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Alzheimer’s Disease (Record no. 503563)

000 -LEADER
fixed length control field 05320nam a22005295i 4500
001 - CONTROL NUMBER
control field 978-0-387-35135-3
003 - CONTROL NUMBER IDENTIFIER
control field DE-He213
005 - DATE AND TIME OF LATEST TRANSACTION
control field 20161121230746.0
007 - PHYSICAL DESCRIPTION FIXED FIELD--GENERAL INFORMATION
fixed length control field cr nn 008mamaa
008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION
fixed length control field 100301s2007 xxu| s |||| 0|eng d
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 9780387351353
-- 978-0-387-35135-3
024 7# - OTHER STANDARD IDENTIFIER
Standard number or code 10.1007/978-0-387-35135-3
Source of number or code doi
050 #4 - LIBRARY OF CONGRESS CALL NUMBER
Classification number RC321-580
072 #7 - SUBJECT CATEGORY CODE
Subject category code PSAN
Source bicssc
072 #7 - SUBJECT CATEGORY CODE
Subject category code MED057000
Source bisacsh
082 04 - DEWEY DECIMAL CLASSIFICATION NUMBER
Classification number 612.8
Edition number 23
245 10 - TITLE STATEMENT
Title Alzheimer’s Disease
Medium [electronic resource] :
Remainder of title Advances in Genetics, Molecular and Cellular Biology /
Statement of responsibility, etc. edited by Sangram S. Sisodia, Rudolph E. Tanzi.
264 #1 - PRODUCTION, PUBLICATION, DISTRIBUTION, MANUFACTURE, AND COPYRIGHT NOTICE
Place of production, publication, distribution, manufacture Boston, MA :
Name of producer, publisher, distributor, manufacturer Springer US,
Date of production, publication, distribution, manufacture, or copyright notice 2007.
300 ## - PHYSICAL DESCRIPTION
Extent X, 286 p. 24 illus., 5 illus. in color.
Other physical details online resource.
336 ## - CONTENT TYPE
Content type term text
Content type code txt
Source rdacontent
337 ## - MEDIA TYPE
Media type term computer
Media type code c
Source rdamedia
338 ## - CARRIER TYPE
Carrier type term online resource
Carrier type code cr
Source rdacarrier
347 ## - DIGITAL FILE CHARACTERISTICS
File type text file
Encoding format PDF
Source rda
505 0# - FORMATTED CONTENTS NOTE
Formatted contents note The Genetics of Alzheimer’s Disease -- APP Biology, Processing and Function -- The Biology of the Presenilin Complexes -- ?-secretase: Physiological Role and Target Validation -- Cognitive Impairment in Transgenic A? and Tau Models of Alzheimer’s Disease -- Cholesterol and ?-Amyloid -- A? Structure and Aggregation -- Signaling Mechanisms that Mediate A? Induced Neuronal Dysfunction -- Beta Amyloid and Excitatory Synapses -- A? Degradation -- Role of A ? Transport and Clearance in the Pathogenesis and Treatment of Alzheimer’s Disease -- Tau Gene Mutations in FTDP-17 Syndromes -- Animal Models of Tauopathy -- Tau and Axonal Transport -- Growth Factors in Alzheimer’s Disease.
520 ## - SUMMARY, ETC.
Summary, etc. Alzheimer’s Disease: Advances in Genetics, Cellular and Molecular Biology provides exciting, comprehensive and up-to-date summaries of the most important recent advances in the genetic, molecular, biochemical, and cell biological studies of AD. The studies and advances described in this volume will help to accelerate the process of rational drug discovery and soon serve to extend and enhance the mental health and lifespan of our burgeoning elderly population. In 1906, Dr. Alois Alzheimer presented the case of his patient, Auguste D., a 51 year-old female admitted to the local asylum who presented with early memory impairments, psychoses, hallucinations and morbid jealousy. Dr. Alzheimer would argue that specific lesions that were present in and around neurons were responsible for dementia. In the ensuing decades, studies of the disorder that affected Auguste D., which would be named Alzheimer’s disease (AD), were largely limited to descriptive neuropathological and psychological assessments of this disease, but with little understanding of the molecular and cellular mechanisms underlying neurodegeneration and dementia. This would change in the 1980s when the protein components of the major neuropathological hallmarks of the disease, senile plaques (and cerebral blood vessel amyloid) and neurofibrillary tangles were first determined. The identification of the ß-amyloid protein (Aß) and the microtubule-associated tau protein as the main components of plaques and tangles, respectively, would pave the way for the molecular genetic era of AD research. By the late-1980s, the genes encoding the ß-amyloid precursor protein (APP) and tau (MAPT) were identified and would subsequently be shown to harbor autosomal dominant mutations causing early-onset familial AD and frontal temporal dementia (FTD), respectively. In the early 1990s, the e4 variant of the apoliprotein E gene (APOE) would be found to be associated with increased risk for late-onset AD. APP mutations increased the generation and subsequent deposition of the neurotoxic peptide, Aß42, in brain while APOE-e4 affected aggregation of Aß into fibrils and its clearance from brain. In 1995, genes encoding presenilin 1 and 2 (PSEN1, PSEN2) were identified, and mutations in MAPT were linked to frontal temporal dementia. Thus, by 1995, the stage was set for molecular studies of age-related dementias with APP, presenilin 1 and 2, APOE, and tau playing the major roles. The vast majority of studies addressing the molecular mechanisms underlying dementia would continue to focus on characterizing the five genes already firmly implicated in the etiology and pathogenesis of these dementing disorders, and these efforts have provided a firm foundation for translational studies that will hopefully serve to take these findings from the bench top to the bedside designing and developing novel ways to diagnose, treat, and prevent these diseases.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element Medicine.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element Neurosciences.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element Pharmacology.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element Geriatrics.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element Neurology.
650 #0 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element Neurobiology.
650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element Biomedicine.
650 24 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element Neurosciences.
650 24 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element Neurobiology.
650 24 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element Neurology.
650 24 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element Pharmacology/Toxicology.
650 24 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element Geriatrics/Gerontology.
650 24 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element Medicine/Public Health, general.
700 1# - ADDED ENTRY--PERSONAL NAME
Personal name Sisodia, Sangram S.
Relator term editor.
700 1# - ADDED ENTRY--PERSONAL NAME
Personal name Tanzi, Rudolph E.
Relator term editor.
710 2# - ADDED ENTRY--CORPORATE NAME
Corporate name or jurisdiction name as entry element SpringerLink (Online service)
773 0# - HOST ITEM ENTRY
Title Springer eBooks
776 08 - ADDITIONAL PHYSICAL FORM ENTRY
Relationship information Printed edition:
International Standard Book Number 9780387351346
856 40 - ELECTRONIC LOCATION AND ACCESS
Uniform Resource Identifier http://dx.doi.org/10.1007/978-0-387-35135-3
912 ## -
-- ZDB-2-SBL
Holdings
Withdrawn status Lost status Damaged status Not for loan Permanent Location Current Location Date acquired Barcode Date last seen Price effective from Koha item type
        PK Kelkar Library, IIT Kanpur PK Kelkar Library, IIT Kanpur 2016-11-21 EBK3850 2016-11-21 2016-11-21 E books

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