https://medicine.nus.edu.sg/medphc/

Department of Pharmacology NUS Medicine, Singapore (2026)

28/05/2026

Calling all International Applicants! ✈️ 🌍

Applications for the 𝐌𝐚𝐬𝐭𝐞𝐫 𝐨𝐟 𝐒𝐜𝐢𝐞𝐧𝐜𝐞 𝐢𝐧 𝐌𝐞𝐝𝐢𝐜𝐚𝐥 𝐏𝐡𝐚𝐫𝐦𝐚𝐜𝐨𝐥𝐨𝐠𝐲 𝐚𝐭 𝐍𝐔𝐒 (Aug 2026 Intake) are closing very soon!

Please submit your applications by 𝟑𝟏𝐬𝐭 𝐌𝐚𝐲 𝟐𝟎𝟐𝟔.

For more information and where to apply please head to our website:

https://medicine.nus.edu.sg/graduatestudies/education/msc-in-medical-pharmacology/

Ensure you have the required documents which include:
1. Academic transcripts and CV
2. Statement of Intent
3. Personal Statement
4. Proof of English proficiency (IELTS or TOEFL)
5. Financial Support documents.

All the best!!

25/05/2026

We are proud to congratulate our faculty members — Prof. Christopher CHEN Li Hsian, Prof. GOH Boon Cher, and Dr. Saima HILAL — on receiving prestigious awards under the 2026 National Medical Research Council (NMRC) Awards.

Prof Christopher Chen and Prof Goh Boon Cher were awarded the Singapore Translational Research Investigator Award (STaR), while Dr Saima Hilal received the Clinician Scientist Award – Investigator (CSA-INV).

These achievements reflect their outstanding contributions to medical research and their continued commitment to advancing healthcare and scientific innovation. We extend our heartfelt congratulations on this well-deserved recognition.

25/05/2026

𝐈𝐍𝐓𝐑𝐎𝐃𝐔𝐂𝐓𝐈𝐎𝐍
Vascular dementia (VaD) is a major therapeutic challenge. Tar DNA-binding protein 43 (TDP-43), known for its role in neurodegeneration, may contribute to VaD pathogenesis under chronic cerebral hypoperfusion (CCH). This study investigates TDP-43 dysregulation in VaD.

𝐌𝐄𝐓𝐇𝐎𝐃𝐒
TDP-43 and phosphorylated TDP-43 (pTDP-43) expression and localization were assessed in a VaD animal model, neuronal cells exposed to oxygen–glucose deprivation (OGD), and post mortem human brain tissues.

𝐑𝐄𝐒𝐔𝐋𝐓𝐒
Bilateral Common Carotid Artery Stenosis (BCAS)-induced CCH led to increased pTDP-43 and aberrant redistribution of both TDP-43 and pTDP-43. In vitro OGD triggered similar mislocalization. Post mortem VaD brains showed no TDP-43 abnormalities, while Alzheimer’s and mixed dementia cases exhibited marked pathology.

𝐃𝐈𝐒𝐂𝐔𝐒𝐒𝐈𝐎𝐍
TDP-43 dysregulation appears early in VaD under hypoperfusive stress, distinguishing it from other dementia subtypes. These findings indicate that TDP‑43 may warrant further investigation as a potential early molecular feature of VaD.

Full Article: https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.71196

19/05/2026

INTRODUCTION

Genome-wide association studies have identified numerous Alzheimer’s disease (AD) susceptibility loci in European populations. However, the genetic architecture of AD in non-European populations remains underinvestigated.
METHODS

We performed a genetic association study in East Asians (N = 8514) to validate known AD loci and identify new susceptibility loci.
RESULTS

We identified LILRB2–LILRB5 as an AD susceptibility locus with ethnic-specific effects between Europeans and East Asians. The lead variant, rs587709-T, was associated with decreased AD risk and increased LILRB5 expression in Europeans. Conversely, in East Asians, the same allele was associated with increased AD risk and increased LILRB2 expression. Furthermore, genome-wide analysis identified TTC3 and FAM135A as candidate susceptibility loci for AD or cognition.
DISCUSSION

The results establish LILRB2–LILRB5 as a cross-ancestry AD-associated locus with ethnic-specific genetic mechanisms and reveal new susceptibility loci, extending the understanding of the genetic etiology of AD.

