Prof. dr. Taruna Ikrar, M.D., M. Biomed, Ph.D.

TRIBUNNEWSWIKI.COM - Prof. dr. Taruna Ikrar, M.D., M. Biomed, Ph.D., is an internationally recognized physician, biomedical scientist, and biomedical educator with more than 20 years of experience in:

• Practicing medicine as a licensed physician at both private and public government hospitals
• Conducting biomedical research in university & hospital settings
• Providing formal academic curriculum development & instruction for undergraduate, doctoral, and post-doctoral biomedical education programs in university and hospital settings.
• Exercising supervisory management and professional development of clinical/research staff in university and hospital settings.

Over the past decade, Prof. Ikrar's ground-breaking biomedical discoveries in biomedical sciences, pharmacology, cardiovascular sciences, and neurosciences have been published in numerous world-class peer-reviewed research journals including Nature, Neuron, Cells, Circulation, Molecular Therapy, American Journal of Cardiology, Journal of Physiology, Current Biology Journal, and Frontiers in Neural Circuits.

They have earned funding from the US National Institutes of Health (NIH). His current research activity is focused on advancing the understanding and treatment of degenerative and infectious diseases, including the Dendritic cell vaccine immunotherapy for COVID-19. [1,2,3,4,5,6,7,8]

Baca: Prof. Dr. Suharso

Baca: Prof. Dr. G.A. Siwabessy

Prof. Ikrar has obtained lawful permanent residence in the United States by qualifying as a physician scientist of extraordinary ability (EB-1 Visa, aka “genius visa”), and is thus recognized by the US Government as an individual with “a level of expertise indicating that the individual is one of that small percentage who have risen to the very top of the field of endeavor".

Currently, Prof. Ikrar has been inaugurated by the President of Indonesia as the Chairman of the Medical Council (Konsil Kedokteran Indonesia). [9,10]

Prof. Ikrar is an Indonesian-born pharmacologist, cardiovascular, and neuroscientist. He has an extensive educational background leading to his current scientific career.

These include earning a B.Sc. in Medicine from the Hasanuddin University in Makassar, Indonesia in 1994 and finishing his residency and receiving an M.D. from the School of Medicine in Hasanuddin University, Makassar, Indonesia in 1997.

Prof. Ikrar continued to pursue an graduate master degree in Pharmacology Medicine (M.Biomed) from the University of Indonesia, Jakarta in 2003.

Following this, he received his Doctorate, Ph.D., for his research work in “Cardiovascular and Vital Control” from Niigata University, Japan in 2008. 

His thesis concerned his invention of a novel functional impact of altered charge and/or size of amino acid residue at the selectivity filter of KCNQ1 potassium channel: Insight into gene therapy for Severe Long QT Phenotype.

Prof. Ikrar continued his postdoctoral research in the Department of Anatomy and Neurobiology, University of California, Irvine, USA (2008-2013). 

Prof. Ikrar received a promotion as an academic specialist staff of neurosciences (2013-2016). In 2016, He also accepted the offer from the Rector of the University of Hasanuddin, as an adjunct professor at the School of Medicine, Department of Neurology.

And in 2017, Prof. Ikrar moved to Pacific Health Sciences University (PHSU) at California, working as a professor of biomedical sciences. In December 2017, Prof Ikrar recruited the Presidential Hospital and Army Central Hospital (Cellcure Center) as a Senior Advisor for the Head of the Presidential Hospital. Finally, Prof. Ikrar, continued his professorship in Malahayati University, School of Medicine, Department of Pharmacology.

Also, since August 19, 2020, Prof. Ikrar was inaugurated as the Chairman of Medical Council, of the Indonesian Medical Council. [11,12,13,14,15,16]

Prof. Ikrar has experimented for more than 20 years. Utilizing his unique background, he currently works on research that combines three large and very important biomedical research areas: pharmacology, cardiology, and neurosciences.

Prof. Ikrar’s work constituted the first demonstration of the mutation of cardiac dysfunctional, belonging to genetic, Arrhythmias’ cardiac diseases.

So, for his achievements, he received the Ministry of Education Sciences and Technology Award for the outstanding Ph.D. thesis in Japan. As a physician, Prof. Dr. Ikrar continued his talent as a visiting Doctor in Bologna University, Italy, to study about cardiac intervention to cure arrhythmia by Implantable Cardioverter-Defibrillations (Pacemaker). An implantable cardioverter-defibrillator (ICD) is a small battery-powered electrical impulse generator which is implanted in patients who are at risk of sudden cardiac death due to ventricular fibrillation and ventricular tachycardia.

