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By: Rian Asmeida Farha binti Ahmad Rejab Nurul Ain binti Razali

Different apolipoprotein E, apolipoprotein A1 and prostaglandin-H2 D- i somerase level in CSF of schizoprenia patients and healthy controls. By: Rian Asmeida Farha binti Ahmad Rejab Nurul Ain binti Razali. Introduction.

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By: Rian Asmeida Farha binti Ahmad Rejab Nurul Ain binti Razali

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  1. Different apolipoprotein E, apolipoprotein A1 and prostaglandin-H2 D-isomerase level in CSF of schizoprenia patients and healthy controls By: RianAsmeidaFarhabinti Ahmad Rejab NurulAinbintiRazali

  2. Introduction • To identify SCZ biomarkers that could help diagnose the disease or give indication about disease pathophysiology. • Transcriptome & Proteome studies: -on SCZ brain tissue – potential biomarkers. -in peripheral fluid [blood & CSF] – have not been validated.

  3. Material & Methods • Subjects : 17 first episode of SCZ patients & 10 healthy controls. CSF: 50μl • Protein extraction & separation - Gel Electrophoresis. • Determination of protein expression & identification - Mass Spectrometry. • Western blot analysis – validate of differentially expressed proteins. • Statistical analysis – to rule out external interference involvement in the different protein expression that was not related to SCZ

  4. Results • 468 matched proteins spots between the groups – significant changes in relative abundance were found for six spots. • Corresponding to 6 distinct protein with apparent altered regulation in the SCZ sample • 3 Downregulated proteins – Transthyretin, TGF-β receptor type1, Coiled-coil domain containing protein 3 precursor. • 3 Upregulated proteins– Apolipoprotein E, Apolipoprotein A1, Prostaglandin- H2 D-isomerase.

  5. Discussion Upregulated protein 1.Apolipoprotein E • In brain, ApoE involves in the metabolism and homeostasis of cholesterol & essential for the formation for axonal myelin sheaths. • Also have critical roles in synaptogenesis, neurite outgrowth and membrane repair & maintenance which might be impaired in SCZ. • Upregulation in SCZ CSF – leads to lower cholesterol level & could lead to disrupted formation of synapses and disturbed cellular membrane formation in SCZ.

  6. 2.Apolipoprotein A1 • ApoA1 function in CNS not completely clear. • Upregulation: - Treatment with anti-psychotic drug : chlorpromazine. • Related to a particular group of patients. • Even so, the upregulation of ApoA1 supports the hypothesis that SCZ is a disorder of phospholipids breakdown.

  7. 3. Prostaglandin- H2 D-isomerase • AA production & degradation is essential to maintain the phospholipids structure of neuron. • Decrease level of AA in RBC membrane phospholipids have been reported in SCZ patients with negative symptoms.

  8. Downregulated proteins • CCDC3 has not previously been related to SCZ, but the CCD are known to be important in genes such as disrupted-in-SCZ-1 [DISC1] • TGFβtranduces signals of proliferation and cellular differentiation from the cell surface to the cytoplasm trough membrane receptors such as TGFβR1 which was downregulated in CSF of SCZ patients.

  9. 3. TTR produces in the choroid plexus, calcification of choroid plexus [due to serotonergichypofunction in SCZ] has been claimed to be neuroradiological hallmark of SCZ especially because of significance association between size of calcified choroid plexus and presence of hallucination in patients.

  10. Conclusion • Upregulation of ApoE, ApoA1 & PTGDS described here confirms the disturbance cholesterol & phospholipids metabolism in SCZ proposed by previously experiment but not clearly identified by genetic analysis • Moreover, the group analyses might be a potential biomarker for SCZ

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