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Serum amyloid P component induces TUNEL-positive nuclei in rat brain after intrahippocampal administration
- Source :
- Brain research. 1145
- Publication Year :
- 2006
-
Abstract
- Serum amyloid P component (SAP)-induced neuronal apoptosis has been demonstrated on the primary culture of embryonic rat cerebral cortex in vitro. Here we present pieces of evidence that cell death is also induced by serum amyloid P component in living rat brain similarly to that in cell culture. Intrahippocampally administered SAP diffuses from the site of injection to the cortical and subcortical area of the rat brain and enters the cells of brain tissue in 1 week. It induces elevation of the number of in situ TdT-mediated dUTP-X nick end-labeled nuclei in the hippocampus, cortex and subcortical structures of rat central nervous system. DNA fragmentation, which is detected by the end labeling reaction, is characteristic to apoptosis. It develops in 4 weeks following exposure. Apoptosis is an important form of cell death in different neurodegenerative diseases including Alzheimer's disease. Our present work reveals that apoptosis can be induced by SAP beyond other hitherto known apoptosis inducing components of neurodegeneration. Hereby SAP seems to be an important component of the process, which leads to expanded neuronal loss in the pathomechanism of neurodegenerative diseases.
- Subjects :
- Male
Programmed cell death
Time Factors
Central nervous system
Neurotoxins
Hippocampus
Apoptosis
Plaque, Amyloid
DNA Fragmentation
Biology
Alzheimer Disease
medicine
In Situ Nick-End Labeling
Animals
Rats, Wistar
Molecular Biology
Serum amyloid P component
Neurons
TUNEL assay
General Neuroscience
Neurodegeneration
Brain
Neurodegenerative Diseases
medicine.disease
Cell biology
Rats
Serum Amyloid P-Component
medicine.anatomical_structure
Cerebral cortex
Nerve Degeneration
biology.protein
Neurology (clinical)
Neuroscience
Developmental Biology
Subjects
Details
- ISSN :
- 00068993
- Volume :
- 1145
- Database :
- OpenAIRE
- Journal :
- Brain research
- Accession number :
- edsair.doi.dedup.....df2407c01ebf24feace8f5ee1fcbbcc2