Education
Max Planck Research School for Neurosciences, Germany PhD in Neuroscience
Max Planck Research School for Neurosciences, Germany MSc in Neuroscience
University of Dhaka, Bangladesh MSc in Biochemistry and Molecular Biology
University of Dhaka, Bangladesh BSc in Biochemistry and Molecular Biology
Positions, Scientific Appointments and Honors
Positions and Employment
Oct 2021- Post doctoral Fellow, Picower Institute for Learning and Memory, MIT, Cambridge, MA, USA
Jan 2021- Sep 2021 Post doctoral scientist, German Center for Neurodegenerative Diseases, Göttingen, Germany
Honors and Awards
2022 EMBO long term fellowship
2021 “Summa Cum Laude” for Doctoral Research
2019 DZNE Team Award
2013 Erasmus Mundus Scholarship for Masters in Neuroscience
2013 Commonwealth Shared Scholarship for Masters in Molecular Medicine (declined)
2012 National Science and Technology Fellowship, Bangladesh
2011 Dean´s Award, University of Dhaka, Bangladesh
2008 Sumitomo Corporation Scholarship Bachelor in Biochemistry and Molecular Biology
2007 National Merit Award, Bangladesh
2005 National Merit Award, Bangladesh
Contributions to Science
Patents
1. Methods and kits for detecting a risk for developing neurological or neurophysiological disorders. Md Rezaul Islam, A Fischer, F Sananbenesi
2. Using Gamma Sensory Entrainment to Rescue Brain Development Defects in Down Syndrome. Dong Shin Park, Md Rezaul Islam, Li-Huei Tsai
Recent publications
1. (2025) Md Rezaul Islam*, Brennan Jackson*, Maeesha Tasnim Naomi, Brooke Schatz, Noah Tan, Mitchell Murdock, Dong Shin Park, Daniela Rodrigues Amorim, Xueqiao Jiang, S. Sebastian Pineda, Chinnakkaruppan Adaikkan, Vanesa Fernandez Avalos, Ute Geigenmuller, Rosalind Mott Firenze, Manolis Kellis, Edward S. Boyden, and Li-Huei Tsai. “Multisensory gamma stimulation enhances adult neurogenesis and improves cognitive function in male mice with Down Syndrome”. in press. (*Equal contribution)
2. (2024) Lalit Kaurani*, Md Rezaul Islam*, Urs Heilbronner, Dennis M. Krüger, Jiayin Zhou, …Farahnaz Sananbenesi, Andre Fischer. “Regulation of Zbp1 by miR-99b-5p in microglia controls the development of schizophrenia-like symptoms in mice”. EMBO Journal. doi: https://doi.org/10.1038/s44318-024-00067-8. *Equal contribution.
3. (2021) Md Rezaul Islam*, Lalit Kaurani*, Tea Berulava, Urs Heilbronner, Monika Budde, Tonatiuh Pena Centeno…Andre Fischer. “A microRNA signature that correlates with cognition and is a target against cognitive decline”. EMBO Molecular Medicine (2021), doi: https://doi.org/10.15252/emmm.202013659.
4. (2021) Md Rezaul Islam, Dawid Lbik, M Sadman Sakib, Raoul Maximilian Hofmann, Tea Berulava, Martí Jiménez Mausbach, …Andre Fischer. “Epigenetic gene expression links heart failure to memory impairment”. EMBO Molecular Medicine (2021), doi: 10.15252/emmm.201911900.
5. (2021) Maria Goldberg*, Md Rezaul Islam*, Cemil Kerimoglu, Camille Lancelin, Verena Gisa, Susanne Burkhardt, Dennis M Krüger, Till Marquardt, Berend Malchow, Andrea Schmitt, Peter Falkai, Farahnaz Sananbenesi, Andre Fischer. “Exercise as a model to identify microRNAs linked to human cognition: a role for microRNA-409 and microRNA-501”. Translational Psychiatry (2021), doi: 10.1038/s41398-021-01627-w
Summary of the previous contributions
Full list of publications is available here: https://scholar.google.com/citations?user=CHyK7OQAAAAJ&hl=en
1. Identification of biomarkers and therapeutic targets for early cognitive decline in aging
Aging is strongly associated with progressive decline in cognitive functions. The treatment of aging-associated cognitive deficits is limited by patient diagnosis at an advanced stage of the pathology. Identification of at-risk individuals of developing dementia is critical for successful therapeutic intervention. To identify biomarkers denoting individuals at risk of cognitive deficits, I led a study (M. R. Islam, Kaurani, et al. 2021) in collaboration with 51 researchers from different research institutes. We report that the expression of a marker consisting of three microRNAs (miR-181a-5p, miR-146a-5p and miR-148a-3p) is increased in the blood of mice along aging and in humans who are at greater risk of developing cognitive deficits. Using models, we show that the increased expression is related to aberrant gene expression and neuronal activity in mice and humans. Targeted inhibition of these microRNAs could rescue cognitive deficits in mouse models for aging and Alzheimer´s disease (AD). This study is promising toward the use of this circulating marker as a population wide screening tool to find individuals at risk, who then can undergo more detailed diagnostic tests e.g., analysis of CSF biomarker or brain imaging. The findings have been published in EMBO Molecular Medicine (M. R. Islam, Kaurani, et al. 2021), see also (Yacovzada and Hornstein 2021), highlighted in its cover of November Issue, 2021. It came to the spotlight through national and international media coverage (a,b), and a related patent is available, in which I am listed as a co-inventor (R. Islam, Fischer, and Sananbenesi 2022).
