Displaying publications 21 - 40 of 48 in total

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  1. Fulltext Rapid-Onset Dystonia-Parkinsonism in a Chinese Girl with a De Novo ATP1A3 c.2267G>A (p.R756H) Genetic Mutation
    Tan AH, Ozelius LJ, Brashear A, Lang AE, Ahmad-Annuar A, Tan CT, et al.
    Mov Disord Clin Pract, 2015 Mar;2(1):74-75.
    PMID: 30713883 DOI: 10.1002/mdc3.12122
  2. Genetic Testing for Parkinson's Disease and Movement Disorders in Less Privileged Areas: Barriers and Opportunities
    Tan AH, Cornejo-Olivas M, Okubadejo N, Pal PK, Saranza G, Saffie-Awad P, et al.
    Mov Disord Clin Pract, 2024 Jan;11(1):14-20.
    PMID: 38291851 DOI: 10.1002/mdc3.13903
  3. Fulltext Underrepresented Populations in Parkinson's Genetics Research: Current Landscape and Future Directions
    Schumacher-Schuh AF, Bieger A, Okunoye O, Mok KY, Lim SY, Bardien S, et al.
    Mov Disord, 2022 Aug;37(8):1593-1604.
    PMID: 35867623 DOI: 10.1002/mds.29126
    BACKGROUND: Human genetics research lacks diversity; over 80% of genome-wide association studies have been conducted on individuals of European ancestry. In addition to limiting insights regarding disease mechanisms, disproportionate representation can create disparities preventing equitable implementation of personalized medicine.

    OBJECTIVE: This systematic review provides an overview of research involving Parkinson's disease (PD) genetics in underrepresented populations (URP) and sets a baseline to measure the future impact of current efforts in those populations.

    METHODS: We searched PubMed and EMBASE until October 2021 using search strings for "PD," "genetics," the main "URP," and and the countries in Latin America, Caribbean, Africa, Asia, and Oceania (excluding Australia and New Zealand). Inclusion criteria were original studies, written in English, reporting genetic results on PD from non-European populations. Two levels of independent reviewers identified and extracted information.

    RESULTS: We observed imbalances in PD genetic studies among URPs. Asian participants from Greater China were described in the majority of the articles published (57%), but other populations were less well studied; for example, Blacks were represented in just 4.0% of the publications. Also, although idiopathic PD was more studied than monogenic forms of the disease, most studies analyzed a limited number of genetic variants. We identified just nine studies using a genome-wide approach published up to 2021, including URPs.

    CONCLUSION: This review provides insight into the significant lack of population diversity in PD research highlighting the immediate need for better representation. The Global Parkinson's Genetics Program (GP2) and similar initiatives aim to impact research in URPs, and the early metrics presented here can be used to measure progress in the field of PD genetics in the future. © 2022 International Parkinson and Movement Disorder Society.

  4. Embracing Monogenic Parkinson's Disease: The MJFF Global Genetic PD Cohort
    Vollstedt EJ, Schaake S, Lohmann K, Padmanabhan S, Brice A, Lesage S, et al.
    Mov Disord, 2023 Feb;38(2):286-303.
    PMID: 36692014 DOI: 10.1002/mds.29288
    BACKGROUND: As gene-targeted therapies are increasingly being developed for Parkinson's disease (PD), identifying and characterizing carriers of specific genetic pathogenic variants is imperative. Only a small fraction of the estimated number of subjects with monogenic PD worldwide are currently represented in the literature and availability of clinical data and clinical trial-ready cohorts is limited.

    OBJECTIVE: The objectives are to (1) establish an international cohort of affected and unaffected individuals with PD-linked variants; (2) provide harmonized and quality-controlled clinical characterization data for each included individual; and (3) further promote collaboration of researchers in the field of monogenic PD.

    METHODS: We conducted a worldwide, systematic online survey to collect individual-level data on individuals with PD-linked variants in SNCA, LRRK2, VPS35, PRKN, PINK1, DJ-1, as well as selected pathogenic and risk variants in GBA and corresponding demographic, clinical, and genetic data. All registered cases underwent thorough quality checks, and pathogenicity scoring of the variants and genotype-phenotype relationships were analyzed.

