Protein Synthesis

Huntingtin is a 350-kilodalton protein of unknown function that is mutated in Huntington's disease (HD), a neurodegenerative disorder. The mutant protein is presumed to acquire a toxic gain of function that is detrimental to striatal neurons in the brain. However, loss of a beneficial activity of wild-type huntingtin may also cause the death of striatal neurons. Here we demonstrate that wild-type huntingtin up-regulates transcription of brain-derived neurotrophic factor (BDNF), a pro-survival factor produced by cortical neurons that is necessary for survival of striatal neurons in the brain. We show that this beneficial activity of huntingtin is lost when the protein becomes mutated, resulting in decreased production of cortical BDNF. This

During normal development of the mammalian central nervous system (CNS), neural stem cells (NSC) give rise to neurons via process of neurogenesis (Kempermann et al., 2004; Zhao et al., 2008). Neurogenesis normally occurs in dentate gyrus (DG) region of the hippocampus and lateral ventricle of sub-ventricular zone (SVZ) (Zhao et al., 2008). Hippocampal neurogenesis plays pivotal role in neurologic and psychiatric disorder like epilepsy, depression, schizophrenia and mood disorders (Antonova et al., 2004; Keller and Roberts, 2008; Lucassen et al., 2006; Zhao et al., 2008). Development of the nervous system is complex, and includes multistep dynamic processes such as proliferation, differentiation, migration, expansion of axons and dendrites, synapse formation, myelination and programmed cell death (Rice and Barone, 2000). These processes required the coordinated expression of cellular and molecular events in a spatial and temporal manner during the brain development (Rice and Barone, 2000; Rodier, 1994). Several growth factors and signal transduction cascades have been implicated in controlling NSC behavior in the developing brain (Faigle and Song, 2013). Among these, members of the Wnt family of secreted glycoprotein thought to be variably influence proliferation and lineage decisions of NSC and their progeny (Clevers et al., 2014).

Long-term potentiation refers to the steady increase in synaptic activity between two neurons which causes persistent strengthening of synaptic activity. Since memory formation is mainly dependent on synaptic strength, LTP seems to play an essential role in memory formation. Contrary to that, long-term depression causes a reduction in synaptic activity between two neurons, causing a decrease in synaptic activity. LTP and LTD are essential for normal functioning of the brain and balance in the ratio of LTP/LTD is needed for homeostasis. The levels and activity of LTP and LTD are majorly dependent on Calcium levels, Calcium-Calmodulin Kinase, NMDARs (N-Methyl-D-Aspartate receptors) and AMPARs (α-amino-3-hydroxy-5-methylisoxazole-4-propionic

Protein Synthesis Protein Synthesis is the process whereby DNA (deoxyribonucleic acid) codes for the production of essential proteins, such as enzymes and hormones. Proteins are long chains of molecules called amino acids. Different proteins are made by using different sequences and varying numbers of amino acids. The smallest protein consists of fifty amino acids and the largest is about three thousand amino acids long. Protein synthesis occurs on ribosomes in the cytoplasm of a cell but is controlled by DNA located in the nucleus.

In the search for the etiology of schizophrenia, several possibilities have been investigated, including psychodynamic, autoimmune, and genetic, but two have been long pitted against each other: neurodevelopmental and neurodegenerative. While there is evidence for both processes, current research is more supportive of a neurodevelopmental etiology. However, schizophrenia will likely not be explained by a single process. Since the current study did not include longitudinal studies, it is difficult to directly support either theory. But, indirect evidence was observed. The presence of ERG abnormalities in healthy high-risk offspring (Hebert et al., 2010) and widening of venules in unaffected co-twins supports neurodevelopment. The OCT findings, on the other hand, more support neurodegeneration. As discussed previously and summarized in Figures 3, 4, and 5, there is a negative correlation between duration of illness and RNFL and macular thickness. This could be secondary to a progressive loss of brain volume as detected by retinal thinning.

Long dsRNA s bind to Dicer to cut into smaller nucleotide fragments/segments. siRNA unwinds when it is catalysed by Argonaut. One strand remained with the Argonaut is the guide strand. The RNA guide strand with Argonaut and other proteins are combined into RNA induced silencing complex (RISC) and the other passenger RNA strand is released into nucleotides.

