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Languages : en
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Author: Heather M. Wilkins
Publisher: Frontiers Media SA
ISBN: 2889743616
Category : Science
Languages : en
Pages : 183
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Author: Fei Yin
Publisher: Frontiers Media SA
ISBN: 2889452530
Category :
Languages : en
Pages : 161
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Book Description
Impairment of energy metabolism is a hallmark of brain aging and several neurodegenerative diseases, such as the Alzheimer’s disease (AD). Age- and disease-related hypometabolism is commonly associated with oxidative stress and they are both regarded as major contributors to the decline in synaptic plasticity and cognition. Neuroinflammatory changes, entailing microglial activation and elevated expression of inflammatory cytokines, also correlate with age-related cognitive decline. It is still under debate whether the mitochondrial dysfunction-induced metabolic deficits or the microglia activation-mediated neuroinflammation is the initiator of the cognitive changes in aging and AD. Nevertheless, multiple lines of evidence support the notion that mitochondrial dysfunction and chronic inflammation exacerbate each other, and these mechanistic diversities have cellular redox dysregulation as a common denominator. This research topic focuses on the role of a metabolic-inflammatory axis encompassing the bioenergetic activity, brain inflammatory responses and their redox regulation in healthy brain aging and neurodegenerative diseases. Dynamic interactions among these systems are reviewed in terms of their causative or in-tandem occurrence and how the systemic environment, –e.g., insulin resistance, diabetes, and systemic inflammation–, impacts on brain function.
Author: A.D. Roses
Publisher: Springer Science & Business Media
ISBN: 3642801099
Category : Medical
Languages : en
Pages : 208
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There is now considerable genetic evidence that the type 4 allele of the apolipoprotein E gene is a major susceptibility factor associated with late-onset Alzheimer's disease, the common form of the disease defined as starting after sixty years of age. The role of apolipoprotein E in normal brain metabolism and in the pathogenesis of Alzheimer's disease are new and exciting avenues of research. This book, written by the most outstanding scientists in this new filed, is the first presentation of results concerning the implications of apolipoprotein E on the genetics, cell biology, neuropathology, biochemistry, and therapeutic management of Alzheimer's disease.
Author: Shiri Stempler
Publisher:
ISBN:
Category :
Languages : en
Pages : 200
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Author: Wen Zhang
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Category :
Languages : en
Pages :
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"An estimated 30 million people worldwide suffer from Alzheimer’s disease (AD), a neurodegenerative disorder characterized by memory loss and progressive cognitive impairment. Despite being the focus of enormous research efforts, there remains a lack of accurate pre-mortem diagnosis and effective treatments against AD. While major discoveries have uncovered some of the important pathophysiological processes underlying this disease, such as the aggregation of amyloid protein plaques and neurofibrillary tangles in the brain, AD continues to evade detection in its pre-symptomatic stages. One of the main hallmarks of AD pathology is a decrease in glucose metabolism that originates in the hippocampus and precuneus brain structures, and eventually spreads throughout the brain. Separately, there is increasing evidence that neuroinflammation plays a role in AD pathogenesis, however it remains unclear whether neuroinflammation and altered brain metabolism are linked. Magnetic resonance spectroscopy (MRS) is a non-invasive imaging technique which can be used to study neurochemistry and brain metabolism in vivo. Specifically, Carbon-13 (13C) MRS enables quantitative assessment of cerebral metabolism such as tricarboxylic acid (TCA) cycling and glutamate/glutamine neurotransmitter cycling rates. The aim of the current study is two-fold; 1) to investigate altered brain metabolism in a rat model of AD using 13C MRS, and 2) to determine the effects, if any, of early treatment with the anti-inflammatory drug, Naproxen, on these metabolic changes. Three rat cohorts, each containing ten rats, were investigated in the study; a wild type control cohort, a transgenic cohort with no treatment, and a transgenic cohort treated with Naproxen from weaning up to 10 months of age. At 16-months of age, all three cohorts underwent 13C MRS imaging during an infusion of [1,6-13C] glucose. The rate of TCA cycle (VTCA), the glutamate-alpha–ketoglutarate exchange rate (VX), and the rate of neurotransmission (VNT) were estimated by fitting the measured time courses of fractional 13C enrichment to a metabolic model. Additionally, concentrations of seven metabolites (N-acetylaspartate, taurine, glutamate, myo-inositol, glutamine, glutathione, glycerophosphocholine (GPC), and phosphocholine (PCh)) were quantified, and concentrations of these metabolites were compared between groups. Myo-Inositol levels were found to be elevated in both untreated and treated transgenic animals relative to wild type animals, suggesting an increase in neuroinflammation. Similarly, there was a significant increase in GPC+PCh concentrations in transgenic control animal relative to wild type animals, but no significant difference was observed between wild type and treated transgenic animals. This finding suggest that AD pathology is associated with elevated levels of both myo-Inositol and GPC-PCh, but that early treatment with anti-inflammatory drugs is only effective at reversing the elevations in GPC-PCh in a persistent way. 13C MRS revealed no difference in metabolic flux rates between treated and untreated transgenic AD rats, but both groups exhibited significantly lower VTCA and VX fluxes relative to the wildtype group. The observation of decreased VTCA in the AD cohorts is consistent with previous PET-based literature of hypometabolism and the confirmation of altered TCA cycle metabolism could serve as a potential biomarker for AD. Treatment with Naproxen did not rescue the impaired metabolism in AD rats, suggesting that the metabolic impairments observed in AD are not linked to neuroinflammation"--