    RESULTS: We collected 3888 variant carriers for our analyses, reported by 92 centers (42 countries) worldwide. Of the included individuals, 3185 had a diagnosis of PD (ie, 1306 LRRK2, 115 SNCA, 23 VPS35, 429 PRKN, 75 PINK1, 13 DJ-1, and 1224 GBA) and 703 were unaffected (ie, 328 LRRK2, 32 SNCA, 3 VPS35, 1 PRKN, 1 PINK1, and 338 GBA). In total, we identified 269 different pathogenic variants; 1322 individuals in our cohort (34%) were indicated as not previously published.

    CONCLUSIONS: Within the MJFF Global Genetic PD Study Group, we (1) established the largest international cohort of affected and unaffected individuals carrying PD-linked variants; (2) provide harmonized and quality-controlled clinical and genetic data for each included individual; (3) promote collaboration in the field of genetic PD with a view toward clinical and genetic stratification of patients for gene-targeted clinical trials. © 2023 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

  5. Fulltext Improved inherited peripheral neuropathy genetic diagnosis by whole-exome sequencing
    Drew AP, Zhu D, Kidambi A, Ly C, Tey S, Brewer MH, et al.
    Mol Genet Genomic Med, 2015 Mar;3(2):143-54.
    PMID: 25802885 DOI: 10.1002/mgg3.126
    Inherited peripheral neuropathies (IPNs) are a group of related diseases primarily affecting the peripheral motor and sensory neurons. They include the hereditary sensory neuropathies (HSN), hereditary motor neuropathies (HMN), and Charcot-Marie-Tooth disease (CMT). Using whole-exome sequencing (WES) to achieve a genetic diagnosis is particularly suited to IPNs, where over 80 genes are involved with weak genotype-phenotype correlations beyond the most common genes. We performed WES for 110 index patients with IPN where the genetic cause was undetermined after previous screening for mutations in common genes selected by phenotype and mode of inheritance. We identified 41 missense sequence variants in the known IPN genes in our cohort of 110 index patients. Nine variants (8%), identified in the genes MFN2, GJB1, BSCL2, and SETX, are previously reported mutations and considered to be pathogenic in these families. Twelve novel variants (11%) in the genes NEFL, TRPV4, KIF1B, BICD2, and SETX are implicated in the disease but require further evidence of pathogenicity. The remaining 20 variants were confirmed as polymorphisms (not causing the disease) and are detailed here to help interpret sequence variants identified in other family studies. Validation using segregation, normal controls, and bioinformatics tools was valuable as supporting evidence for sequence variants implicated in disease. In addition, we identified one SETX sequence variant (c.7640T>C), previously reported as a putative mutation, which we have confirmed as a nonpathogenic rare polymorphism. This study highlights the advantage of using WES for genetic diagnosis in highly heterogeneous diseases such as IPNs and has been particularly powerful in this cohort where genetic diagnosis could not be achieved due to phenotype and mode of inheritance not being previously obvious. However, first tier testing for common genes in clinically well-defined cases remains important and will account for most positive results.
  6. Fulltext LRRK2 N551K and R1398H variants are protective in Malays and Chinese in Malaysia: A case-control association study for Parkinson's disease
    Gopalai AA, Lim JL, Li HH, Zhao Y, Lim TT, Eow GB, et al.
    Mol Genet Genomic Med, 2019 Nov;7(11):e604.
    PMID: 31487119 DOI: 10.1002/mgg3.604
    BACKGROUND: The LRRK2 gene is associated with Parkinson's disease (PD) as a number of mutations within the gene have been shown to be susceptibility factors. Studies on various global populations have determined that mutations such as G2019S, G2385R, and R1628P in LRRK2 increase the risk of developing PD while the N551K-R1398H haplotype is associated with conferring protection against developing PD. Here we report a study looking at the N551K and R1398H variants for the first time in the Malaysian population.

    METHODS: Cases (523) which conformed to the United Kingdom PD Brain Bank Criteria for PD were recruited through trained neurologists and age- and ethnically matched controls (491) were individuals free of any neurological disorder. The N551K and R1398H mutations were genotyped using the Taqman SNP genotyping assay.

    RESULTS: A significant protective association for N551K was found in those of Malay ancestry, with a protective trend seen for R1398H. A meta-analysis of Chinese individuals in this cohort with other published cohorts of Chinese ancestry indicated a significant protective role for N551K and R1398H.

    CONCLUSION: This study reports that the N551K-R1398H haplotype is also relevant to the Malaysian population, with a significant protective effect found in those of Malay and Chinese ancestries.

