Mental illnesses like schizophrenia (SCZ) and major depression disorder (MDD) are devastating brain disorders. The SCZ risk gene, disrupted in schizophrenia 1 (DISC1), has been associated with neuropsychiatric conditions. However, little is known regarding the long-lasting impacts on brain metabolism and behavioral outcomes from genetic insults on fetal NPCs during early life. We have established a new mouse model that specifically interrupts DISC1 functions in NPCs in vivo by a dominant-negative DISC1 (DN-DISC1) with a precise temporal and spatial regulation. Interestingly, prenatal interruption of mouse Disc1 function in NPCs leads to abnormal depression-like deficit in adult mice. Here we took a novel unbiased metabonomics approach to identify
The sixth major case of Endangered Specie. The laboratory Rats are bred every year to serve various scientific purposes. Once the test are complete the rat are rapidly killed, with the result that the variety becomes extinct.
The neurodevelopmental Basis of Schizophrenia. Austin, TX: Landes Co.
Zhan, Y., Paolicelli, R.C., Sforazzini, F., Weinhard, L., Bolasco, G., Pagani, F., Vyssotski, A.L., Bifone, A., Gozzi, A., Ragozzino, D., et al. (2014). Deficient neuron-microglia signaling results in impaired functional brain connectivity and social behavior. Nature neuroscience 17, 400-406.
Proteogenomics is a kind of science field that includes proteomics and genomics. Proteomic consists of protein sequence information and genomic consists of genome sequence information. It is used to annotate whole genome and protein coding genes. Proteomic data provides genome analysis by showing genome annotation and using of peptides that is gained from expressed proteins and it can be used to correct coding regions.Identities of protein coding regions in terms of function and sequence is more important than nucleotide sequences because protein coding genes have more function in a cell than other nucleotide sequences. Genome annotation process includes all experimental and computational stages.These stages can be identification of a gene ,function and structure of a gene and coding region locations.To carry out these processes, ab initio gene prediction methods can be used to predict exon and splice sites. Annotation of protein coding genes is very time consuming process ,therefore gene prediction methods are used for genome annotations. Some web site programs provides these genome annotations such as NCBI and Ensembl. These tools shows sequenced genomes and gives more accurate gene annotations. However, these tools may not explain the presence of a protein. Main idea of proteogenomic methods is to identify peptides in samples by using these tools and also with the help of mass spectrometry.Mass spectrometry searches translation of genome sequences rather than protein database searching. This method also annotate protein protein interactions.MS/MS data searching against translation of genome can determine and identify peptide sequences.Thus genome data can be understood by using genomic and transcriptomic information with this proteogenomic methods and tools. Many of proteomic information can be achieved by gene prediction algorithms, cDNA sequences and comparative genomics. Large proteomic datasets can be gained by peptide mass spectrophotometry for proteogenomics because it uses proteomic data to annotate genome. If there is genome sequence data for an organism or closely related genomes are present,proteogenomic tools can be used. Gained proteogenomic data provides comparing of these data between many related species and shows homology relationships among many species proteins to make annotations with high accuracy.From these studies, proteogenomic data demonstrates frame shifts regions, gene start sites and exon and intron boundaries , alternative splicing sites and its detection , proteolytic sites that is found in proteins, prediction of genes and post translational modification sites for protein.
By introducing a partially functional SMPD1 gene onto the complete knockout (ASMKO) background, a transgenic mouse model of type B NPD has been produced, This results in a mouse with ~ 8 % residual ASM activity in most organs (Marathe et al., 2000 ). Notably, these mice never develop a neurological phenotype and live a normal lifespan. Nevertheless, by ~8–10 months of age they begin to show lipid storage in RES organs. These interpretations provide in vivo evidence that low levels of ASM activity in the brain are likely to prevent neurological disease in ASM patients, and have important applications for the treatment of neurological (type A )ASM-deficient NPD.
Markham, J. A., & Koenig, J. I. (2011). Prenatal stress: Role in psychotic and depressive diseases. Psychopharmacology, 214(1), 89-106.
Recent research has identified three stages of the prodrome. In the first stage of the prodrome, individuals often display the negative symptoms of schizophrenia, including social withdrawal, decline in school functioning, and may also exhibit signs of anxiety or depression (Larson et al., 2010). These individuals also often have a genetic vulnerability to develop schizophrenia, in the form of prior family history of psychosis (Kaur & Cadenhead, 2010). In the ...
... Circuitry and a Road Map for Future Research. The American Journal of Psychiatry, 72-84, 88. doi:10.1176/appi.ajp.2014.13081008
vulnerability factors for bipolar disorder: A review of neuroimaging studies of individuals at high genetic risk for bipolar disorder. Australian & New Zealand Journal of Psychiatry, 47, 1124-1135.
It is not surprising that deficits in serotonin circuits are also seen in depressed patients, as these depletions may interact with and indeed be responsible for falls in norepinephrine levels (a phen...
Biological connections to schizophrenia are not exclusively genes or environment, combination of genes and environment causes schizophrenia (Glick, 2005). Nature’s focus of life is gene electives and nurture is environmental causing direct influence to bump traits, environment and innate potential defining reality in schizophrenia (Glick, 2005). If both genes and environment are correct schizophrenia turns on and each contributes 100% (Glick, 2005). Psychologist cannot account for a single cause of schizophrenia; results from case studies leave multiple genetic factors, psychological assaults, environmental, and hormonal causes that affect brain chemistry (Lifespan, 2009).
Not one gene can cause Schizophrenia by itself. This illness may result from the gene that make important brain chemicals malfunctioning. This malfunctioning may affect the ...
The brain, a component of the nervous system that is located in our skulls is a complex organ that determines almost everything about us, from actions to personality traits. It controls voluntary movement, conscious thinking, language, memory, and emotion (“Brain” 2014). Through the use of brain imaging technologies, psychologists are able to break down the complexity of the active brain and study its particular processes. Such technologies include Positron Emission Topography (PET), Magnetic Resonance Imaging (MRI), Functional Magnetic Resonance Imaging (fMRI), Electroencephalogram (EEG), and Computerized Axial Tomography (CAT). These instruments are useful in the field of neurology, but have their own set of benefits and drawbacks depending on different situations. Hence, this essay will discuss and evaluate the brain technologies of PET and fMRI in its role of investigating the relationship between biological factors and behavior in terms of schizophrenia.
...Elizabeth R. Sowell. "Focus On: Structural And Functional Brain Abnormalities In Fetal Alcohol Spectrum Disorders." Alcohol Research & Health 34.1 (2011): 121-131. Health Source - Consumer Edition. Web. 19 Nov. 2013.
Current evidence suggests that a multifactorial neurodevelopmental model best explains the development of schizophrenia, with multiple genetic and environmental exposures playing roles (McClellan & Stock, 2013).The most important risk factors for vulnerability to schizophrenia are genetic factors where family, twin, and adoption studies support a strong genetic component (Lewis & Lieberman, 2000; McClellan & Stock, 2013; Niemi, Suvisaari, Tuulio-Henriksson, & Lönnqvist, 2003).