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A 15-year-old teenager presented with a 2-month history of headache. Neurological examination was normal except for papilledema. Further lumbar puncture indicated intracranial hypertension (330 mm H2O). Brain magnetic resonance imaging (MRI) was normal but phase contrast-magnetic resonance venography (PC-MRV) (Figure 1(A)) suggested possible left transverse-sigmoid sinus thrombosis; subsequent contrast-enhanced 3D fat-saturated T1 volumetric isotropic turbo spin echo acquisition (VISTA) MRI (Figure 1(B)) confirmed the pathology. Hyper-coagulable panel results (including six steroid sex hormones, antithrombin III, protein C, protein S, lupus anticoagulant, and anticardiolipin antibodies) were all within normal range. In further examination, computed tomography (CT) venography images (Figure 1(C) and (D)) showed that the left jugular vein was compressed by the styloid process, consistent with Eagle syndrome.1 The patient who refused the recommended surgical treatment, however, chose anticoagulant therapy consisting of low-molecular weight heparin subcutaneous injection in addition to new oral anticoagulant. At 18-month follow-up, the patient reported no symptoms remained.
Background: Increasing evidence suggests that neprilysin (NEP) may be the major degrading enzyme of amyloid beta (Aβ) in the brain and the NEP gene has been proposed as a candidate gene for Alzheimer's disease (AD). Association results between the NEP gene and AD are still preliminary. This study investigates the effect of the polymorphisms of −204G/C and 159C/T in the NEP gene on the development of sporadic Alzheimer's disease (SAD) in a southern Chinese community.
Method: 236 sporadic late-onset AD patients were recruited from Guangzhou Psychiatric Hospital in southern China, and 332 healthy elderly controls were enrolled from three old age homes in suburban Guangzhou. NEP and ApoE genotype were determined by PCR–RFLP.
Results: No differences in genotypic and allelic frequencies of −204G/C and 159C/T polymorphisms in NEP were found between AD and control group (for −204G/C genotype: χ2 = 2.34, P > 0.05; for allele: χ2 = 2.31, P > 0.05; for 159C/T genotype: χ2 = 1.34, P > 0.05; for allele: χ2 = 0.88, P > 0.05). Neither was any difference found in genotypic and allelic frequency when stratified by sex or by ApoE ε4 allele (P > 0.05).
Conclusions: Our results suggest that −204G/C and 159C/T polymorphisms of the NEP gene may not be associated with SAD. Moreover, both sex and ApoE ε4 allele do not affect the distribution of NEP gene polymorphisms.
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