  7. Glucocerebrosidase (GBA) gene variants in a multi-ethnic Asian cohort with Parkinson's disease: mutational spectrum and clinical features
    Lim JL, Lohmann K, Tan AH, Tay YW, Ibrahim KA, Abdul Aziz Z, et al.
    J Neural Transm (Vienna), 2022 Jan;129(1):37-48.
    PMID: 34779914 DOI: 10.1007/s00702-021-02421-0
    GBA variants are associated with increased risk and earlier onset of Parkinson's disease (PD), and more rapid disease progression especially with "severe" variants typified by p.L483P. GBA mutation screening studies from South-East Asia, with > 650 million inhabitants of diverse ancestries, are very limited. We investigated the spectrum of GBA variants, and associated clinico-demographic features, in a multi-ethnic PD cohort in Malaysia. Patients (n = 496) were recruited from seven centres, primarily of Chinese (45%), Malay (37%), and Indian (13%) ethnicities. All GBA coding exons were screened using a next-generation sequencing-based PD gene panel and verified with Sanger sequencing. We identified 14 heterozygous GBA alleles consisting of altogether 17 missense variants (8 classified as pathogenic or likely pathogenic for PD) in 25 (5.0%) patients, with a substantially higher yield among early (
  8. Fulltext A Patient with Beta-Propeller Protein-Associated Neurodegeneration: Treatment with Iron Chelation Therapy
    Lim SY, Tan AH, Ahmad-Annuar A, Schneider SA, Bee PC, Lim JL, et al.
    J Mov Disord, 2018 May;11(2):89-92.
    PMID: 29860786 DOI: 10.14802/jmd.17082
    We present a case of beta-propeller protein-associated neurodegeneration, a form of neurodegeneration with brain iron accumulation. The patient harbored a novel mutation in the WDR45 gene. A detailed video and description of her clinical condition are provided. Her movement disorder phenomenology was characterized primarily by limb stereotypies and gait dyspraxia. The patient's disability was advanced by the time iron-chelating therapy with deferiprone was initiated, and no clinical response in terms of cognitive function, behavior, speech, or movements were observed after one year of treatment.
  9. Fulltext Purposeless Groaning in Parkinson's Disease
    Lim SY, Tan AH, Lim JL, Ahmad-Annuar A
    J Mov Disord, 2018 May;11(2):87-88.
    PMID: 29860787 DOI: 10.14802/jmd.18004
    Purposeless groaning has been reported in advanced progressive supranuclear palsy. We present a case of purposeless groaning occurring as a primary complaint in a patient with advanced Parkinson's disease. Purposeless groaning is thought to be a manifestation of disinhibition and perseveration due to frontal-subcortical dysfunction. Proper recognition of this phenomenon will help clinicians to avoid unnecessary investigations and treatment (e.g., prescription of opioid medications).
  10. Fulltext Alternating Hemiplegia of Childhood in a Person of Malay Ethnicity with Diffusion Tensor Imaging Abnormalities
    Tan AH, Ong TL, Ramli N, Tan LK, Lim JL, Azhan MA, et al.
    J Mov Disord, 2019 May;12(2):132-134.
    PMID: 31158946 DOI: 10.14802/jmd.18063
  11. Fulltext Association of LRRK2 Haplotype With Age at Onset in Parkinson Disease
    Xiao B, Deng X, Ng EY, Allen JC, Lim SY, Ahmad-Annuar A, et al.
    JAMA Neurol, 2018 01 01;75(1):127-128.
    PMID: 29131875 DOI: 10.1001/jamaneurol.2017.3363
  12. Fulltext Analysis of non-synonymous-coding variants of Parkinson's disease-related pathogenic and susceptibility genes in East Asian populations
    Foo JN, Tan LC, Liany H, Koh TH, Irwan ID, Ng YY, et al.
    Hum Mol Genet, 2014 Jul 15;23(14):3891-7.
    PMID: 24565865 DOI: 10.1093/hmg/ddu086
    To evaluate the contribution of non-synonymous-coding variants of known familial and genome-wide association studies (GWAS)-linked genes for Parkinson's disease (PD) to PD risk in the East Asian population, we sequenced all the coding exons of 39 PD-related disease genes and evaluated the accumulation of rare non-synonymous-coding variants in 375 early-onset PD cases and 399 controls. We also genotyped 782 non-synonymous-coding variants of these genes in 710 late-onset PD cases and 9046 population controls. Significant enrichment of LRRK2 variants was observed in both early- and late-onset PD (odds ratio = 1.58; 95% confidence interval = 1.29-1.93; P = 8.05 × 10(-6)). Moderate enrichment was also observed in FGF20, MCCC1, GBA and ITGA8. Half of the rare variants anticipated to cause loss of function of these genes were present in healthy controls. Overall, non-synonymous-coding variants of known familial and GWAS-linked genes appear to make a limited contribution to PD risk, suggesting that clinical sequencing of these genes will provide limited information for risk prediction and molecular diagnosis.
  13. Identification of the genomic mutation in Epha4(rb-2J/rb-2J) mice
    Mohd-Zin SW, Abdullah NL, Abdullah A, Greene ND, Cheah PS, Ling KH, et al.
    Genome, 2016 Jul;59(7):439-48.
    PMID: 27373307 DOI: 10.1139/gen-2015-0142
    The EphA4 receptor tyrosine kinase is involved in numerous cell-signalling activities during embryonic development. EphA4 has the ability to bind to both types of ephrin ligands, the ephrinAs and ephrinBs. The C57BL/6J-Epha4rb-2J/GrsrJ strain, denoted Epha4(rb-2J/rb-2J), is a spontaneous mouse mutant that arose at The Jackson Laboratory. These mutants exhibited a synchronous hind limb locomotion defect or "hopping gait" phenotype, which is also characteristic of EphA4 null mice. Genetic complementation experiments suggested that Epha4(rb-2J) corresponds to an allele of EphA4, but details of the genomic defect in this mouse mutant are currently unavailable. We found a single base-pair deletion in exon 9 resulting in a frame shift mutation that subsequently resulted in a premature stop codon. Analysis of the predicted structure of the truncated protein suggests that both the kinase and sterile α motif (SAM) domains are absent. Definitive determination of genotype is needed for experimental studies of mice carrying the Epha4(rb-2J) allele, and we have also developed a method to ease detection of the mutation through RFLP. Eph-ephrin family members are reportedly expressed as numerous isoforms. Hence, delineation of the specific mutation in EphA4 in this strain is important for further functional studies, such as protein-protein interactions, immunostaining and gene compensatory studies, investigating the mechanism underlying the effects of altered function of Eph family of receptor tyrosine kinases on phenotype.
  14. The Prevalence and Distribution of Spina Bifida in a Single Major Referral Center in Malaysia
    Sahmat A, Gunasekaran R, Mohd-Zin SW, Balachandran L, Thong MK, Engkasan JP, et al.
    Front Pediatr, 2017;5:237.
    PMID: 29170734 DOI: 10.3389/fped.2017.00237
    Background: The aim of this study is to review the medical history of patients with spina bifida, encompassing both aperta and occulta types born between the years 2003 until 2016, spanning a 13-year time period. We assessed each patient and maternal parent information, details of the defects, and conditions associated with the primary defect. We also include information on patients' ambulation and education level (where available).

