To see the other types of publications on this topic, follow the link: Genetics factors associated to FTLD.
Books on the topic 'Genetics factors associated to FTLD'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 17 books for your research on the topic 'Genetics factors associated to FTLD.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse books on a wide variety of disciplines and organise your bibliography correctly.
1
Maes, Dominiek, Marina Sibila, and Maria Pieters, eds. Mycoplasmas in swine. CABI, 2021. http://dx.doi.org/10.1079/9781789249941.0000.
Full textAbstract:
Abstract This book contains 14 chapters that discuss the genetics, epidemiology, prevalence, pathogenesis, clinical signs, diagnosis, treatment, prevention and control of Mycoplasma infections in pigs. Chapter 1 discusses the phylogenetics and classification of Mycoplasma species in pigs; Chapter 2 describes the genomic diversity and antigenic variation of Mycoplasma hyopneumoniae strains; Chapter 3 discusses the pathogenesis, virulence factor and pathogenicity of Mycoplasma hyopneumoniae; Chapter 4 discusses the molecular epidemiology, risk factors, transmission and prevalence of Mycoplasma hyopneumoniae, Chapter 5 discusses the clinical signs and gross lesions of Mycoplasma hyopneumoniae infection; Chapter 6 discusses immune responses against Mycoplasma infections; Chapter 7 describes the interactions of Mycoplasma hyopneumoniae with other pathogens and their economic impact; Chapter 8 discusses the diagnosis of Mycoplasma hyopneumoniae infection and its associated diseases; Chapter 9 describes the general control measures against Mycoplasma hyopneumoniae infections; Chapter 10 describes the selection and efficacy of antimicrobials against Mycoplasma hyopneumoniae infections; Chapter 11 discusses the development and efficacy of vaccines against Mycoplasma hyopneumoniae; Chapter 12 describes the eradication of Mycoplasma hyopneumoniae in pig herds; Chapter 13 describes the epidemiology, prevalence, pathogenesis, clinical signs, diagnosis, treatment, prevention and control of Mycoplasma hyorhinis and Mycoplasma hyosynoviae in pig herds and Chapter 14 discusses the epidemiology, prevalence, transmission, pathogenesis, clinical signs, diagnosis, treatment, prevention, control and economic impact of Mycoplasma suis infection in pigs.
2
(Editor), Sankar Adhya, and Susan Garges (Editor), eds. RNA Polymerase and Associated Factors, Part C, Volume 370 (Methods in Enzymology). Academic Press, 2003.
3
Pezzini, Alessandro. Genetics. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0011.
Full textAbstract:
Ischaemic stroke is a heterogeneous multifactorial disorder. Although epidemiological data from twin and family studies provide substantial evidence for a genetic basis for stroke, the contribution of genetic factors identified so far is small. Large progress has been made in single-gene disorders associated with ischaemic stroke, particularly at young age. By contrast, little is known about the genes associated with multifactorial stroke. The reported genome-wide association studies of ischaemic stroke have shown that no single common genetic variant imparts major risk, but data on early-onset disease are scarce in this regard. Larger studies with samples numbering in the thousands are ongoing to identify common variants with smaller effects on risk. This approach, in addition with new analytic techniques, will likely contribute to the identification of additional genes, novel pathways, and eventually novel therapeutic approaches to cerebrovascular disorders in the near future. The aims of this review are to summarize data on clinical, genetic, and epidemiologic aspects of monogenic conditions associated with juvenile ischaemic stroke, to discuss recent findings and methodological limitations regarding the genetics of sporadic ischaemic stroke in this age category, and to provide a brief overview of the potential future approaches to stroke genetics.
4
Levinson, Douglas F., and Walter E. Nichols. Genetics of Depression. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0024.
