Publications by authors named "J Delabar"
Overexpression of the chromosome 21 DYRK1A gene induces morphological defects and cognitive impairments in individuals with Down syndrome (DS) and in DS mice models. Aging neurons of specific brain regions of patients with Alzheimer's disease, DS and Pick's disease have increased DYRK1A immunoreactivity suggesting a possible association of DYRK1A with neurofibrillary tangle pathology. Epigallocatechin-3-gallate (EGCG) displays appreciable inhibition of DYRK1A activity and, contrary to all other published inhibitors, EGCG is a non-competitive inhibitor of DYRK1A.
View Article and Find Full Text PDFEarly markers are needed for more effective prevention of Alzheimer's disease. We previously showed that individuals with Alzheimer's disease have decreased plasma DYRK1A levels compared to controls. We assessed DYRK1A in the plasma of cognitively healthy elderly volunteers, individuals with either Alzheimer's disease (AD), tauopathies or Down syndrome (DS), and in lymphoblastoids from individuals with DS.
View Article and Find Full Text PDFCorrigendum to: DYRK1A interacts with the REST/NRSF-SWI/SNF chromatin remodelling complex to deregulate gene clusters involved in the neuronal phenotypic traits of Down syndrome.
Hum Mol Genet
June 2022
Article Synopsis
- Research on Down syndrome has surged recently, aiming to better understand how trisomy 21 (T21) affects individuals at the molecular and cellular levels.
- The Trisomy 21 Research Society (T21RS) is a leading organization uniting researchers and clinicians in this field, hosting events like the Third International Conference in Barcelona in June 2019.
- The conference attracted 429 attendees and covered significant discoveries related to T21, including cognitive and behavioral challenges, and comorbidities like Alzheimer's disease and leukemia, highlighting advancements in neuroscience, psychology, and therapeutic approaches.
Introduction: An effective therapy has not yet been developed for Alzheimer's disease (AD), in part because pathological changes occur years before clinical symptoms manifest. We recently showed that decreased plasma DYRK1A identifies individuals with mild cognitive impairment (MCI) or AD, and that aged mice have higher DYRK1A levels.
Methods: We assessed DYRK1A in plasma in young/aged controls and in elderly cognitive complainers with low (L) and high (H) brain amyloid load.