    Methods: Data from the Department of Patient Information University of Malaya Medical Centre (UMMC), Malaysia was captured from spina bifida patients (ICD10: Q05 spina bifida). Data involved patients referred to UMMC between 2003 and 2016 and/or born in UMMC within that particular time frame. We filtered and extracted the information according to the data of clinical examination, medical review, and social history provided in the medical records.

    Results: A total of 86 patient records with spina bifida were analyzed. Spina bifida prevalence rate in this study ranged from 1.87 to 8.9 per 1,000 live births depending on weightage. We note that ethnicity was a factor whereby the highest numbers of spina bifida were from Malays (n = 36, 41.86%), followed by equal numbers of Chinese and Indians (n = 24, 27.91%). The highest number of diagnoses reported was myelomeningocele type-spina bifida (n = 39, 45.35%). The most common site of the spina bifida lesion was located at the lumbar region irrespective of aperta or occulta types (n = 23, 26.74%). Data on other associated phenotypes of spina bifida such as hydrocephalus and encephalocele was also captured at 37.21% (n = 32) and 1.16% (n = 1), respectively. In terms of mobility, 32.84% (n = 22/67) of patients between the ages 4 and 16 years old were found to be mobile. As many as 36.07% of patients ranging from 5 to 16 years of age (n = 22/61) received formal education ranging from preschool to secondary school.

    Conclusion: The prevalence of spina bifida in UMMC is as according to international statistics which is in the range of 0.5-10 per 1,000 live births. Majority of the reported cases were males, Malays, full term babies, and of the myelomeningocele phenotype located at the lumbar region.

