National University - Sudan (NUSU)
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Item Association of Platelet Serotonin Levels in Alzheimer’s Disease with Clinical and Cerebrospinal Fluid Markers(Journal of Alzheimer’s Disease, 2016) Tajeddinna,Walid; Fereshtehnejad,Seyed-Mohammad; Ahmed,Mohammed Seed; Yoshitaked,Takashi; Kehr,Jan; Shahnaz,Tasmin; Milovanovic,Micha; Behbahani,Homira; Hoglund ,Kina; Winblad,Bengt; Cedazo-Minguez,Angel; Jelic,Vesna; Jaremo,Petter; Aarsland,DagIntroduction: Serotonin (5-HT) is involved in the pathology of Alzheimer’s disease (AD). Objective: We aimed to measure 5-HT level in platelets in AD and explore its association with cerebrospinal fluid (CSF), AD biomarkers (amyloid- 1-42 (A42), total tau (t-tau), and phosphorylated tau (p-tau)), and clinical symptoms. Methods: 15 patients with AD and 20 patients with subjective cognitive impairment (SCI) were included. 5-HT metabolites were measured, in a specific fraction, using high performance liquid chromatography with electrochemical detection (HPLC- ECD). Results: Significantly lower 5-HT concentrations were observed in AD patients compared to SCI patients both after normal- ization against total protein (p = 0.008) or platelet count (p = 0.019). SCI patients with lower 5-HT level have higher AD CSF biomarkers, total tau (p = 0.026) and tau/A42 ratio (p = 0.001), compared to those with high 5-HT levels. Conclusion: AD patients have reduced platelet 5-HT levels. In SCI, lower 5-HT content was associated with a higher AD-CSF biomarker burden.Item Pharmacological Modulations of the Serotonergic System in a Cell-Model of Familial Alzheimer’s Disease(Journal of Alzheimer’s Disease, 2016) Tajeddinna,Walid; Persson,Torbjorn; Garridoa,Javier Calvo; Ahmed,Mohammed Seed; Maiolia,Silvia; Vijayaraghavan,Swetha; Kazokoglua,Mehmet Selim; Fernandez,Cristina Parrado; Yoshitaked,Takashi; Kehrd,Jan; Francisb,Paul; Winblada,Bengt; Hoglund ,Kina; Mingueza,Angel Cedazo; Aarsland,DagSerotonin (5-HT) plays a central role in the integrity of different brain functions. The 5-HT homeostasis is regulated by many factors, including serotonin transporter (SERT), monoamine oxidase enzyme (MAO), and several 5-HT receptors, including the 5-HT1B. There is little knowledge how the dynamics of this system is affected by the amyloid- (A) burden of Alzheimer’s disease (AD) pathology. SH-SY5Y neuroblastoma cells transfected with the amyloid precursor protein (APP) gene containing the Swedish mutations causing familial AD (APPswe), were used as a model to explore the effect of A pathology on 5-HT1B and related molecules including the receptor adaptor protein (p11), SERT and MAOA gene expression, and MAOA activity after treatment with selective serotonin reuptake inhibitor (SSRI) (sertraline), and a 5-HT1B receptor antagonist. Sertraline led more than 70 fold increase of 5-HT1B gene expression (p < 0.001), an increased serotonin turnover in both APPswe and control cells and reduced intracellular serotonin levels by 75% in APPswe cells but not in controls (p > 0.05). Treatment with the 5-HT1B receptor antagonist increased SERT gene-expression in control cells but not in the APPswe cells. 5-HT and 5-HT1B antagonist treatment resulted in different p11 expression patterns in APPswe cells compared to controls. Although MAOA gene expression was not changed by APPswe overexpression, adding 5-HT lead to a significant increase in MAOA gene expression in APPswe but not control cells. These findings suggest that the sensitivity of the 5-HT1B receptor and related systems is affected by APPswe overexpression, with potential relevance for pharmacologic intervention in AD. This may at least partly explain the lack of effect of SSRIs in patients with AD and depression.Item Highlighting the Effect of Pro‑inflammatory Mediators in the Pathogenesis of Periodontal Diseases and Alzheimer’s Disease(Journal of Pharmacy and Bioallied Sciences, 2024) Hashim, Nada; Babiker, Rasha; Mohammed, Riham; Chaitanya, Nallan CSK; Rahman, Muhammed M.; Gismalla, BakriAlzheimer’s disease (AD) is a neurological condition that is much more common as people get older. It may start out early or late. Increased levels of pro‑inflammatory cytokines and microglial activation, both of which contribute to the central nervous system’s inflammatory state, are characteristics of AD. As opposed to this, periodontitis is a widespread oral infection brought on by Gram‑negative anaerobic bacteria. By releasing pro‑inflammatory cytokines into the systemic circulation, periodontitis can be classified as a “low‑grade systemic disease.” Periodontitis and AD are linked by inflammation, which is recognized to play a crucial part in both the disease processes. The current review sought to highlight the effects of pro‑inflammatory cytokines, which are released during periodontal and Alzheimer’s diseases in the pathophysiology of both conditions. It also addresses the puzzling relationship between AD and periodontitis, highlighting the etiology and potential ramifications.