Alpha- and beta-synuclein expression in Parkinson disease with and without dementia

Katrin Beyer, Lourdes Ispierto, Pilar Latorre, Eduardo Tolosa, Aurelio Ariza

Research output: Contribution to journalArticleResearchpeer-review

18 Citations (Scopus)

Abstract

Parkinson disease (PD) is the most important movement disorder and about 50% of patients develop dementia over the time. PD belongs to the group of Lewy body disorders. Alpha-synuclein (AS) is the main component of Lewy bodies and its aggregation is a key event in the pathogenesis of PD. Beta-synuclein (BS) inhibits AS aggregation in vitro and in vivo and has been shown to interact directly with AS regulating its functionality and preventing its oligomerization. Recently, we have described a molecular subgroup of DLB characterized by the drastic BS reduction in cortical areas. In this study we have analyzed the expression of two BS transcripts and the main AS transcript SNCA140, in frozen samples of three brain areas, temporal cortex, caudate nucleus and pons, from patients with PD and PDD in comparison with controls. Relative mRNA expression was determined by real-time PCR with SybrGreen, neuron-specific-enolase as housekeeping gene and the deltadeltaCt method. The most important difference in BS and AS mRNA expression between PD and PDD was found in the caudate nucleus, where BS mRNA was overexpressed in PD and AS mRNA diminished in PDD. Our findings provide new insights into the pathogenesis of dementia in PD, indicating that differential BS and AS expression in the caudate nucleus may represent one of the molecular mechanisms involved in these complex diseases. © 2011 Elsevier B.V.
Original languageEnglish
Pages (from-to)112-117
JournalJournal of the Neurological Sciences
Volume310
Issue number1-2
DOIs
Publication statusPublished - 15 Nov 2011

Keywords

  • Alpha-synuclein
  • Beta-synuclein
  • Differential isoform expression
  • mRNA expression
  • Parkinson disease
  • Parkinson disease dementia

Fingerprint Dive into the research topics of 'Alpha- and beta-synuclein expression in Parkinson disease with and without dementia'. Together they form a unique fingerprint.

Cite this