کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3063967 | 1580398 | 2014 | 6 صفحه PDF | دانلود رایگان |

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.
Journal: Journal of Neuroimmunology - Volume 276, Issues 1–2, 15 November 2014, Pages 18–23