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BackgroundAlzheimer’s disease (AD) is the most common form of dementia and patients often have visual disorders. Mild cognitive impairment (MCI) is characterized by a memory deficit when compared with those of a similar age and education level which could indicate an earlier onset of AD. The aim of this study is to measure the changes of the retinal nerve fiber layer (RNFL) thickness of AD and MCI patients in comparison with the normal age controls.MethodsThe RNFL thickness was assessed using optical coherence tomography (OCT) in patients with MCI, AD (mild, moderate and severe) and the age matched controls.ResultsThe thickness of RNFL in the superior quadrant and total mean values are gradually and significantly decreased from MCI to severe AD when compared to that in the controls. There is also a significant reduction of the retinal nerve fiber layer in the inferior quadrant in severe AD patients.ConclusionsOur data indicate that the retinal nerve fiber layer degeneration is paralleled with dementia progression. Owing to its non-invasive and cost effective nature, monitoring RNFL thickness may have a value in assessing disease progression and the efficacy of any treatments.

Endothelial dysfunction leads to worse cognitive performance in Alzheimer's dementia (AD). While both cerebrovascular risk factors and endothelial dysfunction lead to activation of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and E-selectin, it is not known whether these biomarkers extend the diagnostic repertoire in reflecting intracerebral structural damage or cognitive performance. A total of 110 AD patients and 50 age-matched controls were enrolled. Plasma levels of VCAM-1, ICAM-1 and E-selectin were measured and correlated with the cognitive performance, white matter macro-structural changes, and major tract-specific fractional anisotropy quantification. The AD patients were further stratified by clinical dementia rating score (mild dementia, n=60; moderate-to-severe dementia, n=50). Compared with the controls, plasma levels of VCAM-1 (p< 0.001), ICAM-1 (p=0.028) and E-selectin (p=0.016) were significantly higher in the patients, but only VCAM-1 levels significantly reflected the severity of dementia (p< 0.001). In addition, only VCAM-1 levels showed an association with macro- and micro- white matter changes especially in the superior longitudinal fasciculus (p< 0.001), posterior thalamic radiation (p=0.002), stria terminalis (p=0.002) and corpus callosum (p=0.009), and were independent of, age and cortical volume. These tracts show significant association with MMSE, short term memory and visuospatial function. Meanwhile, while VCAM-1 level correlated significantly with short-term memory (p=0.026) and drawing (p=0.025) scores in the AD patients after adjusting for age and education, the significance disappeared after adjusting for global FA. Endothelial activation, especially VCAM-1, was of clinical significance in AD that reflects macro- and micro-structural changes and poor short term memory and visuospatial function.

BackgroundThe correlation between intracranial pressure (ICP) and intraocular pressure (IOP) is still controversial in literature and hence whether IOP can be used as a non-invasive surrogate of ICP remains unknown. The aim of the current study was to further clarify the potential correlation between ICP and IOP.MethodsThe IOP measured with Goldmann applanation tonometer was carried out on 130 patients whose ICP was determined via lumber puncture. The Pearson correlation coefficient between ICP and IOP was calculated, the fisher line discriminated analysis to evaluate the effectivity of using IOP to predict the ICP level.ResultsA significant correlation between ICP and IOP was found. ICP was correlated significantly with IOP of the right eyes (p < 0.001) and IOP of the left eyes (p = 0.001) and mean IOP of both eyes (p < 0.001), respectively. However, using IOP as a measurement to predict ICP, the accuracy rate was found to be 65.4%.ConclusionOur data suggested that although a significant correlation exists between ICP and IOP, caution needs to be taken when using IOP readings by Goldmann applanation tonometer as a surrogate for direct cerebrospinal fluid pressure measurement of ICP.

PURPOSE. To characterize whether the activation of Rac1 is involved in the inflammatory effects produced by Amadori-glycated albumin (AGA) in retinal microglia and to further explore the pathologic pathways of AGA-induced retinal microglial activation and inflammation via a microRNA-dependent mechanism.METHODS. Primary rat retinal microglia were separated and cultured. The levels of TNF-a mRNA and soluble TNF-a produced by the retinal microglia in response to AGA were measured with quantitative RT-PCR (qRT-PCR) and ELISA. In addition, the GTPase activity of Rac1 was measured using a Rac activation assay kit. Luciferase reporter assays were used to validate the regulation of a putative target of microRNA-124 (miR-124).RESULTS. Amadori-glycated albumin significantly stimulated the expression of TNF-a mRNA and protein in cultured retinal microglial cells in a dose-and time-dependent manner. MicroRNA-124 expression was consistently suppressed by AGA, and the inhibitory effect was controlled by histone deacetylases (HDACs). Amadori-glycated albumin induced an increase in Rac1 activation in a dose-and time-dependent manner. Furthermore, our data indicated that Rac1 activation-mediated reactive oxygen species production stimulates p65 NF-jB phosphorylation and induces TNF-a release from retinal microglial cells. Finally, we demonstrated that miR-124 directly controls Rac1 expression.CONCLUSIONS. The current study indicated that AGA-induced retinal microglial activation and inflammation occur via a miR-124-dependent mechanism.

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A patient developed drug-induced myopathy during long-term treatment with telbivudine for chronic HBV. To promptly detect this reversible adverse event, monitoring of serum CK level and recognition of myopathic signs and symptoms are necessary. Further investigations are needed to clarify the possible mechanism of telbivudine-induced myopathy.