Journal coverage
Patent
Islam, Rezaul, Andre Fischer, and Farahnaz Sananbenesi. 2022. Methods and kits for detecting a risk for developing neurological or neurophysiological disorders. WIPO 2022144402:A1. World Patent, filed December 29, 2021, and issued July 7, 2022. https://patents.google.com/patent/WO2022144402A1/en.
2. Role of risk factors in Brain dysfunctions
Brain dysfunctions and related diseases pose a significant burden in the modern world. Understanding the role of various risk factors in brain dysfunctions at the molecular level will help us design better strategies to maintain brain homeostasis and promote cognitive resilience. Besides genetic factors, different risk factors can shape brain functions (Wendeln et al. 2018) and cause cognitive deficits. For example, patients with cardiac dysfunctions (CARD), who display changes in RNA methylation(Berulava et al. 2020), have an increased risk of developing dementia. However, the underlying molecular mechanisms remained unknown until I led a recent study (M. R. Islam, Lbik, et al. 2021) using a transgenic mouse model for CARD. In this study, we found that CARD is related to dysregulation of hippocampal gene expression, loss of neuronal H3K4Me3, an euchromatin mark, and poor performance in hippocampus-dependent memory tasks. Oral administration of Vorinostat could ameliorate these pathologies. This study shed light on novel therapeutic avenues to alleviate dementia in patients with CARD. It has been published in EMBO Molecular Medicine (M. R. Islam, Lbik, et al. 2021), see also (Condorelli and Matteoli 2021).
In another study, together with colleagues, I have found that early-life-stress, another risk factor, can affect Schizophrenia pathology through modulation of molecular processes related to inflammasome activation (Kaurani et al. 2024). In this study, analyzing high throughput small RNAome in blood of 331 healthy and 242 Schizophrenia (SZ) patients and integrating the results to those from post-mortem brains, I identified miR-99b-5p as a key player in Schizophrenia. In mice, inhibition of miR-99b-5p triggered SZ-like symptoms, microglial inflammation, and synaptic pruning. We discovered Zbp1 as a novel miR-99b-5p target, and targeting it with antisense oligos mitigated the SZ-like effects. The study provides promising therapeutic target(s) for RNA therapy in Schizophrenia (Kaurani et al. 2024).
Islam, Md Rezaul, Dawid Lbik, M. Sadman Sakib, Raoul Maximilian Hofmann, Tea Berulava, Martí Jiménez Mausbach, Julia Cha, et al. 2021. “Epigenetic Gene Expression Links Heart Failure to Memory Impairment.” EMBO Molecular Medicine 13 (3). https://doi.org/10.15252/emmm.201911900.
*Equal contributions
Journal coverage
3. Physical Exercise to improve cognitive performance
Physical exercise has been linked to improved cognition, which can be transmitted to the next generation (Benito et al. 2018). However, the molecular mechanism that underlies the cognitive benefit remains poorly understood. To address this, in a study (Goldberg et al. 2021) (published in Translational Psychiatry, in which I am co-first and co-corresponding author), I analyzed small RNA sequencing data of healthy humans who participated in a physical training and found two microRNAs related to cognitive benefit. Employing relevant in vitro models, we observed that the expression of the two microRNAs is critical to maintain neuronal structure and activity (Goldberg et al. 2021). In another study, we reported a hippocampal single nuclei RNA-seq data resource after four weeks of voluntary exercise (Methi et al. 2024).
