Instructions and marking rubric for Annotated Bibliography assignment Topic: The Frontotemporal Dementia and Amyotrophic Lateral Sclerosis Disease Spectrum In your review you should consider one (or...

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Instructions and marking rubric for Annotated Bibliography assignment Topic: The Frontotemporal Dementia and Amyotrophic Lateral Sclerosis Disease Spectrum In your review you should consider one (or more) of the following questions: · Is there any convincing evidence to suggest these two diseases do not exist on a spectrum? · What molecular pathways may lead to neuronal death in FTD/ALS spectrum? · How can a common underlying pathway(s) explain the heterogeneity in clinical presentation of FTD/ALS patients? · Are there any underlying molecular mechanisms that can explain where patients fall on the FTD/ALS clinical spectrum? It would be great if you look into the pathological features of the above^ Please look at sample as to how they did it and see how they wrote their title and what they wanted to focus on · pathological features of the two diseases (disease mechanisms) molecular neuropathology of both - neurodengeneration · - tdp43 Provide a draft title of your planned review. Select 3 appropriate primary research articles broadly relevant to your chosen review focus Write an annotation for each of the 3 primary research articles. Include in your annotation: 1) The citation: provide the full bibliographic citation. Any standard journal citation format that provides authors, date, full title and publicatiobn information is fine (eg Journal of Neuroscience) (1 mark) 2) Introduction: Indicate the content or scope of the paper (1 mark) 3) Aims & Research methods: Identify the aim/s of the paper and the key research methods that were used. (1 mark) 4) Scope: Identify the main results and conclusions of the authors (1 mark) 5) Usefulness (to your research review topic): Highlight special features. Identify strengths. Point out in what way the paper relates to themes or concepts that will be the topic of your review (2 marks) 6) Limitations: Identify any limitations of the paper (1 mark) 7) Conclusions: Provide an overall conclusion/interpretation of the paper (1 mark) 8) Reflection: Explain how this work illuminates your review topic or how it will/will not fit in with your further research. Discuss the relevance of this paper to the topic of your review. Present your view/reaction to this paper. (2 marks) The word limit for sections 2-8 (ie NOT including the citation) of EACH annotation is 250 words (there is no minimum word count). Total 10 marks for each annotation =Total mark /30) Do not forget to include a DRAFT TITLE for your review Some really useful suggestions and a helpful example can be found on the UNSW student site below. We strongly encourage you to have a look at: https://student.unsw.edu.au/annotated-bibliography Fetal exposure to drugs of abuse: some effects on neurogenesis in the case of cocaine (78) Bahi, A, Dreyer J (2004) Cocaine-induced expression changes of axon guidance molecules in the adult rat brain. Molecular and Cellular Neuroscience 28: 275-291. This study contained an experiment using adult rats to investigate the effects of acute and chronic administration of cocaine on brain development. The main aim was to determine if axon guidance molecules are up- or down-regulated post-treatment using DNA microarray and quantitative real-time PCR. The study found that mRNA expression of Sempahorins followed an identical pattern of changes of both up- and down-regulation in the nucleus accumbens and in the ventral tegmental area most notably in chronically treated rats. In addition to these areas, expression changes of Ephs and Ephrins were observed in the caudate putamen and the hippo-campus. This study confirmed all microarray data with real-time PCR as well as included 39 molecules to ensure a testable variety, however it is important to note that the rats used were adults which could affect its implications for early developmental processes. The authors concluded that an alternation in the mesolimbic dopamine system induces malformation of synaptic connections and therefore neuroplasticity in reward and memory centres to produce cognitive deficits from cocaine consumption. In terms of relevance for my literature review, I will be focusing on pre-natal and early development of the cortex and subcortical structures which requires a basis in axon guidance molecules as cues for neurogenesis. I think that this paper is useful as evidence for the effects of cocaine on processes that are most prolific in the human fetal and neonatal stages and possible detriments as a result. Frankfurt M, Wang H, Marmolejo N, Bakshi K, Friedman E (2009) Prenatal cocaine increases dendritic spine density in cortical and subcortical brain regions of the rat. Developmental Neuroscience 31: 71-75. This study involved an experiment on pregnant rats and the brains of their offspring in order to investigate the effects of cocaine as opposed to saline. The aim was to observe differences in the density of dendritic spines in both the cortex and subcortex with the data later analysed by two-way ANOVA. The rats were injected with cocaine (or placebo in the control group) from gestation day 2 until they gave birth where at postnatal day 21 pups’ brains were removed. The results of analyses showed that dendritic spine density was increased in the cortex and sub-cortex of pups in the hippocampus, medial prefrontal cortex, striatum, nucleus accumbens and medial hypothalamic nucleus. The strengths of this study include the fact that they used both sexes and found the effects to be the same as well as using a simultaneous control group instead of older data. A limitation is that they only experimented with one dose and timeframe and could establish a clearer trend with further manipulation of these variables. The conclusion relates to reward circuitry and points to the issue that the exact mechanism behind increased dendritic spine density remains unclear. I think this is relevant to my literature review because it shows that cocaine administration affects both cortical and subcortical areas which I will explore in turn. I also think that a specific focus on dendritic spines in the context of neuro-genesis is unique and is noteworthy to be included in my final report. Grewen K, Burchinal M, Vachet C, Gouttard S, Gilmore JH (2014) Prenatal cocaine effects on brain structure in early infancy. NeuroImage 101: 114-123. This study investigated the effects of prenatal drug exposure on infants using three groups: those exposed to cocaine, those exposed to a variety of other substances excluding cocaine and a control group with no drug exposure at all. The aim of the study was to compare anatomical features between the groups and therefore attribute significant changes to the variable of drug exposure using MRI scanning and subsequently, an automatic segmentation tool for analysis. The researchers found that infants with cocaine history had lower grey matter volumes in the prefrontal and frontal areas of the brain and had higher volumes of cerebrospinal fluid in these areas as well as in the parietal cortex. Overall, greatest differences were observed in the dorsal prefrontal cortex. Some strengths in the methodology include use of descriptive statistics and inferential analyses to account for factors such as birth weight, head circumference, gender, race and maternal characteristics and they further adjusted for varying levels of substance use. The main limitation is the lack of evidence to translate these anatomical effects into cognitive functions and later substance abuse potential through a longitudinal study. The research paper concludes that there could be a link between the highlighted structural changes and possible functional impact and this is relevant to my topic looking at early infancy as a crucial period. I think that in terms of neurodevelopmental toxicity, it is particularly important as one of the only human studies available due to understandable ethical concerns.