GM1 is a ganglioside that impacts neuronal plasticity, repair mechanisms, and the release of neurotrophins in the brain. GM1 promotes neuronal growth and survival by modulating tyrosine kinase receptors for neurotrophic factors. GM1’s neurotrophic action is exerted on dopaminergic neurons by interacting with the GDNF receptor complex, Ret tyrosine kinase, and GFR alpha-1

Muscle protein synthesis is a common term used in the lifting world. Often people do not actually understand what this actually is. Muscle protein synthesis is a natural process that our bodies go through after any type of work the muscles do to repair, grow, and become stronger. While weightlifting, muscles are breaking down, becoming damaged and our bodies repairs itself through muscle protein synthesis. After leaving the gym and eat protein the body takes the protein and moves it into the cells to repair it. This window will last between 36-48 hours until the muscle is rebuilt and recover, experienced lifters will have a shorter duration (Leal). As long as loads are stressing the body it will respond with muscle protein synthesis.

BDNF is a member of the neurotrophin family, which includes nerve growth factor, neurotrophin-3, neurotrophin-4/5, and neurotrophin-6 (Poo, 2001). BDNF is broadly expressed in the developing and adult mammalian brain (Poo, 2001), as well as in several peripheral tissues, such as the muscle (Cassiman et al., 2001) and adipose tissue (Sornelli et al., 2009). BDNF plays an important role in various aspects of developmental and adult brain plasticity, including proliferation, differentiation, and survival of neurons, neurogenesis, synaptic plasticity, and cognitive function (Monteggia et al., 2004).

Attempts to cure or slow down the progression of Parkinson’s disease have largely failed; researchers in this paper maintain this is obviously a direct result of the lack of insight into the pathogenesis of the disease. Parkinson’s disease is the product of the deaths of a number of dopaminergic (dopamine-secreting) neurons in the substantia nigra pars compacta region (SNc) of the brain. But what causes these deaths? In the paper “‘Rejuvenation’ protects neurons in mouse models of Parkinson’s disease,” Chen and researchers find that older neurons in the SNc are unusually reliant on calcium channels and that after blocking these channels, the cells are “rejuvenated” and begin acting like their juvenile counterparts; as a

There is a critical need to design a novel strategy targeting ASD risk genes involved in the Wnt pathway. The major gap in current knowledge that we will address in this proposal is to determine how PV neuron- specific CTNNB1 KO affects animal behaviors and to what extent Wnt agonists reverse the behavioral deficits. We expect to identify the defect that is involved in PV neurons specific to CTNNB1 knockout mice. Moreover, we have identified several bioactive compounds with diverse mechanisms of action that can potentiate the Wnt pathway in human NPCs, including approved drugs and probes suitable for in vivo use31, 32. Repurposing these drugs for ASD will be exciting because they act through different mechanisms than current experimental therapies now. Our cKO mice provide an ideal animal model to examine the extent to which targeting Wnt pathway can ameliorate the behavioral deficits. If small molecules targeting Wnt pathway in this study can alleviate behavioral deficits, a whole new "druggable" pathway will further identify more active molecules/drugs that can be directly applied to the ASD patients. This contribution will be significant because it is an important step to allow modulation of the Wnt signaling pathway at interneurons and may lead to development of a pharmacologic approach to correct ASD-related behavioral defects, thereby improving the lives of ASD patients. What is learned in this study will be applicable to other ASDs caused by mutations associated with

Researchers used BrdU pulsing to identify the target cells they wanted to monitor for possible growth and change. In order to evaluate the effects of aspirin on oligodendroglia in vitro, multiple aspects were studied. Cultures of neural stem cells and OPC’s were taken, incubated, stained, and treated with varying doses of aspirin. Cells are analyzed under the electron microscope to see the effects aspirin may have on oligodendrocyte lineage and development, as well as OPC proliferation and differentiation. Specific stains are used as markers for the cells being targeted as well as the processes they may be undergoing, such as proliferation.

The authors took extracellular electrophysiological recording to examine the functional change from hippocampus on parabionts. They found isochronic parabionts stayed at baseline level for long-term potentiation, but can be maintained at above baseline level in heterochronic parabionts. From these functional results, they concluded that young blood is capable to potentiate synaptic plasticity in aged mice.

It is clear to neurobiologists that aging results in a decrease in brain size as well as a decrease in the efficiency of brain functions. It has been a widely held belief that aging causes neurons to die and for the overall number of neurons to decrease as one reaches old age. Studies

Protein synthesis is one of the most fundamental biological processes. To start off, a protein is made in a ribosome. There are many cellular mechanisms involved with protein synthesis. Before the process of protein synthesis can be described, a person must know what proteins are made out of. There are four basic levels of protein organization. The first is primary structure, followed by secondary structure, then tertiary structure, and the last level is quaternary structure. Once someone understands the makeup of a protein, they can then begin to learn how elements can combine and go from genes to protein. There are two main processes that occur during protein synthesis, or peptide formation. One is transcription and