Synaptic Plasticity and the Mechanism of Alzheimer's Disease

Synaptic Plasticity and the Mechanism of Alzheimer's Disease PDF Author: Dennis J. Selkoe
Publisher: Springer Science & Business Media
ISBN: 3540763309
Category : Medical
Languages : en
Pages : 186

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Book Description
A biochemical hypothesis - that Alzheimer’s disease (AD) is a progressive cerebral amyloidosis caused by the aggregation of the amyloid b-protein (Ab) - preceded and enabled the discovery of etiologies. This volume serves as a record focused on bringing together investigators at the forefront of elucidating the structure and function of hippocampal synapses with investigators focused on understanding how early assemblies of Ab may compromise some of these synapses.

Synaptic Plasticity and the Mechanism of Alzheimer's Disease

Synaptic Plasticity and the Mechanism of Alzheimer's Disease PDF Author: Dennis J. Selkoe
Publisher: Springer Science & Business Media
ISBN: 3540763309
Category : Medical
Languages : en
Pages : 186

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Book Description
A biochemical hypothesis - that Alzheimer’s disease (AD) is a progressive cerebral amyloidosis caused by the aggregation of the amyloid b-protein (Ab) - preceded and enabled the discovery of etiologies. This volume serves as a record focused on bringing together investigators at the forefront of elucidating the structure and function of hippocampal synapses with investigators focused on understanding how early assemblies of Ab may compromise some of these synapses.

The Molecular Mechanisms of Synaptic Plasticity Impairments in Alzheimer's Disease

The Molecular Mechanisms of Synaptic Plasticity Impairments in Alzheimer's Disease PDF Author: Gong-Ping Liu
Publisher: Frontiers Media SA
ISBN: 2889744841
Category : Science
Languages : en
Pages : 147

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Book Description


Synaptic Plasticity and the Mechanism of Alzheimer's Disease

Synaptic Plasticity and the Mechanism of Alzheimer's Disease PDF Author: Dennis J. Selkoe
Publisher: Springer
ISBN: 9783540845553
Category : Medical
Languages : en
Pages : 183

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Book Description
A biochemical hypothesis - that Alzheimer’s disease (AD) is a progressive cerebral amyloidosis caused by the aggregation of the amyloid b-protein (Ab) - preceded and enabled the discovery of etiologies. This volume serves as a record focused on bringing together investigators at the forefront of elucidating the structure and function of hippocampal synapses with investigators focused on understanding how early assemblies of Ab may compromise some of these synapses.

Neuroplasticity

Neuroplasticity PDF Author: Victor Chaban
Publisher: BoD – Books on Demand
ISBN: 1789231949
Category : Medical
Languages : en
Pages : 206

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Book Description
This book provides comprehensive and up-to-date insights into emerging research trends on neuroplasticity with current or future treatments for neurodevelopment and neurodegenerative diseases. The authors discuss structural and functional changes associated with cortical remapping, sensory substitution, synaptic and non-synaptic compensatory plasticity due to brain damage, brain training, chronic pain, meditation, music, exercise and related states. Key features include pathogenesis, and existing and new therapies together with a pharmacological and non-pharmacological approach in clinical treatment and management. The authors are established experts that contributed significantly to a better understanding of the etiology of neuroplasticity. This book is recommended to healthcare providers, clinical scientists, students and patients.

Apolipoprotein E and Alzheimer’s Disease

Apolipoprotein E and Alzheimer’s Disease PDF Author: A.D. Roses
Publisher: Springer Science & Business Media
ISBN: 3642801099
Category : Medical
Languages : en
Pages : 208

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Book Description
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.

Magnesium in the Central Nervous System

Magnesium in the Central Nervous System PDF Author: Robert Vink
Publisher: University of Adelaide Press
ISBN: 0987073052
Category : Medical
Languages : en
Pages : 354

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Book Description
The brain is the most complex organ in our body. Indeed, it is perhaps the most complex structure we have ever encountered in nature. Both structurally and functionally, there are many peculiarities that differentiate the brain from all other organs. The brain is our connection to the world around us and by governing nervous system and higher function, any disturbance induces severe neurological and psychiatric disorders that can have a devastating effect on quality of life. Our understanding of the physiology and biochemistry of the brain has improved dramatically in the last two decades. In particular, the critical role of cations, including magnesium, has become evident, even if incompletely understood at a mechanistic level. The exact role and regulation of magnesium, in particular, remains elusive, largely because intracellular levels are so difficult to routinely quantify. Nonetheless, the importance of magnesium to normal central nervous system activity is self-evident given the complicated homeostatic mechanisms that maintain the concentration of this cation within strict limits essential for normal physiology and metabolism. There is also considerable accumulating evidence to suggest alterations to some brain functions in both normal and pathological conditions may be linked to alterations in local magnesium concentration. This book, containing chapters written by some of the foremost experts in the field of magnesium research, brings together the latest in experimental and clinical magnesium research as it relates to the central nervous system. It offers a complete and updated view of magnesiums involvement in central nervous system function and in so doing, brings together two main pillars of contemporary neuroscience research, namely providing an explanation for the molecular mechanisms involved in brain function, and emphasizing the connections between the molecular changes and behavior. It is the untiring efforts of those magnesium researchers who have dedicated their lives to unraveling the mysteries of magnesiums role in biological systems that has inspired the collation of this volume of work.

