Growth associated protein (GAP-43): Cloning and the development of a sensitive ELISA for neurological disorders

被引:8
|
作者
Gnanapavan, Sharmilee [1 ]
Yousaf, Nasim [2 ]
Heywood, Wendy [3 ]
Grant, Donna [1 ]
Mills, Kevin [3 ]
Chernajovsky, Yuti [2 ]
Keir, Geoff [1 ]
Giovannoni, Gavin [4 ]
机构
[1] Inst Neurol, Dept Neuroimmunol, London WC1N 3BG, England
[2] Queen Mary Univ London, Bone & Joint Res Unit, William Harvey Res Unit, Barts & London Sch Med & Dent, London, England
[3] UCL, Inst Child Hlth, Clin & Mol Genet Unit, Biochem Grp, London, England
[4] Queen Mary Univ London, Blizzard Inst, London, England
关键词
GAP-43; Neuroplasticity; CSF; Biomarker; ELISA; NEUROFIBRILLARY TANGLE DENSITY; RAT-BRAIN; CEREBROSPINAL-FLUID; MULTIPLE-SCLEROSIS; PHOSPHOPROTEIN B-50; ALZHEIMERS-DISEASE; MEMBRANES; PHOSPHORYLATION; LOCALIZATION; PLASTICITY;
D O I
10.1016/j.jneuroim.2014.07.008
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
GAP-43 has been studied in the rodent and mammalian brain and shown to be present specifically in areas undergoing axonal elongation and synapse formation. GAP-43 was cloned using the baculovirus expression system and purified. A sandwich ELISA was developed using the recombinant GAP-43 as standard and validated. CSF GAP-43 levels were analysed in benign intracranial hypertension, movement disorders, multiple sclerosis, neuropathy, CNS infections, motor neuron disease, and headache (neurological controls). GAP-43 levels were low in all disorders analysed (in particular motor neuron disease; p = 0.001, and movement disorders and multiple sclerosis; p < 0.0001) compared to controls, aside from CNS infections. GAP-43 is preferentially reduced in the CSF of neurological disorders associated with neurodegeneration. (C) 2014 Published by Elsevier B.V.
引用
收藏
页码:18 / 23
页数:6
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