Full textAbstract:
Major depressive disorder (MDD) is a common and heterogeneous complex trait. Twin heritability is 35%–40%, perhaps higher in severe/recurrent cases. Adverse life events (particularly during childhood) increase risk. Current evidence suggests some overlap in genetic factors among MDD, bipolar disorder, and schizophrenia. Large genome-wide association studies (GWAS) are now proving successful. Polygenic effects of common SNPs are substantial. Findings implicate genes with effects on synaptic development and function, including two obesity-associated genes (NEGR1 and OLFM4), but not previous “candidate genes.” It can now be expected that larger GWAS samples will produce additional associations that shed new light on MDD genetics.
5
Brown, Matthew. Genetics of spondyloarthropathies. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0041.
Full textAbstract:
Spondyloarthropathies are a diverse group of conditions, of which ankylosing spondylitis is the prototypic disease, with shared clinical features, genetic risk factors, and histopathological characteristics. These conditions are highly familial and heritable. Several genes have been associated with spondyloarthropathies, with genes in the IL-23 signalling pathway being shared by the major types of spondyloarthritis. These discoveries have already led to the development and successful clinical introduction of novel treatments for psoriasis and psoriatic arthritis, and major advances in our understanding of the pathogenesis of the conditions. Many more genes remain to be identified which are involved in these common conditions; identifying these genes is likely to be highly informative as to their causes.
6
Brown, Matthew. Genetics of spondyloarthropathies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0041_update_003.
Full textAbstract:
Spondyloarthropathies are a diverse group of conditions, of which ankylosing spondylitis is the prototypic disease, with shared clinical features, genetic risk factors, and histopathological characteristics. These conditions are highly familial and heritable. Several genes have been associated with spondyloarthropathies, with genes in the IL-23 signalling pathway being shared by the major types of spondyloarthritis. These discoveries have already led to the development and successful clinical introduction of novel treatments for psoriasis and psoriatic arthritis, and major advances in our understanding of the pathogenesis of the conditions. Many more genes remain to be identified which are involved in these common conditions; identifying these genes is likely to be highly informative as to their causes.
7
Bekris, Lynn M., and James B. Leverenz. Genetics of Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0010.
Full textAbstract:
A great deal has been discovered about Neurodegenerative disorders (NDDs) including Alzheimer’s disease, Parkinson’s disease, frontotemporal dementia, dementia with Lewy bodies . This includes genetic variants associated with both sporadic and autosomal dominant NDDs. These findings have been crucial in our understanding the underlying factors that drive neuropathological changes and in clarifying the time line of biomarker changes in presymptomatic autosomal dominant mutation carriers. While much is still to be learned, these findings will play an important role in the future of neurodegenerative prediction, diagnosis, and treatment. This chapter summarizes the current genetic knowledge related to both the sporadic and autosomal dominant forms of neurodegenerative disease.
8
Reichborn-Kjennerud, Ted, and Kenneth S. Kendler. Genetics of Personality Disorders. Edited by Christian Schmahl, K. Luan Phan, Robert O. Friedel, and Larry J. Siever. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199362318.003.0003.
Full textAbstract:
This chapter reviews the evidence for genetic contributions to the etiology of personality disorders (PDs) as defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM; 5th ed.). This approach and some of the controversial issues associated with its development are briefly described in the first section. The second section evaluates the evidence for genetic influence on DSM PDs from family and twin studies using quantitative genetic methods. Studies that move beyond individual PDs are also reviewed, together with studies on the extent to which common genetic factors influence PDs and normal personality traits and PDs and pathological personality trait domains. Stability of genetic influences on PDs over time are also examined. Molecular genetic studies are reviewed in the third section. The fourth section deals with gene environment interplay, and the final section discusses future directions in the exploration of genetic influences on PDs.
9
Eyre, Steve, and Jane Worthington. Genetics of rheumatoid arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0040.