  15. Fulltext DTI Profiles for Rapid Description of Cohorts at the Clinical-Research Interface
    Lock C, Kwok J, Kumar S, Ahmad-Annuar A, Narayanan V, Ng ASL, et al.
    Front Med (Lausanne), 2018;5:357.
    PMID: 30687707 DOI: 10.3389/fmed.2018.00357
    Normal pressure hydrocephalus (NPH) is a syndrome comprising gait disturbance, cognitive decline and urinary incontinence that is an unique model of reversible brain injury, but it presents as a challenging spectrum of disease cohorts. Diffusion Tensor Imaging (DTI), with its ability to interrogate structural white matter patterns at a microarchitectural level, is a potentially useful tool for the confirmation and characterization of disease cohorts at the clinical-research interface. However, obstacles to its widespread use involve the need for consistent DTI analysis and interpretation tools across collaborator sites. We present the use of DTI profiles, a simplistic methodology to interpret white matter injury patterns based on the morphology of diffusivity parameters. We examined 13 patients with complex NPH, i.e., patients with NPH and overlay from multiple comorbidities, including vascular risk burden and neurodegenerative disease, undergoing extended CSF drainage, clinical assessments, and multi-modal MR imaging. Following appropriate exclusions, we compared the morphology of DTI profiles in such complex NPH patients (n = 12, comprising 4 responders and 8 non-responders) to exemplar DTI profiles from a cohort of classic NPH patients (n = 16) demonstrating responsiveness of white matter injury to ventriculo-peritoneal shunting. In the cohort of complex NPH patients, mean age was 71.3 ± 7.6 years (10 males, 2 females) with a mean MMSE score of 21.1. There were 5 age-matched healthy controls, mean age was 73.4 ± 7.2 years (1 male, 4 females) and mean MMSE score was 26.8. In the exemplar cohort of classic NPH patients, mean age was 74.7 ± 5.9 years (10 males, 6 females) and mean MMSE score was 24.1. There were 9 age-matched healthy controls, mean age was 69.4 ± 9.7 years (4 males, 5 females) and mean MMSE score was 28.6. We found that, despite the challenges of acquiring DTI metrics from differing scanners across collaborator sites and NPH patients presenting as differing cohorts along the spectrum of disease, DTI profiles for responsiveness to interventions were comparable. Distinct DTI characteristics were demonstrated for complex NPH responders vs. non-responders. The morphology of DTI profiles for complex NPH responders mimicked DTI patterns found in predominantly shunt-responsive patients undergoing intervention for classic NPH. However, DTI profiles for complex NPH non-responders was suggestive of atrophy. Our findings suggest that it is possible to use DTI profiles to provide a methodology for rapid description of differing cohorts of disease at the clinical-research interface. By describing DTI measures morphologically, it was possible to consistently compare white matter injury patterns across international collaborator datasets.
  16. Fulltext A Perspective on the Role of microRNA-128 Regulation in Mental and Behavioral Disorders
    Ching AS, Ahmad-Annuar A
    Front Cell Neurosci, 2015;9:465.
    PMID: 26696825 DOI: 10.3389/fncel.2015.00465
    MiRNAs are short, non-coding RNA molecules that regulate gene expression post-transcriptionally. Over the past decade, misregulated miRNA pathways have been associated with various diseases such as cancer, neurodegenerative diseases, and neurodevelopmental disorders. In this article, we aim to discuss the role played by miR-128 in neuropsychiatric disorders, and highlight potential target genes from an in silico analysis of predicted miR-128 targets. We also discuss the differences of target gene determination based on a bioinformatics or empirical approach. Using data from TargetScan and published reports, we narrowed the miR-128 target gene list to those that are known to be associated with neuropsychiatric disorders, and found that these genes can be classified into 29 gene clusters and are mostly enriched in cancer and MAPK signaling pathways. We also highlight some recent studies on several of the miR-128 targets which should be investigated further as potential candidate genes for therapeutic interventions.
  17. Fulltext A Novel Occulta-Type Spina Bifida Mediated by Murine Double Heterozygotes EphA2 and EphA4 Receptor Tyrosine Kinases
    Abdullah NL, Mohd-Zin SW, Ahmad-Annuar A, Abdul-Aziz NM
    Front Cell Dev Biol, 2017;5:105.
    PMID: 29312933 DOI: 10.3389/fcell.2017.00105
