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Alzheimer’s disease is a neurodegenerative disease characterized by the impairment of cognitive function and loss of memory, affecting millions of individuals worldwide. With the dramatic increase in the prevalence of Alzheimer’s disease, it is expected to impose extensive public health and economic burden. However, this burden is particularly heavy on the caregivers of Alzheimer’s disease patients eliciting neuropsychiatric symptoms that include mood swings, hallucinations, and depression. Interestingly, these neuropsychiatric symptoms are shared across symptoms of bipolar disorder, schizophrenia, and major depression disorder. Despite the similarities in symptomatology, comorbidities of Alzheimer’s disease and these neuropsychiatric disorders have not been studied in the Alzheimer’s disease model. Here, we explore the comprehensive changes in gene expression of genes that are associated with bipolar disorder, schizophrenia, and major depression disorder through the microarray of an Alzheimer’s disease animal model, the forebrain specific PSEN double knockout mouse. To analyze the genes related with these three neuropsychiatric disorders within the scope of our microarray data, we used selected 1207 of a total of 45,037 genes that satisfied our selection criteria. These genes were selected on the basis of 14 Gene Ontology terms significantly relevant with the three disorders which were identified by previous research conducted by the Psychiatric Genomics Consortium. Our study revealed that the forebrain specific deletion of Alzheimer’s disease genes can significantly alter neuropsychiatric disorder associated genes. Most importantly, most of these significantly altered genes were found to be involved with schizophrenia. Taken together, we suggest that the synaptic dysfunction by mutation of Alzheimer’s disease genes can lead to the manifestation of not only memory loss and impairments in cognition, but also neuropsychiatric symptoms.

The experimental results regarding to the effects of ultraviolet (UV) light illumination on the characteristics of hydrogenated amorphous silicon (a-Si:H) thin film transistors (TFT's) have been presented. The device parameters of a-Si:H TFT, such as threshold voltage, field-effect mobility, and subthreshold slope, have been degraded by electrical stress and visible light illumination, but substantially improved by UV radiation. This may be attributed to an annealing effect on the dangling-bond defects, involving a number of phonons generated by absorption of high energy UV photons in the a-Si:H TFT channel. It has been also observed that the off-current of a-Si:H TFT decreases remarkably while the on-current changes very little. From the experimental results, we report that the improved on/off current ratio of a-Si:H TFT may be achieved by UV radiation.

We presents a new model for the series resistance of an amorphous silicon (a-Si) thin film transistor (TFT) with an inverted-staggered configuration, considering the current spreading under the source and the drain contacts as well as the space charge limited current. The calculated results of our model have been in good agreements with the measured data over a wide range of applied voltage, gate-to-source and gate-to-drain overlap length, channel length, and operating temperature. Our model shows that the relative contribution of the series resistances to the current-voltage (I-V) characteristics of the a-Si TFT in the linear regime is more significant at low drain and high gate voltages, for short channel and small overlap length, and at low operating temperature, which has been verified successfully by the experimental measurements.