Image restoration using a two-dimensional lorentzian probability model

It is known that the distribution of intensity gradients along separate horizontal and vertical directions in an image of a general scene often has a sharp peak with a long tail. This property, can be described by a Lorentzian probability function, and is the basis of an efficient nonlinear one-dimensional restoration algorithm. It can also superresolve a two-dimensional separable image. This paper discusses the gradient distribution in a general two-dimensional image and shows that the distribution of the maximum gradient at any picture point is also Lorentzian. This has been used to develop an iterative two-dimensional restoration algorithm. It starts by evaluating the likelihood of the intensity gradients within a Wiener filtered image. Then a nonlinear correction term is introduced which increases this likelihood under mean square error criterion. The method is applied to synthetic images and to a 94 GHz passive millimetre wave image. This new two-dimensional method is shown to be superior to the previous one-dimensional algorithm which had to be applied separately along two orthogonal directions. © 2000 Taylor & Francis Group, LLC

What have we learned from the streptozotocin-induced animal model of sporadic Alzheimer's disease, about the therapeutic strategies in Alzheimer's research

Experimental models that faithfully mimic the developmental pathology of sporadic Alzheimer's disease (sAD) in humans are important for testing the novel therapeutic approaches in sAD treatment. Widely used transgenic mice AD models have provided valuable insights into the molecular mechanisms underlying the memory decline but, due to the particular β-amyloid-related gene manipulation, they resemble the familial but not the sporadic AD form, and are, therefore, inappropriate for this purpose. In line with the recent findings of sAD being recognised as an insulin resistant brains state (IRBS), a new, non-transgenic, animal model has been proposed as a representative model of sAD, developed by intracerebroventricular application of the betacytotoxic drug streptozotocin (STZ-icv). The STZ-icv-treated animals (mostly rats and mice) develop IRBS associated with memory impairment and progressive cholinergic deficits, glucose hypometabolism, oxidative stress and neurodegeneration that share many features in common with sAD in humans. The therapeutic strategies (acetylcholinesterase inhibitors, antioxidants and many other drugs) that have been tested until now on the STZ-icv animal model have been reviewed and the comparability of the drugs' efficacy in this non-transgenic sAD model and the results from clinical trials on sAD patients, evaluated

Validation and pilot application of [ 18F]FDG-PET in evaluation of a metabolic therapy for Alzheimer's disease

Here we describe methods for application of quantitative fluorodeoxyglucose positron emission tomography ([ 18F]FDG-PET) measures of brain glucose metabolism in multi-centre clinical trials for Alzheimer's disease. We validated methods and demonstrated their use in the context of a treatment trial with the PPARγ agonist Rosiglitazone XR versus placebo in mild to moderate AD patients. Novel quantitative indices related to the combined forward rate constant for [ 18F]FDG uptake $({K}-{i}^{index})$ and to the rate of cerebral glucose utilization $(CM{R}-{glu}^{index})$ were applied. Active treatment was associated with a sustained but not statistically significant trend from the first month for higher mean values in both. However, neither these nor another analytical approach recently validated using data from the Alzheimer's Disease Neuroimaging Initiative suggested that active treatment decreased the progression of decline in brain glucose metabolism. Rates of brain atrophy were similar between active and placebo groups and measures of cognition also did not demonstrate clear group differences. Our study demonstrates the feasibility of using [ 18F]FDG-PET as part of a multi-centre therapeutics trial and describes new measures that can be employed. It suggests that Rosiglitazone is associated with an early increase in whole brain glucose utilisation, but not with any biological or clinical evidence for slowing progression over the period of study in the selected patient group

A Multi-Center Randomized Proof-of-Concept Clinical Trial Applying [18F]FDG-PET for Evaluation of Metabolic Therapy with Rosiglitazone XR in Mild to Moderate Alzheimer's Disease

Here we report the first multi-center clinical trial in Alzheimer's disease (AD) using fluorodeoxyglucose positron emission tomography ([18F]FDG-PET) measures of brain glucose metabolism as the primary outcome. We contrasted effects of 12 months treatment with the PPARγ agonist Rosiglitazone XR versus placebo in 80 mild to moderate AD patients. Secondary objectives included testing for reduction in the progression of brain atrophy and improvement in cognition. Active treatment was associated with a sustained but not statistically significant trend from the first month for higher mean values in Kiindex and CMRgluindex, novel quantitative indices related to the combined forward rate constant for [18F]FDG uptake and to the rate of cerebral glucose utilization, respectively. However, neither these nor another analytical approach recently validated using data from the Alzheimer's Disease Neuroimaging Initiative indicated that active treatment decreased the progression of decline in brain glucose metabolism. Rates of brain atrophy were similar between active and placebo groups and measures of cognition also did not suggest clear group differences. Our study demonstrates the feasibility of using [18F]FDG-PET as part of a multi-center therapeutics trial. It suggests that Rosiglitazone is associated with an early increase in whole brain glucose metabolism, but not with any biological or clinical evidence for slowing progression over a 1 year follow up in the symptomatic stages of AD