Protein aggregation in Parkinson’s disease
V. Gundersen,
V. Gundersen
Department of Anatomy and the CMBN, University of Oslo, Oslo, Norway; Department of Neurology, Oslo University Hospital, Rikshospitalet, Oslo, Norway
Search for more papers by this authorV. Gundersen,
V. Gundersen
Department of Anatomy and the CMBN, University of Oslo, Oslo, Norway; Department of Neurology, Oslo University Hospital, Rikshospitalet, Oslo, Norway
Search for more papers by this authorVidar Gundersen, Department of Anatomy and the CMBN, University of Oslo, Oslo, Norway; Department of Neurology, Oslo University Hospital, Rikshospitalet, Oslo, Norway Tel.: +47 22 85 14 96Fax: +47 22 85 12 78e-mail: [email protected]
Conflicts of interest: none.
Abstract
Gundersen V. Protein aggregation in Parkinson’s disease. Acta Neurol Scand: 2010: 122 (Suppl. 190): 82–87. © 2010 John Wiley & Sons A/S.
Parkinson’s disease (PD) is a primary neurodegenerative movement disorder. In most cases it occurs as a sporadic type of disease, but there are also rare familial forms. Pathologically Parkinson’s disease is characterized by loss of dopaminergic neurons in the compact part of substantia nigra. As a part of the neurodegenerative process protein aggregates will accumulate as Lewy bodies in dopaminergic neurons (1). In addition, non-dopaminergic neurons are known to be affected in Parkinsons’s disease, for example, in several brain stem nuclei and the olfactoric bulb (2–4). The pathogenic process underlying the death of dopaminergic neurons is far from fully understood. Along with mitochondrial dysfunction, excitotoxicity, neuroinflammation and oxidative stress (5–8), recent evidence indicates that accumulation of protein filaments in Lewy bodies actively takes part in the degeneration of neurons. This will be further discussed below.
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