Alzheimer's Disease: Cellular and Molecular Aspects of Amyloid beta

Alzheimer's Disease: Cellular and Molecular Aspects of Amyloid beta PDF Author: J. Robin Harris
Publisher: Springer Science & Business Media
ISBN: 0387232265
Category : Science
Languages : en
Pages : 416

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Book Description
To understand Alzheimer's disease (AD) is one of the major thrusts of present-day clinical research, strongly supported by more fimdamental cellular, biochemical, immunological and structural studies. It is these latter that receive attention within this book. This compilation of 20 chapters indicates the diversity of work currently in progress and summarizes the current state of knowledge. Experienced authors who are scientifically active in their fields of study have been selected as contributors to this book, in an attempt to present a reasonably complete survey of the field. Inevitably, some exciting topics for one reason or another have not been included, for which we can only apologize. Standardization of terminology is often a problem in science, not least in the Alzheimer field; editorial effort has been made to achieve standardization between the Chapters, but some minor yet acceptable personal / author variation is still present, i. e. P-amyloid/amyloid-P; Ap42/Apl-42/APi. 42! The book commences with a broad survey of the contribution that the range of available microscopical techniques has made to the study of Alzheimer's amyloid plaques and amyloid fibrillogenesis. This chapter also serves as an Introduction to the book, since several of the topics introduced here are expanded upon in later chapters. Also, it is significant to the presence of this chapter that the initial discovery of brain plaques, by Alois Alzheimer, utilized light microscopy, a technique that continues to be extremely valuable in present-day AD research.

Learning, Memory, and Synaptic Plasticity in Alzheimer's Model Mice

Learning, Memory, and Synaptic Plasticity in Alzheimer's Model Mice PDF Author: Jason Knight Clark
Publisher:
ISBN:
Category :
Languages : en
Pages : 546

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Book Description
Alzheimer's disease (AD) is a neurodegenerative disease of aging thought to be initiated by production of Amyloid-[beta] peptide, which leads to synaptic dysfunction and progressive memory loss, and the eventual formation of [beta]-Amyloid plaques and neurofibrillary Tau tangles. Working memory is one of the first cognitive impairments in AD. We therefore wanted to explore the cellular mechanisms underlying working memory impairments in AD utilizing a well-known triple transgenic mouse model of Alzheimer's disease (3xTg-AD) carrying mutations in APP, PS1, and Tau. We evaluated working memory using an 8-arm radial maze, and synaptic transmission and plasticity using an ex vivo hippocampal slice preparation to measure field Excitatory Post-Synaptic Potentials (fEPSP) in the CA1 region of ventral hippocampus. Unexpectedly, young 3xTg-AD mice at 3 months of age, typically considered to be presymptomatic, were significantly impaired in the spatial working memory task compared to Nontransgenic (NonTg) control mice. Measurements of fEPSPs to evaluate Long-Term Potentiation (LTP) as an indicator of long-term synaptic plasticity showed the NMDA receptor-dependent component of LTP (NMDAR LTP) was reduced in 3xTg-AD mice compared to NonTg mice. The remaining non-NMDA receptor-dependent component of LTP (non-NMDAR LTP) however was increased, resulting in a total LTP that was not different between 3xTg-AD and NonTg mice. At 8 months of age, 3xTg-AD mice were again significantly impaired in the spatial working memory task, and NMDAR LTP was again reduced in 3xTg-AD mice. The non-NMDAR LTP however was also reduced in 3xTg-AD mice, resulting in a total LTP that was now reduced in 3xTg-AD mice. The majority (>90%) of non-NMDAR LTP is mediated by Voltage-Dependent Calcium Channels (VDCC), and attempts to block LTP using NMDAR and VDCC antagonists were unsuccessful, indicating 3xTg-AD mice have compensatory mechanisms for LTP expression that occur independently of NMDAR or non-NMDAR dependent mechanisms. In addition, 3xTg-AD mice also showed impairments in short-term synaptic plasticity and basal synaptic transmission at both 3 and 8 months of age. These impairments in synaptic transmission and plasticity coincide with impairments in spatial working memory, and understanding the nature of these altered mechanisms may lead to therapeutic targets for disorders such as AD.

The Neurobiology of Alzheimer's Disease

The Neurobiology of Alzheimer's Disease PDF Author: Study Group on the Pharmacology of Memory Disorders Associated with Aging. Meeting
Publisher:
ISBN:
Category : Medical
Languages : en
Pages : 460

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Book Description
The overall goal of the International Study Group on the Pharmacology of Memory Disorders Associated with Ageing is to point out discoveries that shed light on the potential causes of Alzheimer's disease, its pathogenesis, and the biological mechanisms that could underlie its cure. This eighth meeting in the series, aims to stimulate research in dementia and increase the transfer of information from the basic sciences to physicians and the pharmaceutical industry."

Genes, Environment and Alzheimer's Disease

Genes, Environment and Alzheimer's Disease PDF Author: Orly Lazarov
Publisher: Academic Press
ISBN: 0128028858
Category : Psychology
Languages : en
Pages : 449

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Book Description
Genes, Environment and Alzheimer's Disease discusses the role that activities such as exercise can play in cardiovascular health, while also highlighting the fact that the last 10 years have brought great discoveries in the strong environmental component of brain disorders, neurodegeneration, and cognitive decline. It is now clear that brain insult is an environmental risk factor for AD, while on the other hand, lifestyle components such as exercise and level of education may play a protective role, delaying the onset and/or severity of the disease. Evidence from experiments in rodent models of Alzheimer’s disease contributes major insight into the molecular mechanisms by which the environment plays its role in AD. Additionally, there are diseases related to lifestyle that may lead to AD. This volume reviews new discoveries related to all these factors, serving as a translational tool for clinicians and researchers interested in genetic and environmental risk factors for the disease. Provides the first volume to link genetic and environmental risk factors for Alzheimer’s disease and dementia Aids researchers and clinicians in understanding the basic mechanisms of Alzheimer’s disease and cognitive decline Brings the basic science and clinical perspectives together in a single volume, facilitating translational possibilities Includes a range of molecular to behavioral components assembled into a single volume that creates an excellent resource for basic and clinical neuroscientists