Full textAbstract:
A range of epidemiological studies have clearly established that susceptibility to rheumatoid arthritis (RA) is determined by both genetic and environmental factors. Studies over the last five decades have used a variety of approaches to identify the genetic variants associated with disease. HLA DRB1 was the first RA susceptibility locus to be discovered and has the largest effect size. We describe current understanding of the complexities of HLA association for RA. Linkage and small-scale association studies prior to 2007 provided convincing evidence for only one more RA susceptibility locus, PTPN22. Major breakthroughs in high-throughput genotyping and systematic discovery and mapping of hundreds of thousands of single nucleotide polymorphisms (SNPs) led to large-scale genome-wide association studies used for the first time for RA in 2007. This approach has had a dramatic impact on our knowledge of the susceptibility loci for RA, such that over 60 risk variants have now been robustly identified. We present an overview of these studies and the loci that have been identified. We consider how this knowledge is contributing to a greater understanding of the aetiology and pathology of the disease and in turn how this can influence management of patients presenting with an inflammatory arthritis. We consider some of the unanswered questions and the approaches that will need to be taken to address them.
10
Eyre, Steve, Jane Worthington, and Sebastien Viatte. Genetics of rheumatoid arthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0040_update_003.
Full textAbstract:
A range of epidemiological studies have clearly established that susceptibility to rheumatoid arthritis (RA) is determined by both genetic and environmental factors. Studies over the last five decades have used a variety of approaches to identify the genetic variants associated with disease. HLA DRB1 was the first RA susceptibility locus to be discovered and has the largest effect size. We describe current understanding of the complexities of HLA association for RA. Linkage and small-scale association studies prior to 2007 provided convincing evidence for only one more RA susceptibility locus, PTPN22. Major breakthroughs in high-throughput genotyping, and systematic discovery and mapping of hundreds of thousands of single nucleotide polymorphisms (SNPs) led to large-scale genome-wide association studies used for the first time for RA in 2007. Widespread utilization of this approach has had a dramatic impact on our knowledge of the susceptibility loci for RA, such that over 100 risk variants have now been robustly identified. We present an overview of these studies and the loci that have been identified. We consider how this knowledge is contributing to a greater understanding of the aetiology and pathology of the disease, and in turn how this can influence management of patients presenting with an inflammatory arthritis. We consider some of the unanswered questions and the approaches that will need to be taken to address them.
11
McCurdy-McKinnon, Danyale, and Jamie D. Feusner. Neurobiology of Body Dysmorphic Disorder : Heritability/Genetics, Brain Circuitry, and Visual Processing. Edited by Katharine A. Phillips. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190254131.003.0020.
Full textAbstract:
This chapter covers studies addressing neurobiologic factors that may contribute to body dysmorphic disorder (BDD). There are indications that neurobiologic abnormalities are associated with symptoms in BDD. This includes evidence that the susceptibility for BDD may be partly heritable and that there may be shared genetic factors among the obsessive-compulsive and related disorders (of which BDD is a member) as a group. In addition, studies of brain circuitry in BDD implicate white matter and structural connectivity abnormalities as playing possible roles in the pathophysiology of BDD. Furthermore, studies of visual processing suggest that disturbances in visual perception and visuospatial information processing, characterized by heightened attention to detail and impairment in holistic and global assessment, are also contributory.
12
Tackett, Jennifer L., Avantè J. Smack, and Kathleen W. Reardon. Examining Relational Aggression in an Individual Differences Context. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190491826.003.0010.
Full textAbstract:
Individual differences, such as normal-range personality, personality pathology, and genetics (specifically behavioral genetics), are variables or constructs that can be used to distinguish people. Individual differences have also been used to understand differences in antisocial behavior, including relational aggression, and can help inform the scientific conceptualization of this behavior. This chapter summarizes evidence for individual differences in relational aggression in three dimensions: normal-range personality, personality pathology, and behavioral genetics. Relationally aggressive behaviors are associated with normal-range personality traits, including high negative affect and low interpersonal and intrapersonal self-regulation. Relational aggression also overlaps with personality pathology. With regard to genetics, relational aggression can be explained by genetic factors and also shows substantial influences from environmental factors. Taken together, relational aggression is probably influenced by a number of internal and external factors, and individual differences research highlights potential heterogeneity in the construct.
13
Sampaio-Barros, Percival, and Rafael Valle-Oñate. Axial spondyloarthritis in Latin America. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0029.