Full Article: https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.71219

11/05/2026

Among the transcriptional regulators of cell fate, c-Myc is one of the most frequently deregulated oncogenes, exerting pleiotropic effects on cellular metabolism, survival, and stress adaptation. C-Myc occupies a pivotal position at the intersection of autophagy and senescence, two essential, yet paradoxical processes in cancer biology. Autophagy can both suppress tumor formation and support the survival of established tumors. In contrast, senescence acts as a barrier to malignant transformation but can also promote tumor progression through the senescence-associated secretory phenotype. C-Myc modulates both autophagy and senescence in a highly context-dependent manner. It acts as either an inducer or a suppressor depending on cellular state and microenvironmental conditions. This dual regulatory capacity underscores its role as a central hub in cell fate decisions. In this review, we first summarize how c-Myc, autophagy, and senescence contribute to tumor biology. We then highlight the molecular mechanisms through which c-Myc regulates autophagy and senescence. We examine how these interactions influence cancer progression. Finally, we discuss emerging therapeutic strategies and clinical trials targeting the c-Myc-mediated autophagy/senescence axis. We also address future challenges and opportunities for exploiting this network in precision oncology.

Full Article: https://www.sciencedirect.com/science/article/abs/pii/S0304383526000789?via%3Dihub

05/05/2026

As in art, the ability of nucleic acids to be designed and synthesized as a novel treatment modality is limited only by the imagination. Nucleic acids of virtually all sizes and forms can be synthesized on demand, from short antisense oligonucleotides to large mRNAs and to entire chromosomes. Given the genetic basis of cancer, nucleic acid-based therapy is a particularly promising avenue for anticancer therapeutic development. This has led to a profusion of studies exploring strategies to utilize nucleic acid-based drugs to treat cancer, with some approaches demonstrating great potential for clinical translation. In this review, we summarize the various nucleic acid-based strategies being developed for cancer therapy. We also provide a comprehensive overview of current efforts to enhance the potency and safety of nucleic acid-based drugs, exploring advances in nucleotide composition, design, and delivery strategies.
Full Article: https://www.cell.com/molecular-therapy-family/molecular-therapy/fulltext/S1525-0016(25)00812-3?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1525001625008123%3Fshowall%3Dtrue

27/04/2026

Abstract

Introduction: This study examined whether selective serotonin reuptake inhibitors (SSRIs) treatment influenced cognitive trajectory and progression to Alzheimer's disease (AD) dementia in amnestic mild cognitive impairment (MCI) patients, stratified by AD pathology.

Methods: Four hundred fifty-seven amnestic MCI participants in the ADNI database were analyzed. AD pathology was determined by baseline amyloid beta (Aβ) and tau positron emission tomography. Kaplan-Meier survival analysis and Cox proportional hazards models evaluated MCI-to-AD progression. Linear mixed models analyzed longitudinal cognitive trajectories, amyloid accumulation, and cortical thickness.

Results: SSRI treatment showed no significant effect on AD dementia progression (hazard ratio = 1.64, 95% confidence interval: 0.61 to 4.38) or cognitive trajectories, regardless of AD pathology. No significant differences in Aβ accumulation or cortical thickness were observed between SSRI users and non-users. External validation confirmed no significant SSRI effect on AD progression or cognitive decline.

Discussion: SSRI treatment was not associated with long-term cognitive effects in amnestic MCI, irrespective of underlying AD pathology.

Highlights: SSRI treatment was not associated with long-term AD dementia risk in MCI. SSRI treatment had no impact on long-term cognitive performance changes in MCI. SSRI treatment did not affect Aβ accumulation or cortical thickness in MCI. SSRIs had no effect on MCI progression, regardless of underlying AD pathology.

Full Article: https://pubmed.ncbi.nlm.nih.gov/41292493/

20/04/2026

Global warming is expanding mosquito habitats and increasing mosquito-borne diseases. In tropical and sub-tropical regions, chikungunya virus (CHIKV) transmitted by Aedes mosquitoes has become a major concern due to the debilitating chronic joint disease it causes. Mosquito saliva contains bioactive factors that enhance viral infection, with sialokinin identified as a key contributor to vascular leakage and viral spread in mice. Here, we demonstrate that sialokinin binds to neurokinin receptors and restricts the activation of human myeloid cells. Mechanistically, sialokinin facilitates early viral dissemination, as evidenced by increased viral load in the contralateral footpad at 1 day post-infection, and significantly reduces circulating CD169+ monocytes while suppressing IFN-γ-producing T-cell-driven inflammation, as reflected by reduced joint footpad swelling in female CHIKV-infected mice. Clinically, patients with severe CHIKV disease exhibited higher levels of IgG antibodies against sialokinin, which correlated with higher viral loads and systemic inflammatory markers. Our findings highlight the multifaceted role of sialokinin in facilitating early viral dissemination and modulating host immunity during CHIKV infection. Given the growing threat of mosquito-borne diseases in a warming, disease-burdened world, targeting mosquito salivary factors like sialokinin could offer a novel therapeutic strategy to mitigate viral-induced inflammation and improve clinical outcomes.

