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Behavioral Neurogenetics

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Cover of 'Behavioral Neurogenetics'

Table of Contents

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    Book Overview
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    Chapter 178 Behavioural Genetics of Childhood Disorders.
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    Chapter 179 Rare Genomic Deletions and Duplications and their Role in Neurodevelopmental Disorders
  4. Altmetric Badge
    Chapter 180 Using Zebrafish to Unravel the Genetics of Complex Brain Disorders
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    Chapter 181 Behavioral Genetics of Neurodegenerative Disorders.
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    Chapter 182 Toward a Mechanistic Understanding of How Variability in Neurobiology Shapes Individual Differences in Behavior.
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    Chapter 183 Schizophrenia Genes: On the Matter of Their Convergence.
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    Chapter 184 Gene × Environment Interaction Models in Psychiatric Genetics
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    Chapter 185 Behavioral Genetics of Affective and Anxiety Disorders
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    Chapter 186 Behavioural Genetics of the Serotonin Transporter.
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    Chapter 187 Genetic Factors Modulating the Response to Stimulant Drugs in Humans
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    Chapter 188 The Cognitive Genetics of Neuropsychiatric Disorders
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    Chapter 189 Forward Genetic Approaches to Understanding Complex Behaviors
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    Chapter 190 Mouse Models of the 5-HTTLPR × Stress Risk Factor for Depression
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    Chapter 191 Behavioral and Pharmacogenetics of Aggressive Behavior
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    Chapter 192 Selectively Bred Rodents as Models of Depression and Anxiety
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    Chapter 193 Stress-Induced Deficits in Cognition and Emotionality: A Role for Glutamate
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    Chapter 194 Susceptibility Genes for Schizophrenia: Mutant Models, Endophenotypes and Psychobiology
  19. Altmetric Badge
    Chapter 195 Genetic Models of Sensorimotor Gating: Relevance to Neuropsychiatric Disorders
  20. Altmetric Badge
    Chapter 196 Applications of Second Generation Sequencing Technologies in Complex Disorders
Attention for Chapter 181: Behavioral Genetics of Neurodegenerative Disorders.
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Chapter title
Behavioral Genetics of Neurodegenerative Disorders.
Chapter number 181
Book title
Behavioral Neurogenetics
Published in
Current topics in behavioral neurosciences, January 2012
DOI 10.1007/7854_2011_181
Pubmed ID
Book ISBNs
978-3-64-227858-7, 978-3-64-227859-4
Authors

Galimberti D, Scarpini E, Daniela Galimberti, Elio Scarpini, Galimberti, Daniela, Scarpini, Elio

Abstract

Alzheimer's disease (AD) is the most common cause of dementia in the elderly, and is typically characterized by memory loss. In addition, during the disease progression, most patients develop behavioural and psychiatric symptoms of dementia (BPSD). Frontotemporal Lobar Degeneration (FTLD) is the most frequent neurodegenerative disorder with a presenile onset. It is characterized mainly by behavioural disturbances, whereas memory is conserved. The two major neuropathologic hallmarks of AD are extracellular Amyloid beta (Ab) plaques and intracellular neurofibrillary tangles (NFTs). Conversely, in FTLD the deposition of tau has been observed in a number of cases, but in several brains there is no deposition of tau but instead a positivity for ubiquitin. In some families these diseases are inherited in an autosomal dominant fashion. Genes responsible for familial AD include the Amyloid Precursor Protein (b-APP), Presenilin 1 (PS1)and Presenilin 2 (PS2). The majority of mutations in these genes are often associated with a very early onset (40–50 years of age). Regarding FTLD, the first mutations described are located in the Microtubule Associated Protein Tau gene(MAPT). Tau is a component of microtubules, which represent the internal support structures for the transport of nutrients, vesicles, mitochondria and chromosomes within the cell. Mutations in MAPT are associated with an early onset of the disease (40–50 years), and the clinical phenotype is consistent with Frontotemporal Dementia (FTD). Recently, mutations in a second gene, named progranulin(GRN), have been identified in some families with FTLD. The pathology associated with these mutations is most frequently characterized by the immunostaining of TAR DNA Binding Protein 43 (TDP-43), which is a transcription factor. The clinical phenotype associated with GRN mutations is highly heterogeneous,including FTD, Progressive Aphasia, Corticobasal Syndrome, and AD. Age at disease onset is variable, ranging from 45 to 85 years of age. The majority of cases of AD and FTLD are however sporadic, and likely several genetic and environmental factors contribute to their development. Concerning AD, it is known that the presence of the e4 allele of the Apolipoprotein E gene is a susceptibility factor,increasing the risk of about 4 fold. A number of additional genetic factors,including cytokines, chemokines, Nitric Oxide Synthases, contribute to the susceptibility for the disease. Some of them also influence the risk to develop FTLD.Variability in serotonin transporter gene could influence the development of BPSD. In this chapter, current knowledge on molecular mechanisms at the basis of AD and FTLD, as well as the role of genetics, will be presented and discussed.

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Mendeley readers

The data shown below were compiled from readership statistics for 51 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 51 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 9 18%
Researcher 8 16%
Student > Master 6 12%
Other 5 10%
Professor 4 8%
Other 9 18%
Unknown 10 20%
Readers by discipline Count As %
Agricultural and Biological Sciences 10 20%
Medicine and Dentistry 9 18%
Neuroscience 6 12%
Biochemistry, Genetics and Molecular Biology 5 10%
Pharmacology, Toxicology and Pharmaceutical Science 2 4%
Other 8 16%
Unknown 11 22%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 22 January 2015.
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#13,719,522
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Outputs from Current topics in behavioral neurosciences
#309
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#234,212
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Outputs of similar age from Current topics in behavioral neurosciences
#28
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