0000000000008737

AUTHOR

Thomas Van Groen

showing 4 related works from this author

A Novel 1,4-Dihydropyridine Derivative Improves Spatial Learning and Memory and Modifies Brain Protein Expression in Wild Type and Transgenic APPSweD…

2015

Ca2+ blockers, particularly those capable of crossing the blood-brain barrier (BBB), have been suggested as a possible treatment or disease modifying agents for neurodegenerative disorders, e.g., Alzheimer's disease. The present study investigated the effects of a novel 4-(N-dodecyl) pyridinium group-containing 1,4-dihydropyridine derivative (AP-12) on cognition and synaptic protein expression in the brain. Treatment of AP-12 was investigated in wild type C57BL/6J mice and transgenic Alzheimer's disease model mice (Tg APPSweDI) using behavioral tests and immunohistochemistry, as well as mass spectrometry to assess the blood-brain barrier (BBB) penetration. The data demonstrated the ability …

Genetically modified mouseMalePathologymedicine.medical_specialtyDihydropyridinesTime Factorsmedicine.drug_classTransgeneSpatial Learninglcsh:MedicineMice TransgenicBlood–brain barrierAnxiolyticGyrus CinguliHippocampus03 medical and health sciences0302 clinical medicineHomer Scaffolding ProteinsMemorymedicineAnimalsHumanslcsh:Science030304 developmental biology0303 health sciencesMultidisciplinaryAmyloid beta-PeptidesGlutamate Decarboxylaselcsh:RDihydropyridineWild typeBrainmedicine.disease3. Good healthMice Inbred C57BLmedicine.anatomical_structureAnti-Anxiety AgentsBlood-Brain BarrierSynaptic plasticitylcsh:QAlzheimer's diseaseCarrier ProteinsNeuroscience030217 neurology & neurosurgerymedicine.drugResearch ArticlePloS one
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Subchronic administration of auranofin reduced amyloid-β plaque pathology in a transgenic APPNL-G-F/NL-G-F mouse model

2020

Abstract Alzheimer’s disease (AD) is the most common cause of dementia. Neuropathological processes, including the accumulation of amyloid-β (Aβ) plaques and neurofibrillary tangles, and neuroinflammation, lead to cognitive impairment at middle and eventually later stages of AD progression. Over the last decade, focused efforts have explored repurposed drug approaches for AD pathophysiological mechanisms. Recently, auranofin, an anti-inflammatory drug, was shown to have therapeutic potential in a number of diseases in addition to rheumatoid arthritis. Surprisingly, no data regarding the effects of auranofin on cognitive deficits in AD mice or the influence of auranofin on Aβ pathology and n…

0301 basic medicinePathologymedicine.medical_specialtyAuranofinGlial fibrillary acidic proteinbiologybusiness.industryAmyloid betaGeneral NeuroscienceGlutamate decarboxylaseHippocampusPathophysiology03 medical and health sciences030104 developmental biology0302 clinical medicineSynaptic plasticitybiology.proteinMedicineNeurology (clinical)businessMolecular Biology030217 neurology & neurosurgeryNeuroinflammationDevelopmental Biologymedicine.drugBrain Research
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Mildronate improves cognition and reduces amyloid-β pathology in transgenic Alzheimer's disease mice

2013

Mildronate, a carnitine congener drug, previously has been shown to provide neuroprotection in an azidothymidine-induced mouse model of neurotoxicity and in a Parkinson's disease rat model. The aim of this study was to investigate the effects of mildronate treatment on cognition and pathology in Alzheimer's disease (AD) model mice (APP(SweDI)). Mildronate was administered i.p. daily at 50 or 100 mg/kg for 28 days. At the end of treatment, the animals were behaviorally and cognitively tested, and brains were assessed for AD-related pathology, inflammation, synaptic markers, and acetylcholinesterase (AChE). The data show that mildronate treatment significantly improved animal performance in w…

Genetically modified mousePathologymedicine.medical_specialtybiologyNeurotoxicityHippocampusWater mazemedicine.diseaseAcetylcholinesteraseNeuroprotectionCellular and Molecular Neurosciencechemistry.chemical_compoundchemistrySynaptic plasticitymedicineSynaptophysinbiology.proteinPsychologyJournal of Neuroscience Research
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Memory-enhancing and brain protein expression-stimulating effects of novel calcium antagonist in Alzheimer’s disease transgenic female mice

2016

The prevalence of Alzheimer's disease (AD) is higher in females than in males, and causes more severe cognitive, memory and behavioral impairments. Previously, in male transgenic (Tg) APPSweDI mice, we reported that the novel lipophilic 1,4-dihydropyridine (DHP) derivative AP-12 crossed the blood-brain barrier, blocked neuronal and vascular calcium channels, changed brain protein expression and improved behavior. In this study, we used female Tg APPSweDI mice to assess the effects of AP-12 on behavior, and brain protein expression, with a particular focus on those of the GABAergic system. The results showed that in female Tg mice, similar to male Tg mice, AP-12 improved spatial learning/mem…

Male0301 basic medicineCingulate cortexDihydropyridinesmedicine.medical_specialtyElevated plus mazeVesicular Inhibitory Amino Acid Transport ProteinsHippocampusMice TransgenicWater mazeBiologyHippocampal formationGyrus CinguliHippocampusArticleAmyloid beta-Protein PrecursorMice03 medical and health sciences0302 clinical medicineAlzheimer DiseaseMemoryInternal medicineNeuroplasticitymedicineAnimalsGABAergic NeuronsMaze LearningPharmacologyAmyloid beta-PeptidesNeuronal PlasticityGlutamate DecarboxylaseCalcium Channel BlockersUp-RegulationDisease Models Animal030104 developmental biologyEndocrinologyAnti-Anxiety AgentsBlood-Brain BarrierSynaptic plasticityGABAergicCalciumFemale030217 neurology & neurosurgeryPharmacological Research
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