Full Article: https://www.nature.com/articles/s41467-025-64468-x

13/04/2026

Cortical cerebral microinfarcts are associated with brain atrophy in cross-sectional studies, with further investigation using longitudinal datasets being warranted. Moreover, little is known about their combined impact on cognition. This study aimed to establish the association between cortical cerebral microinfarcts and brain volume loss over time and explore whether they synergistically contribute to cognitive decline.

A total of 475 patients, aged 72.7 ± 7.9 years, were enrolled from a memory clinic cohort, who underwent neuroimaging and neuropsychological assessments at least twice over 5 years. Cortical cerebral microinfarcts and other cerebrovascular disease were assessed using 3-T MRI. Brain volumes were calculated semi-automatically using FreeSurfer. Cognitive function was assessed using a neuropsychological test battery including six domains. Linear mixed-effect models were utilized to examine the association between cortical cerebral microinfarcts and brain volume loss and their interaction on cognitive decline. Estimated marginal means were derived to plot global cognitive trajectories.

Cortical cerebral microinfarcts were associated with a greater decrease over 2 years in total brain volume [β = −1.94 (−3.07, −0.82) at Year 2, P-interaction with time < 0.001], grey matter volume [β = −1.00 (−1.69, −0.30) at Year 2, P-interaction = 0.002] and white matter volume [β = −0.95 (−1.54, −0.35) at Year 2, P-interaction < 0.001]. Brain volume loss was more pronounced in patients with multiple microinfarcts. Patients with high brain volume loss and cortical cerebral microinfarcts, particularly multiple microinfarcts, exhibited significantly lower global cognitive scores [single microinfarct: β = −1.83 (−2.68, −0.97) at Year 5, P-interaction with time < 0.001; multiple microinfarcts: β = −3.13 (−4.21, −2.05) at Year 5, P-interaction < 0.001]. The synergistic effects were more significant in the domains of executive function, memory, language and visuospatial function. Global cognitive trajectories revealed greater cognitive decline in patients with high brain volume loss and single or multiple microinfarcts, with the latter showing the steepest slope.

This study established a longitudinal association between cortical cerebral microinfarcts and brain atrophy progression, with higher microinfarct burden associated with more pronounced brain volume loss. Furthermore, cortical cerebral microinfarcts and brain atrophy showed synergistic effects on cognitive decline. These findings highlight the importance of investigating the role of mixed pathologies in the development of cognitive impairment and dementia in future research.

Full Article: https://academic.oup.com/brain/article/148/11/3924/8232732

07/04/2026

𝐀𝐃𝐕𝐀𝐍𝐂𝐄𝐃 𝐂𝐎𝐔𝐑𝐒𝐄: 𝐄𝐒𝐒𝐄𝐍𝐓𝐈𝐀𝐋𝐒 𝐎𝐅 𝐃𝐑𝐔𝐆 𝐃𝐈𝐒𝐂𝐎𝐕𝐄𝐑𝐘, 𝐃𝐄𝐒𝐈𝐆𝐍, 𝐀𝐍𝐃 𝐃𝐄𝐕𝐄𝐋𝐎𝐏𝐌𝐄𝐍𝐓 𝟐–𝟔 𝐅𝐞𝐛𝐫𝐮𝐚𝐫𝐲 𝟐𝟎𝟐𝟔

The Department of Pharmacology, NUS Yong Loo Lin School of Medicine, recently hosted an engaging week with 46 undergraduate students from 11 universities across China, studying medicine, and bioscience. Their curiosity, insightful questions, and enthusiasm for drug development made the sessions incredibly energizing. It is always a privilege to interact with the next generation of scientists and healthcare innovators. This intensive program explored the full landscape of modern drug development from small-molecule and biologic discovery to clinical translation and commercialization. Students examined how pharmacokinetics, pharmacovigilance, diagnostics, and regulatory science shape therapeutic innovation and market access.

Department of Pharmacology NUS Medicine

28/05/2026

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