Proteomics

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Correction of cognitive deficits in mouse models of Down syndrome by pharmacological inhibitor of DYRK1A


ABSTRACT: Down Syndrome (DS) results from the trisomy of human chromosome 21 (HSA21). It is still the most frequent intellectual disability, affecting 1 newborn per 700 births. Among candidate genes explaining intellectual disabilities seen in DS patients, the dual specificity tyrosine-phosphorylation regulated kinase 1A, DYRK1A, is located in the DS critical region of chromosome 21. DYRK1A has become a major screening target for the development of selective and potent pharmacological inhibitors. We here investigated the effects of a relatively selective DYRK1A inhibitor, Leucettine 41 (hereafter L41) in three different trisomic mouse models with increasing genetic complexity, Tg(Dyrk1a), Ts65Dn and Dp1Yey. Leucettines are derived from the marine sponge alkaloid Leucettamine B.

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Brain

SUBMITTER: Antigoni Manousopoulou  

LAB HEAD: Spiros D Garbis

PROVIDER: PXD008419 | Pride | 2018-10-17

REPOSITORIES: Pride

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Publications


Growing evidence supports the implication of DYRK1A in the development of cognitive deficits seen in Down syndrome (DS) and Alzheimer's disease (AD). We here demonstrate that pharmacological inhibition of brain DYRK1A is able to correct recognition memory deficits in three DS mouse models with increasing genetic complexity [Tg(<i>Dyrk1a</i>), Ts65Dn, Dp1Yey], all expressing an extra copy of <i>Dyrk1a</i> Overexpressed DYRK1A accumulates in the cytoplasm and at the synapse. Treatment of the three  ...[more]

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