Fluorodeoxyglucose (FDG) positron emission tomography (PET) measures the decline in the regional cerebral metabolic rate for glucose, offering a reliable metabolic biomarker even on presymptomatic Alzheimer's disease (AD) patients. PET scans provide functional information that is unique and unavailable using other types of imaging. However, the computational efficacy of FDG-PET data alone, for the classification of various Alzheimers Diagnostic categories, has not been well studied. This motivates us to correctly discriminate various AD Diagnostic categories using FDG-PET data. Deep learning has improved state-of-the-art classification accuracies in the areas of speech, signal, image, video, text mining and recognition. We propose novel methods that involve probabilistic principal component analysis on max-pooled data and mean-pooled data for dimensionality reduction, and multilayer feed forward neural network which performs binary classification. Our experimental dataset consists of baseline data of subjects including 186 cognitively unimpaired (CU) subects, 336 mild cognitive impairment (MCI) subjects with 158 Late MCI and 178 Early MCI, and 146 AD patients from Alzheimer's Disease Neuroimaging Initiative (ADNI) dataset. We measured F1-measure, precision, recall, negative and positive predictive values with a 10-fold cross validation scheme. Our results indicate that our designed classifiers achieve competitive results while max pooling achieves better classification performance compared to mean-pooled features. Our deep model based research may advance FDG-PET analysis by demonstrating their potential as an effective imaging biomarker of AD.
The primary objective of this review is to understand the role of different inflammatory mediators, mechanisms involved in the disease pathogenesis and to identify new therapeutic approaches involved in the treatment of neurodegerative diseases. Neuronflammation is like a two-edged sword because in acute conditions, or at low levels, it deals with the anomaly and is healing in nature. However, in chronic conditions, or at continued high levels it causes massive damage to the viable host tissue. Neuroinflammation accelerates the progression of neurodegeneration in Parkinson's disease (PD), Alzheimer's disease (AD) and amyotrophic lateral sclerosis (ALS). This review aims to study different inflammatory mediators like prostaglandins, cytokines, microglial activation, astrocytic activation, etc and understand the underlying mechanisms (deposition of misfolded proteins, oxidative stress, lipidperoxidation, mitochondrial dysfunctioning) involved in the disease pathogenesis. This range of inflammatory mediators and underlying pathogenic mechanisms provides a variety of potential targets for new anti-inflammatory agents.
Objective: To study the synergetic effect of Melatonin and Simvastatin on brain of albino mice of Swiss strain. Materials and methods: The neuroprotective activity was studied in LPS and STZ induced learning and memory deficit model. In this combined neuroprotective effect of melatonin and simvastatin against LPS and STZ was investigated the synergistic effect. Neuroprotective activity was evaluated by comparing behavioural (learning and memory) and biochemical (GSH, MDA, Cholinesterases) parameters. There was significant Results and discussion: decrease in MDA level and AChE level, as compare to disease group in Melatonin (**p<0.001) and Simvastatin (*p<0.05), Melatonin + Simvastatin (***p<0.001) and significant increase in GSH level respectively, in LPS and STZ memory impairment model. There was significant decrease in escape latency time and no. of crossing behavior in all groups in comparison of session 1-5 except the disease group in LPS and STZ model. Data indicates that Conclusion: combined administration of melatonin and simvastatin improve the behavioral and biochemical parameters in comparison to the administration of their individual doses. Biochemical parameters showed significant decrease (**p<0.01) in MDA level, AChE level and increase in (***p<0.001) GSH level which is equivalent to standard drug.
Objective:Materials To study the neuroprotective effect of Sodium butyrate against CdCl induced dementia in rats. 2 and methods: The neuroprotective activity of HDAC inhibitor, sodium butyratewas evaluated against CdCl induced 2 dementia in adult male Albino Wistar rats. A number of behavioral (Elevated plus maze and Morris water maze; Assessment of learning and memory) and biochemical (brain/ serum levels of nitrite/nitrate, Aortic Superoxide Anion, calcium, GSH, TBARS, CAT, AChE) parameters were assessed.In comparison to the Results and discussion: disease control, administration of sodium butyrate (HDACi) significantly attenuates the CdCl induced behavioral 2 alternations like learning and memory impairment; andincreased the brain/serum levels of acetylcholinesterase (AChE), catalase (CAT), reduced glutathione (GSH), thiobarbituric acid reactive species (TBARS), brain calcium levels, aortic superoxide anionand nitrite/nitrate levels.The results clearly indicate that oxidative stress Conclusion: and lipid peroxidation are the primary mechanisms involved in the pathogenesis of CdCl induced dementia.The 2 research aims to identify and implement the therapeutic potential of HDACi in the treatment of dementia. It is concluded that a target based drug research against pathogenic mechanisms like oxidative stress and lipidperoxidation may help to alleviate ailments associated with neurodegeneration.
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