*Equal contributions,
§corresponding author (designed the project and provided mentorship to Maria Goldberg)
4. Application of non-invasive therapeutic approaches for treatment of brain diseases
Non-invasive sensory gamma stimulation at 40Hz using light and sound has previously been linked with improved cognitive performance in mouse models and patients with AD. In a recent study, we showed that multisensory gamma stimulation promotes glymphatic clearance of amyloid (Murdock et al. 2024). Analyzing scRNA-seq from the mouse cortex of an AD mouse model, I showed that the gamma stimulation induced gene expression changes in astrocytes related to membrane trafficking (Murdock et al. 2024), which was then subsequently validated. Moreover, we observed beneficial effects of the sensory gamma stimulation in other contexts of brain pathologies and brain diseases. For example, we observed that the gamma stimulation could alleviate chemo-brain pathology and cognitive impairment induced by chemotherapy in mice (Kim et al. 2024). In this study, I analyzed the scRNA-seq data from the mouse hippocampus and found that the stimulation plus chemotherapy treatment altered gene expression changes in oligodendrocytes (Kim et al. 2024). In another study, we showed that the gamma stimulation mitigates the effects of demyelination induced by cuprizone in mice (Rodrigues-Amorim et al. 2024). In a more recent study in the lab of Dr. Tsai, along with colleagues at MIT, investigated the effects of the gamma stimulation in Ts65Dn mice, a mouse model of Down Syndrome (DS). Of note, DS shares similar pathology and cognitive decline to AD. For three weeks, mice were exposed daily to one hour of stimulation or, as a control, one hour of ambient light and sound. Mice receiving the stimulation showed improved object recognition and spatial working memory. In the hippocampus, I found that stimulation upregulated genes related to synaptic organization and downregulated genes related to aging and AD at the single nuclei level. Moreover, I demonstrated increased adult neurogenesis following the chronic stimulation that could be linked to enhanced expression of TCF4, a transcription factor, which is known to facilitate adult neurogenesis. Together, our data indicated that sensory gamma stimulation can boost memory in DS mice and thus may have therapeutic potential for dementia in individuals with DS (Islam et al. 2024). Additionally, I contributed as co-first author to another study which we proposed combination of sensory stimulation and microglial depletion as a new therapeutic approach for promoting neuroprotective effects (Adaikkan*, Islam*, Bozzelli* et al). Excitingly, we observed that combining sensory gamma stimulation with microglia depletion led to enhanced neuroprotective effects compared to sensory gamma stimulation alone. At the single cell transcriptomics level, I discovered that the combined treatment increased gene co-expression of a gene module in interneurons, and hub genes of this module included Mef2c, a transcription factor that has been linked with cognitive resilience in an earlier study from Dr Tsai. The manuscript related to these findings is in preparation (Adaikkan*, Islam*, Bozzelli* et al) for submission.
Islam, Md Rezaul, Brennan Jackson, Maeesha Tasnim Naomi, Brooke Schatz, Noah Tan, Mitchell Murdock, Dong Shin Park, et al. 2024. “Multisensory Gamma Stimulation Enhances Adult Neurogenesis and Improves Cognitive Function in Male Mice with Down Syndrome.” Neuroscience. bioRxiv. https://www.biorxiv.org/content/10.1101/2024.10.03.616486v2
5. To better understand the transcriptomic circuits in vulnerable vascular cell type(s) in dementia
In a recent study with Dr. Tsai, I investigated the vulnerability of capillary endothelial cells, one of the vascular cell subtypes, and compared the gene expression networks in 427 individuals from ROSMAP cohorts with and without AD. When compared to the controls, I identified a perturbed gene module in aged human brains with dementia. Interestingly, this module indicated modified lipid processing and a putative endothelial-to-mesenchymal transition, suggesting a loss of endothelial cellular identity in AD. We hypothesized that these phenotypes were driven by increased inflammation. I collaboratively tested these hypotheses using human iPSC-derived 2D endothelial cells and a 3D iPSC-derived blood-brain-barrier (iBBB) model. With this in vitro modeling, we have validated the aberrant endothelial cell phenotypes following cytokine-induced inflammation. Upon analyzing the endothelial cell transcriptomics after cytokines treatment in vitro, I identified inflammation-related upstream gene regulatory factors. Excitingly, pretreatment of the endothelial cells with small-molecule inhibitors targeting these factors rescued the inflammation-driven phenotypes in endothelial cells. The manuscript based on these findings is currently in preparation (Islam* and Pinals* et al).
6. Application of bioinformatics analyses in other studies
Additionally I offered my bioinformatics skills to colleagues to better understand molecular processes related to Parkinson's disease (Paiva et al. 2018), synucleinopathy (Xylaki et al. 2023), sleep (Hu et al. 2020), knockout effect of a histone methyltransferase (Michurina et al. 2022), 3D tissue engineered muscle differentiation (Shahriyari et al. 2022), and to investigate hippocampal synaptic RNAome (Epple et al. 2021). Moreover, as an undergrad, I analyzed in silico Quercetin´s potential as a therapeutic drug for AD (Islam et al. 2013).
Md Rezaul Islam, Aubhishek Zaman, Iffat Jahan, Rajib Chakravorty, Sajib Chakraborty, 2013. “In silico QSAR analysis of quercetin reveals its potential as therapeutic drug for Alzheimer's disease.”
Complete list of publications is available here: https://scholar.google.com/citations?user=CHyK7OQAAAAJ&hl=en