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P Raeymaekers

Researcher at University of Antwerp

Publications -  33
Citations -  1413

P Raeymaekers is an academic researcher from University of Antwerp. The author has contributed to research in topics: Genetic linkage & Gene mapping. The author has an hindex of 17, co-authored 33 publications receiving 1393 citations.

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Duplication in chromosome 17p11.2 in Charcot-Marie-Tooth neuropathy type 1a (CMT 1a). The HMSN Collaborative Research Group.

TL;DR: It is proposed that the duplication in 17p11.2 itself is the disease causing mutation in all the HMSN I families analyzed, and different allelic combinations were found segregating with the duplicates in different families linkage disequilibrium was not a significant factor.
Journal ArticleDOI

Estimation of the size of the chromosome 17p11.2 duplication in Charcot-Marie-Tooth neuropathy type 1a (CMT1a). HMSN Collaborative Research Group.

TL;DR: The discrepancy between the genetic and physical map distances suggests that the 17p11.2-p12.2 region is extremely prone to recombinational events and may be a contributing factor to the genetic instability of this chromosomal region.
Journal ArticleDOI

Association analysis of the 5-HT2c receptor and 5-HT transporter genes in bipolar disorder

TL;DR: Results suggest that variations in these genes may be responsible for a minor increase in susceptibility for bipolar disorder in women.
Journal Article

Localization of the mutation in an extended family with Charcot-Marie-Tooth neuropathy (HMSN I).

TL;DR: This work extensively analyzed a multi-generation Charcot-Marie-Tooth family by using molecular genetic techniques in order to localize the CMT gene defect and found that the mutation is most likely located on the chromosome 17p arm, distal of D17S71.
Journal Article

CAG repeat expansions in bipolar and unipolar disorders.

TL;DR: The findings of anticipation in BP disorders and in UPR must be interpreted with caution because of the possible presence of numerous ascertainment biases, but they support the hypothesis that pathological TREs are implicated in the transmission of thesemore disorders.