Full textAbstract:
Latin American countries are often characterized by a significant miscegenation among whites, blacks, and Amerindians. These heterogeneous populations frequently represent a challenge for the design of studies analysing the genetics, incidence, and prevalence of rheumatic diseases. In this setting, axial spondyloarthritis (axSpA) frequently shows an increased associated peripheral involvement, compared with the homogeneous population. Genetic and socioeconomic factors can be associated with this clinical presentation, although further studies are necessary to confirm this hypothesis. Regarding treatment, Latin American spondyloarthritis (SpA) patients also show a higher prescription of corticosteroids, methotrexate, and sulfasalazine than European series. This chapter presents and discusses the many aspects related to the presentation of axSpA in Latin America.
14
Brugha, Traolach S. History and development of the concept of autism. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198796343.003.0001.
Full textAbstract:
This first chapter covers autism definitions, concepts of autism, of atypical and typical development, and the valuable idea of neuro-diversity. The historical emergence of autism is then described including the contributions of Kanner, Asperger, and Wing, the autism triad, and autism as a spectrum condition. Current official definitions are then introduced. The development of clinical research is then considered. A section on the factors associated with autism in adulthood follows. Manifestations in the population, and epidemiology from birth to old age are set out. Psychiatric epidemiology and psychiatric genetics, and the testing of disease concepts are introduced briefly.
15
Saraiya, Ami, Deep Joshipura, and Alice Gottlieb. Psoriasis treatment. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0026.
Full textAbstract:
Psoriasis is an immune-mediated skin disease that is associated with various factors, including genetics, stress, infections, and environmental triggers. Numerous treatment options exist for plaque psoriasis including topical therapy, phototherapy, systemic therapy, and biological therapy. In order to select a treatment for a patient, a clinician must consider many aspects. First, one must assess the impact and burden of the disease on a patient as well as a patient’s expectations from therapy. Other important factors to consider include the severity of skin disease, location of psoriatic plaques, comorbidities and presence of psoriatic arthritis, efficacy of different treatments, potential side-effects, safety, and cost. In this chapter, an evidence-based review is presented on the treatment armamentarium for psoriasis as well as new biological treatments and those under investigation. In order to guide practitioners, several treatment algorithms are provided and others are referenced from the literature.
16
Doherty, Anne. The biological basis of adjustment disorders (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198786214.003.0005.
Full textAbstract:
The biological basis of adjustment disorders examines the evidence for the biological factors associated with this common diagnosis. Although adjustment disorder is usually characterized as a disorder of psychological adjustment to life stressors, and while it shares overlapping psychopathology with both normal stress response and with major depression, there is evidence that the diagnosis may have pathophysiological characteristics that distinguish it from both. This chapter explores the evidence supporting underlying theories derived from diverse fields including genetics, neuroimaging, and neuroendocrine and neurotransmitter functioning, and considers how the pharmacological management of adjustment disorder is linked to said theories. It discusses the gaps in our knowledge and considers the causes for the relative lack of interest in this diagnosis compared with other diagnoses.
17
McBurney, John W. Pesticides and Neurodegenerative Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190490911.003.0008.
Full textAbstract:
Neurodegenerative diseases, which are characterized by neuronal degeneration, include Alzheimer disease (AD), Parkinson disease (PD), and amyotrophic lateral sclerosis (ALS). Their worldwide prevalence is increasing as the global population ages. The causes reflect interactions between genetics and environmental factors such as increasing urbanization, industrialization, and widespread use of chemicals, including insecticides, fungicides, and herbicides. Epidemiologic data suggest that exposure to many of these pesticides increases the risk of neurodegeneration. The best-defined mechanism for this association is mitochondrial toxicity resulting in increased reactive oxygen species. In PD and AD, the associated accumulation of aggregates of insoluble, misfolded proteins results in the formation of Lewy bodies and neurofibrillary tangles, respectively. Pesticide exposures can be reduced by modifying food choices and applying integrated pest management in schools, businesses, and homes. Medical professionals can counsel patients about limiting exposure to pesticides and decreasing the risk of neurodegenerative disorders.