    Members of the Eph receptor tyrosine kinase have previously been implicated in cranial neural tube development. Failure of neural tube closure leads to the devastating conditions known as anencephaly and spina bifida. EphA2 and EphA4 are expressed at the tips of the closing spinal neural folds prior and during neural tube closure. We investigated the possible role of murine EphA2 and EphA4 during the last step of primary neural tube closure, which is adhesion and fusion. The individual mouse knockouts of EphA2 and EphA4 per se do not exhibit neural tube defects (NTDs). The embryos generated by the crossing of double heterozygotes Epha2tm1Jrui/+Epha4rb-2J/+ displayed NTDs with a wide degree of severity including close exencephaly and close spina bifida (spina bifida occulta). Interestingly, mutants displaying NTDs had skin covering the underlying lesion. The tissue sections revealed the elevated neural folds had not adhered and fused. The phenotypes seen in Epha2tm1Jrui/+Epha4rb-2J/+ double heterozygous embryos suggest both genes play a compensatory role with each other in the adhesion and fusion of the neural tube. In this study, there exists a >50% penetrance of NTDs in the mouse mutants, which genetically have a single allele each of EphA2 and EphA4 absent.
  18. Fulltext Editorial: Genetic and molecular diversity in Parkinson's disease
    Abdul Murad NA, Sulaiman SA, Ahmad-Annuar A, Mohamed Ibrahim N, Mohamed W, Md Rani SA, et al.
    Front Aging Neurosci, 2022;14:1094914.
    PMID: 36589546 DOI: 10.3389/fnagi.2022.1094914
  19. Mutation analysis of genes within the dynactin complex in a cohort of hereditary peripheral neuropathies
    Tey S, Ahmad-Annuar A, Drew AP, Shahrizaila N, Nicholson GA, Kennerson ML
    Clin Genet, 2016 Aug;90(2):127-33.
    PMID: 26662454 DOI: 10.1111/cge.12712
    The cytoplasmic dynein-dynactin genes are attractive candidates for neurodegenerative disorders given their functional role in retrograde transport along neurons. The cytoplasmic dynein heavy chain (DYNC1H1) gene has been implicated in various neurodegenerative disorders, and dynactin 1 (DCTN1) genes have been implicated in a wide spectrum of disorders including motor neuron disease, Parkinson's disease, spinobulbar muscular atrophy and hereditary spastic paraplegia. However, the involvement of other dynactin genes with inherited peripheral neuropathies (IPN) namely, hereditary sensory neuropathy, hereditary motor neuropathy and Charcot-Marie-Tooth disease is under reported. We screened eight genes; DCTN1-6 and ACTR1A and ACTR1B in 136 IPN patients using whole-exome sequencing and high-resolution melt (HRM) analysis. Eight non-synonymous variants (including one novel variant) and three synonymous variants were identified. Four variants have been reported previously in other studies, however segregation analysis within family members excluded them from causing IPN in these families. No variants of disease significance were identified in this study suggesting the dynactin genes are unlikely to be a common cause of IPNs. However, with the ease of querying gene variants from exome data, these genes remain worthwhile candidates to assess unsolved IPN families for variants that may affect the function of the proteins.
  20. Fulltext COVID-19 pandemic: Lessons learned for undergraduate research training
    Ibrahim K, Ahmad-Annuar A
    Biochem Mol Biol Educ, 2022 09;50(5):476-478.
    PMID: 36054325 DOI: 10.1002/bmb.21665
    This article reports a session from the virtual international 2021 IUBMB/ASBMB workshop, "Teaching Science on Big Data." The awareness of using publicly available research data sets for undergraduate training is low in certain parts of the world. Final year projects always revolve around wet-lab based projects. The challenges occur during COVID-19 pandemic when it forces full lockdown to the nation, but at the same time faculty members need to provide consistent training to the students and projects to work with. We aim to identify supervisors in the faculty that are ready to convert their proposed project from wet-lab to an online-based project. As coordinators of the course we created an online survey to identify projects that can be converted into dry-lab/online projects. Our surveys identified only 32.5% projects implemented dry-lab/online based projects. Most academicians described that they are not ready or familiar to apply changes for their research design. With the unknown future of the world living with COVID-19 and directional changes of life science research toward big data driven research indeed we should be ready to adopt such changes. Awareness on reusing public data sets as tools for research should be provided to strengthen undergraduate training. Life science undergraduates should be exposed to reusing public data sets as these materials are readily available case studies that allow in depth exploration to answer specific research questions. Members of the faculty should take part to pave the way for them, ensuring that they understand that life science research revolves around a multidisciplinary field.
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