Seladin-1 transcription is linked to neuronal degeneration in Alzheimer’s disease
Section snippets
Human post-mortem material
Post-mortem samples (Kuopio Brain Bank) obtained since 1991 were evaluated. This study is part of the project focusing on risk genes of AD that has been approved by the local ethical committee, and the use of tissue by the Office of Legal Health Care Affairs. The patients had been clinically assessed by neurologists and the diagnosis of AD was based on the NINCDS-ADRDA (McKhann et al., 1984) and diagnosis of other dementias on the DSM-III-R criteria (American Psychiatric Association, 1987) (
Seladin-1 transcription in human brain tissue
Differential transcription of seladin-1 in temporal and occipital cortical post-mortem brain samples of demented and non-demented subjects was studied using the semi-quantitative RT-PCR method (Fig. 1A). The relative transcription of seladin-1 in human temporal cortex was highly correlated with the transcription in occipital cortex (R=0.767; P<0.001). Thus, to detect averaged differences between these two cortices, we used the ratio of seladin-1 transcription in temporal versus occipital cortex
Discussion
We studied the relative transcription of seladin-1 in temporal and occipital cortices in demented and non-demented subjects using a semi-quantitative RT-PCR method. We found a decrease in the transcription of seladin-1 in temporal cortex when compared to occipital cortex in AD. The seladin-1 transcription was linked with the hallmark lesions of AD, NPs and NFTs whereas no linkage was found between seladin-1 transcription and Aβ. In addition, we investigated the changes in seladin-1
Acknowledgements
The authors thank Marjo Heikkinen, Petra Mäkinen, Tarja Kauppinen, Heikki Luukkonen and Hannu Tiainen for their excellent technical help. The study was supported by the Health Research Council of the Academy of Finland, EVO Grants (5142, 5152 and 5510) of Kuopio University Hospital and the EU 5th Framework Programme (QLK6-CT-1999-02112).
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