Author: Ralph N. Martins
Publisher: John Wiley & Sons
ISBN: 1119356792
Category : Technology & Engineering
Languages : en
Pages : 654
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Book Description
Understanding the impact of diet, exercise, genetics, and hormones on the risk and development of Alzheimer’s and other neurogenerative diseases Diet is widely known to impact on neurological function. Nevertheless, academic texts discussing this relationship are relatively few in number. This book therefore fills an important gap in the current literature. Opening with an overview of neurodegenerative diseases, particularly Alzheimer’s disease, the text then focuses on explaining the means by which glycemic control and lipid metabolism – and associated nutritional and lifestyle variables – may factor into such disorders’ prevention and treatment. An international group of experts in the fields of food science and neurodegeneration have contributed chapters that examine Alzheimer’s disease within a broad range of contexts. Offering dietary, genetic, and hormonal perspectives, the authors explore topics ranging from sugar consumption to digestive fermentation, and Alzheimer’s disease animal models to the cognition-enhancing effects of physical exercise. Also included are overviews of the latest research into current and developing methods of treatment and diagnosis, as well as differential diagnostics. This groundbreaking book: Explores how glucose metabolism, insulin resistance, lipid metabolism, and high intake of refined carbohydrates are linked to Alzheimer's disease Discusses how genetic makeup can impact risk of Alzheimer’s and Parkinson’s disease Examines cognitive changes in neurodegeneration, lists current tests for determining cognitive impairment, and provides information concerning differential diagnosis Discusses potential advantages of increasing antioxidant and micronutrient intake Reviews hormonal influences on neurodegeneration Examines the links between protein intake and Alzheimer’s disease. Neurodegeneration and Alzheimer's Disease is an essential resource for researchers, medical practitioners, dietitians, and students with an interest in neurological diseases and their diagnosis and risk factors, as well as diet-related conditions such as diabetes and obesity. Lifestyle and diet influence neurodegeneration risk, and a better understanding of this evidence amongst health professionals will hopefully lead to greater public awareness of how to reduce the likelihood of these widespread conditions.
Author: Francisco Gonzalez-Lima
Publisher: Springer Science & Business Media
ISBN: 9780306460241
Category : Medical
Languages : en
Pages : 312
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Book Description
As a satellite to the 27th meeting of the Society for Neuroscience held October 28 in New Orleans, this symposium was dedicated to Dr. Margaret T.T. Wong-Reiley, developer of the method of cytochrome oxidase histochemical mapping of metabolism in the brain, on the 20th anniversary of this breakthrough. In this first ever compilation of papers applying this technique to the study of Alzheimer's, the 22 contributors--including Dr. Wong-Reiley--overview the role of cytochrome oxidase in cellular energy metabolism and neuronal activity and the methodology for its study via specific application examples. Part II treats the hypothesis that cytochrome inhibition may predict potential neurodegeneration, through discussions of animal models and genetic vulnerability of regions of the brain. Annotation copyrighted by Book News, Inc., Portland, OR
Author: Don Kulasiri
Publisher: World Scientific
ISBN: 1800610130
Category : Medical
Languages : en
Pages : 416
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Book Description
Alzheimer's disease (AD) is the leading cause of dementia and, unfortunately, remains incurable. The social, emotional and financial implications of AD are immeasurable, and about 47 million people worldwide are affected by AD or other forms of dementia. As lifespans are improved by healthcare systems worldwide, age-associated neurodegenerative diseases are imposing an increasing challenge to science. It is becoming imperative for us to understand the causes of these diseases, AD in particular, at molecular and cellular levels. Starting with the broader picture from a biological perspective, this book takes the reader through fascinating dynamics within and outside of neurons in the brain.Alzheimer's Disease: Biology, Biophysics and Computational Models helps the reader to understand AD from mechanistic and biochemical perspectives at intra- and inter-cellular levels. It focuses on biochemical pathways and modeling associated with AD. Some of the recent research on biophysics and computational models related to AD are explained using context-driven computational and mathematical modeling and essential biology is discussed to understand the modeling research.
Author:
Publisher: Academic Press
ISBN: 012823122X
Category : Medical
Languages : en
Pages : 322
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Book Description
Metabolic Drivers and Bioenergetic Components of Neurodegenerative Disease reviews how the different aspects of metabolic dysfunction and consequent pathology associated with neurodegenerative diseases, including Alzheimer’s and Parkinson’s, can be targeted by novel treatment approaches. Topics covered include Cellular Senescence in Aging and Age-Related Disorders: Implications for Neurodegenerative Diseases; Repurposing GLP1 agonists for Neurodegenerative Diseases; Ketotherapeutics for Neurodegenerative Diseases; Enhancing Mitophagy as a Therapeutic Approach for Neurodegenerative Diseases; Harnessing Neurogenesis in the Adult Brain – A Role in Type 2 Diabetes Mellitus and Alzheimer’s disease; and much more. Summarizes the impact of the metabolic hypothesis on underlying mechanisms of neurodegenerative diseases Presents novel, potential treatment strategies based on the metabolic hypothesis for neurodegenerative diseases
