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Background and Purpose-Vascular pathology and Alzheimer disease (AD) pathology have been shown to coexist in the brains of dementia patients. We investigated how cognitive impairment could be exacerbated in a rat model of combined injury through the interaction of chronic cerebral hypoperfusion and amyloid beta (A␤) toxicity. Methods-In Wistar rats, chronic cerebral hypoperfusion was modeled by permanent occlusion of bilateral common carotid arteries (BCCAo). Further, AD pathology was modeled by bilateral intracerebroventricular A␤ (A␤ toxicity) using a nonphysiological A␤ peptide (A␤ 25 to 35). The experimental animals were divided into 4 groups, including sham, single injury (A␤ toxicity or BCCAo), and combined injury (BCCAo-A␤ toxicity) groups (nϭ7 per group) . Cerebral blood flow and metabolism were measured using small animal positron emission tomography. A Morris water maze task, novel object location and recognition tests, and histological investigation, including neuronal cell death, apoptosis, neuroinflammation, and AD-related pathology, were performed. Results-Spatial memory impairment was synergistically exacerbated in the BCCAo-A␤ toxicity group as compared to the BCCAo or A␤ toxicity groups (PϽ0.05). Compared to the sham group, neuroinflammation with microglial or astroglial activation was increased both in multiple white matter lesions and the hippocampus in other experimental groups. AD-related pathology was enhanced in the BCCAo-A␤ toxicity group compared to the A␤ toxicity group. Conclusion-Our experimental results support a clinical hypothesis of the deleterious interaction between chronic cerebralhypoperfusion and A␤ toxicity. Chronic cerebral hypoperfusion-induced perturbation in the equilibrium of AD-related pathology may exacerbate cognitive impairment in a rat model of combined injury. (Stroke. 2011;42:2595-2604.)Key Words: Alzheimer disease Ⅲ amyloid beta Ⅲ chronic cerebral hypoperfusion Ⅲ Morris water maze Ⅲ vascular dementia A lzheimer disease (AD) and vascular dementia are the most common causes of cognitive decline in the aging population. 1 Accumulation of insoluble amyloid beta (A␤) in the brain has been identified as the major culprit for the cognitive impairment observed in AD patients. 2 Because senile plaques composed of the A␤ peptide have been found in the brains of AD patients, 2 extensive research has focused on the amyloid hypothesis to explain AD pathology.A hypothesis emphasizing the interaction between AD and vascular pathologies has recently emerged. [3][4][5] The Nun study and other clinico-pathological studies 6 -8 have revealed that patients with AD exhibit concomitant vascular lesions in the brain. Further, epidemiological studies have shown that the major risk factors for AD mostly coincide with those for vascular dementia. 4 The Rotterdam study, 9 a large population-based prospective study, reported an increased prevalence of atherosclerosis in patients either with AD or Received March 11, 2011; accepted March 31, 2011 A converging hypothesis involving chronic ...

In this paper, we propose new algorithms to determine the antenna location for downlink distributed antenna systems (DASs) in single-cell and two-cell environments. We consider the composite fading channel which includes small and large scale fadings. First, for the single-cell DAS, we formulate the optimization problem of distributed antenna (DA) port locations by maximizing the lower bound of the expected signal to noise ratio (SNR). In comparison to the conventional algorithm based on the squared distance criterion which requires an iterative method, our problem generates a closed form solution. Next, for the two-cell DAS, we propose a gradient ascent algorithm which determines the optimum DA locations by maximizing the lower bound of the expected signal to leakage ratio (SLR). In our work, we consider selection transmission, maximal ratio transmission and zero-forcing beamforming (ZFBF) under sum power constraint and study equal gain transmission and scaled ZFBF under per-antenna power constraint. Simulation results show that our proposed algorithms based on both the SNR and the SLR criteria offer a capacity gain over the conventional centralized antenna systems.Index Terms-Distributed antenna systems, antenna placement.

In this paper, we investigate a behavior of the cell average ergodic capacity for distributed antenna systems (DAS) in a composite fading channel model which contains small-scale and large-scale fadings. For small-scale Rayleigh fadings, based on the proof of asymptotic normality, the mean and the variance of the instantaneous capacity were recently presented as a closed form solution. However, this solution is too complicated to be applied directly for obtaining the average ergodic capacity over a cell. In this work, we derive a simple and accurate expression for the ergodic capacity by utilizing the high signal to noise ratio (SNR) analysis. Our simple solution provides meaningful insight on how the ergodic capacity is affected as SNR, pathloss and antenna configurations change. Also it is useful for capturing quantitative performance measures such as the multiplexing gain and the power offset. In addition, we analyze the cell average ergodic capacity by taking into account the shadowing effect and the pathloss on the basis of our results on the small-scale fadings. These expressions lead to some insights on the performance of DAS under practical environments. Finally, numerical results confirm the validity of our analytical results.

In this paper, we study single cell multi-user downlink distributed antenna systems (DAS) where antenna ports are geographically separated in a cell. First, we derive an expression of the ergodic sum rate for the DAS in the presence of pathloss. Then, we propose a transmission selection scheme based on the derived expressions which does not require channel state information at the transmitter. Utilizing the knowledge of distance information from a user to each distributed antenna (DA) port, we consider the optimization of pairings of DA ports and users to maximize the system performance. Based on the ergodic sum rate expressions, the proposed scheme chooses the best mode maximizing the ergodic sum rate among mode candidates. In our proposed scheme, the number of mode candidates are greatly reduced compared to that of ideal mode selection. In addition, we analyze the signal to noise ratio cross-over point for different modes using the sum rate expressions. Through Monte Carlo simulations, we show the accuracy of our derivations for the ergodic sum rate. Moreover, simulation results with the pathloss modeling confirm that the proposed scheme produces the average sum rate identical to the ideal mode selection with significantly reduced candidates.