6533b836fe1ef96bd12a0908
RESEARCH PRODUCT
β-Amyloid-induced activation of Caspase-3 in primary cultures of rat neurons
Marta LlansolaNuria MarínFrancisco Bosch-morellBelén RomeroFrancisco J. RomeroVicente FelinoJoaquín Romásubject
AgingTime FactorsAmyloidProteolysisApoptosisCaspase 3medicineAnimalsCells CulturedCaspaseNeuronsAmyloid beta-Peptidesbiologymedicine.diagnostic_testCaspase 3NeurodegenerationIntrinsic apoptosismedicine.diseaseMolecular biologyPeptide FragmentsRatsEnzyme Activationmedicine.anatomical_structureApoptosisCaspasesImmunologybiology.proteinNeuronDevelopmental Biologydescription
It is known that beta-amyloid peptide (Abeta) contributes to the neurodegeneration in Alzheimer's disease (AD) and operates through activation of an apoptotic pathway. Apoptotic signal is driven by a family of cysteine proteases called caspases. The beta-amyloid precursor protein (APP) is directly and efficiently cleaved by caspases during apoptosis, resulting in elevated beta-amyloid peptide formation. Cerebellar neurons from rat pups were treated with the aged Abeta(25-35) at 1 and 5 microM and fluorescence assays of caspase activity performed over 4 days. We observed an increase in caspase activity after 48 h treatment in both 1 and 5 microM treated cells, then (72-96 h) caspase activity decreased to control values. The data presented support the hypothesis that Abeta(25-35)-induced apoptosis is mediated by the activation of Caspase-3 and that this is a transient effect.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2000-10-01 | Mechanisms of Ageing and Development |