Molecular Mechanisms of Dementia / Edition 1

Molecular Mechanisms of Dementia / Edition 1

ISBN-10:
0896033716
ISBN-13:
9780896033719
Pub. Date:
11/01/1996
Publisher:
Springer-Verlag New York, LLC
ISBN-10:
0896033716
ISBN-13:
9780896033719
Pub. Date:
11/01/1996
Publisher:
Springer-Verlag New York, LLC
Molecular Mechanisms of Dementia / Edition 1

Molecular Mechanisms of Dementia / Edition 1

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Overview

The past decade has witnessed a revolution in the attempts of scientists to understand the molecular basis of dementia. Although dementia, as defined by global cogni­ tive decline involving gradual loss of memory, reasoning, judgment, and orientation, presents most commonly in the form of Alzheimer's disease (AD), an assortment of other less common disorders, such as prion and Pick's disease, can also lead to symp­ toms that are similar to those observed in patients with AD. The primary goal of Molecular Mechanisms of Dementia is to address the various mechanisms and multi­ faceted approaches currently being employed to more clearly delineate the etiological and pathogenic events responsible for the onset of dementia. Perhaps the greatest boon to obtaining a clearer understanding of the causes of AD has come from genetic and molecular biological studies carried out over the past decade. At the genetic level, it has become increasingly clear that AD is a heteroge­ neous disorder that can be broadly classified into two categories. "Late onset" (>60 yr) cases, which account for the vast majority of AD, genetically involve "susceptibility" genes representing risk factors for the disease (e. g. , inheritance of the 84 allele of the Apolipoprotein E gene). In many cases, the susceptibility gene can act as a "modifier" that modulates the pathogenic cascade occurring subsequent to a separate etiological event "initiating" or "causing" the disorder.

Product Details

ISBN-13: 9780896033719
Publisher: Springer-Verlag New York, LLC
Publication date: 11/01/1996
Series: Contemporary Neuroscience
Edition description: 1997
Pages: 312
Product dimensions: 7.01(w) x 10.00(h) x 0.04(d)

About the Author

Wasco, Wilma (Massachusetts General Hospital); Tanzi, Rudolph E. (Massachusetts General Hospital)

The contributors represent the specialties of neurology, pharmacology, genetics and aging research, Alzheimer's disease research, anatomy and neurobiology, chemistry, and pathology. Most are from universities, research institutes, and academic hospitals in the U.S., Italy, Canada, and the U.K. Institutions prominently represented include Univ of Kentucky, UC-Irvine, Univ of Western Ontario, Case Western Reserve Univ, Massachusetts General Hospital, and Univ of Arkansas for Medical Sciences.

Table of Contents

1 Etiological Clues from Gene Defects Causing Early Onset Familial Alzheimer’s Disease.- 2 Potential Biological Mechanisms of ApoE in Alzheimer’s Disease.- 3 Understanding the Biology and Molecular Pathogensis of Alzheimer’s Disease in Transgenic Mice Expressing Amyloid Precursor Proteins.- 4 Mechanism for—-Amyloid Overproduction in Alzheimer Disease: Possible Antisense RNA-Mediated Generation of a 5?-Truncated?APP mRNA Encoding 12-kDa C-Terminal Fragment of—APP, the Immediate Precursor of A?.- 5 Apoptosis and Alzheimer’s Disease.- 6 The—-Amyloid Model of Alzheimer’s Disease: Conformation Change, Receptor Cross-Linking, and the Initiation of Apoptosis.- 7 Energy/Glucose Metabolism in Neurodegenerative Diseases.- 8 Calcium Homeostasis and Free Radical Metabolism as Convergence Points in the Pathophysiology of Dementia.- 9—-Amyloid-Derived Free Radical Oxidation: A Fundamental Process in Alzheimer’s Disease.- 10 Inflammatory Pathways: Implications in Alzheimer’s Disease.- 11 Inflammatory Mediators in Alzheimer’s Disease.- 12— Protein and the Neurofibrillary Pathology of Alzheimer’s Disease.- 13 Anatomy of Pathological Alterations in Alzheimer’s Disease.- 14 Cerebral Zinc Metabolism in Alzheimer’s Disease.- 15 Potassium Channels and Calcium Release: Pat ho physiological and Diagnostic Implications for Alzheimer’s Disease.- 16 Pick Disease.- 17 Ischemia.- 18 Prion Diseases and Dementia.
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