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RESEARCH PRODUCT
Early increased density of cyclooxygenase-2 (COX-2) immunoreactive neurons in Down syndrome
Juan NacherCarlos CrespoJosé Miguel Blasco-ibáñezEmilio VareaMaria Muletsubject
0301 basic medicinemedicine.medical_specialtyDown syndromelcsh:MedicineMice TransgenicDiseasePathology and Forensic Medicineneuroinflammationmicroglia</i>Mice03 medical and health sciences0302 clinical medicineInternal medicinemedicineAnimalsHumansPostnatal dayNeuroinflammationNeuronschemistry.chemical_classificationMicrogliabiologybusiness.industryNeurodegenerationlcsh:RBrainmedicine.disease<i>Ts65Dn030104 developmental biologyEndocrinologymedicine.anatomical_structureEnzymechemistryCyclooxygenase 2biology.proteinNeurology (clinical)CyclooxygenaseDown SyndromebusinessNeuroscienceAlzheimer’s disease030217 neurology & neurosurgerydescription
iNeuroinflammation is one of the hallmarks of Alzheimer's disease. One of the enzymes involved in neuroinflammation, even in early stages of the disease, is COX-2, an inducible cyclooxygenase responsible for the generation of eicosanoids and for the generation of free radicals. Individuals with Down syndrome develop Alzheimer's disease early in life. Previous studies pointed to the possible overexpression of COX-2 and correlated it to brain regions affected by the disease. We analysed the COX-2 expression levels in individuals with Down syndrome and in young, adult and old mice of the Ts65Dn mouse model for Down syndrome. We have observed an overexpression of COX-2 in both, Down syndrome individuals and mice. Importantly, mice already presented an overexpression of COX-2 at postnatal day 30, before neurodegeneration begins; which suggests that neuroinflammation may underlie the posterior neurodegeneration observed in individuals with Down syndrome and in Ts65Dn mice and could be a factor for the premature appearance of Alzheimer's disease./i.
year | journal | country | edition | language |
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2017-07-06 | Folia Neuropathologica |