By Roger N. Rosenberg, Stanley Prusiner MD, Salvatore DiMauro MD, Robert L. Barchi MD PhD, Eric J. Nestler
One hundred ten of the world's most excellent professionals discover the most recent advances in molecular and mobile neurobiology and molecular neurogenetics and their implications for the advance of pharmacologic or gene treatment for sufferers with genetic illnesses of the fearful approach. The third version encompasses a new part on psychiatric illnesses, 26 extra new chapters, and a fair more suitable scientific concentration, providing useful counsel on a whole variety of illnesses and the jobs that molecular biology and genetics play of their analysis and management.the most modern advances in molecular research.
- Includes a brand-new part on Psychiatric illnesses, edited through Dr. Eric J. Nestler, that includes chapters on demanding situations in Psychiatric Genetics · melancholy · Bipolar problems · Schizophrenia · Obsessive-Compulsive illness and Tourette's Syndrome · Molecular and Genetic foundation of habit · and Autism.
- Offers new chapters on Degenerative illnesses and Protein Processing and Prion ailments, authored through Dr. Stanley B. Prusiner, winner of the 1997 Nobel Prize in medication for his study defining the molecular and genetic foundation of the spongiform encephalopathies and the expression of the prion gene lower than either physiologic and pathologic conditions.
- Incorporates new facts and insights from the research and sequencing of the human genome into 3 new chapters at the Human Genome undertaking and Neurological illness, Gene treatment, and moral concerns in prognosis and Therapy.
- Features 21 extra new chapters: Animal versions (mice, worms, flies) · Gene Targeting/Gene Mapping · Genotype/Phenotype Correlations · Mitochondrial problems because of Mutations within the Nuclear Genome · Mitochondria in Neurodegenerative issues · Lysosomal Membrane issues - LAMP-2 Deficiency · Alzheimer's sickness and comparable Dementias · circulation issues · Neuronopathies · Limb Girdle Muscular Dystrophies · Congenital Myopathies · Hereditary Inclusion - physique Myopathies · Facioscapulohumeral Muscular Dystrophy · The Phakomatoses: problems of dermis and mind · ailment of Galactose Metabolism · problems of Glucose shipping · Congenital issues of Glycosylation · problems of Glutathione Metabolism · Friedreich Ataxia and Iron Metabolism · The effect of Alpha Tocopherol, Caloric limit and Genes on lifestyles Span · and A Neurologic Gene Map.
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Extra info for The Molecular and Genetic Basis of Neurologic and Psychiatric Disease
Example text
Nat Genet. 1999;23: 471â 473. 8Brown LY, Brown SA. Alanine tracts: the expanding story of human illness and trinucleotide repeats. Trends Genet. 2004;20:51â 58. Fleischer B. Ã ber myotonische Dystrophie mit Katarakt. Albercht von Graefes. Arch Klin Ophthalmol. 1918;96:91â 133. Penrose LS. The problem of anticipation in pedigrees of dystrophia myotonica. Ann Eugenics. 1948;14:125â 132. Liquori CL, Ricker K, Moseley ML, et al. Myotonic dystrophy type 2 caused by a CCTG expansion in intron 1 of ZNF9.
Pedigrees in Figures 2-1H and 2-1I show families with defects in a maternally or paternally imprinted gene, respectively. In the family H, the gene is only expressed when inherited from the father, while a mutant allele transmitted from the mother is inactive. Therefore, the disease phenotype is only apparent when the mutant allele is inherited from a father. However, in family I, the gene is expressed only when inherited from the mother. Thus, a mutant allele transmitted from a father is inactive.
Some genes may require twowild-type alleles for normal function. In such case, heterozygotes for loss-of-function mutations may reveal phenotypes that can transmit as dominant traits because of the insufficient amount of gene products (haploinsufficiency). Two other mutational mechanisms can explain a dominant inheritance pattern. When a translated mutant protein interferes with the function of a normal (wild-type) protein that is produced from the normal allele, the condition is referred to as resulting from a dominant-negative effect (or antimorphic mutations).