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- Host:
- Primary antibody reactivity:Mouse
- Description:Corticotropin Releasing Factor Mouse/Rat ELISA
- Size:1 kit
- Environmentally Preferable:
- Regulatory Status:RUO
- Cat. No.:102552-158
- Supplier no.:RSCYK131R
CRF serves as a potential neurochemical marker of early dementia and possible early AD.
- Calibration Range: 0.078–2.5 ng/mL
- Brain extract, Plasma-Citrate, Plasma-EDTA, Plasma-Heparin: 50 uL/well
Corticotropin releasing factor (CRF, also CRH) was initially isolated from ovine hypothalamus by Vale et al., in 1981, and identified as a novel neuropeptide comprising 41 amino acid residues with molecular weight 4758. Later human CRF and rat CRF were also isolated and identified. The mouse CRF peptide is identical at amino acid level to the rat and human CRF peptides. CRF in anterior pituitary promotes the synthesis and secretion of ACTH, a main factor of hypothalamus-pituitary-adrenal (HPA) axis. In the rat and human, CRF distributes mainly in hypothalamus, but it was also found in spinal cord, stomach, spleen, duodenum, adrenal and placenta. In addition, immunochemical evidence supported the wide distribution of the peptide throughout the central nervous system (CNS) such as olfactory bulb, retina and central auditory system in the rat. In mouse brain extracts, the highest concentrations of CRF-like immunoreactivity (CRF-LI) has been detected in the median eminence and hypothalamus and also existing in the amygdala, thalamus, frontal cortex, medulla/pons and cerebellum by radioimmunoassay. However because of the wide distribution, it is still disputing about CRF whether its blood level can reflect only the function of HPA axis. The relationships between CRF and stress, CRF and Alzheimer disease (AD) were attracted much attention recently. In fact the peptide was also suggested to regulate endocrine, autonomic and behavioral responses to stress, based on an experiment with acute and chronic stress rat models that showed endocrine function changes similar to those seen in patients with depression CRF in serial cerebrospinal fluid (CSF) of patients with depression was strikingly reduced as compared to those of normal subjects. The mean CRF and ACTH levels in the CSF of AD patients were significantly lower than those of healthy controls. Only in the cortices of those with mild dementia, CRF was reduced significantly, thus CRF was proposed to serve as a potential neurochemical marker of early dementia and possible early AD.