Institutional Repository
  • Επιστημονικές Δημοσιεύσεις Μελών ΠΘ (ΕΔΠΘ)
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  •   University of Thessaly Institutional Repository
  • Επιστημονικές Δημοσιεύσεις Μελών ΠΘ (ΕΔΠΘ)
  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ.
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Autoantibodies to alpha-synuclein in inherited Parkinson's disease

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Author
Papachroni, K. K.; Ninkina, N.; Papapanagiotou, A.; Hadjigeorgiou, G. M.; Xiromerisiou, G.; Papadimitriou, A.; Kalofoutis, A.; Buchman, V. L.
Date
2007
DOI
10.1111/j.1471-4159.2006.04365.x
Keyword
alpha-synuclein
autoantibody
Parkinson's disease
CENTRAL-NERVOUS-SYSTEM
MOUSE MODEL
DOPAMINERGIC-NEURONS
T-CELLS
IMMUNIZATION
EXPRESSION
ALZHEIMERS
PROTEIN
PERSYN
Biochemistry & Molecular Biology
Neurosciences
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Abstract
Neurodegeneration in Parkinson's disease (PD) is accompanied by a local immune reaction in the affected brain regions. It is well established that alpha-synuclein is directly implicated in the pathogenesis of PD. Development of the disease is often associated with changes of expression and cellular compartmentalisation of this protein; moreover, its oligomers or protofibrils are often released to the CSF and plasma of patients. Aggregated alpha-synuclein can trigger the activation of microglia; however, its capacity to induce production of specific autoantibodies (AAb) has not been assessed. In this study, we examined the presence of AAb against synuclein family members in the peripheral blood serum of PD patients and control individuals. Presence of AAb against beta-synuclein or gamma-synuclein showed no association with PD. Multi-epitopic AAb against alpha-synuclein were detected in 65% of all patients tested and their presence strongly correlated with an inherited mode of the disease but not with other disease-related factors. The frequency of the presence of AAb in the studied group of patients with sporadic form of PD was not significantly different from the frequency in the control group but very high proportion (90%) of patients with familial form of the disease were positive for AAb against alpha-synuclein. We hypothesise that these AAb could be involved in pathogenesis of the inherited form of PD.
URI
http://hdl.handle.net/11615/31639
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  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ. [9728]
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ΕΣΠΑ 2007-2013
 

 

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Η δικτυακή πύλη της Ευρωπαϊκής Ένωσης
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ΕΣΠΑ 2007-2013