The device is programmed to detect cardiac arrhythmia and correct it by delivering a jolt of electricity.

In current variants, the ability to revert ventricular fibrillation has been extended to include both atrial and ventricular arrhythmias as well as the ability to perform biventricular pacing in patients with congestive heart failure or bradycardia. [11]

When he was in the University of California, Irvine, He found some discoveries about cell-type specific regulation of cortical excitability through the Allatostatin receptor system, as a basic therapy for epileptic disorder, and a new technique to do the mapping of the brain.

Baca: Prof. Dr. Zudan Arif Fakhrulloh (Dirjen Dukcapil)

Baca: RSUP Prof. Dr. R. D. Kandou

He has also applied for a patent with high precision and fasts functional mapping of cortical circuitry through a combination of voltage-sensitive dye imaging and laser scanning photo-stimulation. [1,2,3,4,5,6,7,8]

Currently, Prof. Ikrar has more than 100 international journal publications. Formerly, he has an appointment with the University of California, Irvine as an academic specialist staff.

He was the President of the Center for Interregional Study and the Vice President for the International Indonesian Scholar Association.

Also, he is a member of the American College of Clinical Pharmacology, the American Society of Gene and Cell Therapy, the American College of Cardiology, the American Heart Association, the Society for Neurosciences, the International Heart Research Association, the Asia Pacific Hearth Rhythms Association, and the Japanese Cardiologist Association.

Prof. Ikrar directs a research team investigating the neural circuit defects that directly underlie changes in drug additives behavior and result in cognitive deficits in animal models and human subjects.

This is to address novel cortical circuit mechanism by examining how genetic alterations of dopamine receptor affect emergent properties of single cells and neural populations in medial prefrontal cortex using the D2R mutant mouse. [1,2,3,4,5,6,7,8]

Prof. Ikrar is an expert Medical Doctor with multi-talents as we can see from his discovery, belonging to the large medical field: pharmacologist, cardiologist, and neuroscientist; with ability to cure of cardiovascular, heart disease, and brain disorder.

Also, he has the deeper knowledge of pharmacology, genetics, electrophysiology, ion channels, stem cells, confocal imaging, and clinical trials.

He better understands from the basic science to clinical application, has been conducting translational research, and performing advanced research, such as drug and clinical therapy, preventive medicine, stem cell therapy, and gene therapy. [11]

Throughout his graduate studies, Prof. Ikrar focused on the field of cardiovascular and vital control research, where a cardiovascular disease may refer to any disease that affects the cardiovascular system of some living organism, in particular “cardiac diseases”, namely vascular diseases of the brain and kidney, or even peripheral arterial diseases.

The causes of such cardiovascular diseases are diverse, but atherosclerosis and/or hypertension are the most common causes of such harmful ailments; with age also causing a great number of physiological and morphological changes that may greatly alter cardiovascular functions and lead to subsequently increased risk of cardiovascular disease, even in a healthy individual.

Experts in medical sciences believe that it is extremely important to pursue research in cardiovascular diseases because these diseases are the leading cause of death.

In 2008, 30% of all global deaths (17.3 million) were attributed to cardiovascular diseases (WHO, 2008) with the leading cause of all the deaths in the USA (~0.6 million of 2.5 million) are caused by cardiovascular diseases (CDC 2011).

More specifically, researchers project that by 2030, over 23 million people will die from cardiovascular diseases annually.

The primary cause of the cardiovascular diseases is the Long QT syndrome (LQTS), a cardiac disorder characterized by a prolonged QT interval, which predisposes a patient to syncope and sudden arrhythmic death. Prof. Ikrar discovered in 2008 that a prolonged QT interval most commonly results from reductions in either the rapidly (IKr) or the slowly (IKs) activating delayed rectifier K+ current.

Throughout graduate school, Prof. Ikrar studied the role of KCNQ1, otherwise known as KVLQT1, a voltage-gated K+ channel α-subunit that forms a tetrameric complex in the plasma membrane and selectively conducts K+ ions.

Although homomeric KCNQ1 channels are functional, it has become increasingly evident that at least some of the physiological functions of KCNQ1 require its coassembly with a single transmembrane domain ancillary subunit minK (known as KCNE1) to form the cardiac IKs. Mutation of KCNQ1 can lead to dysfunction of this channel, causing cardiac LQTS, with serious subsequent arrhythmias such as ventricular fibrillation and cardiac arrest, a major cause of death for many throughout, not only the United States, but also the world.

Prof. Ikrar was the first scientist to discover an I313K mutation in a female patient with LQTS and to also present her clinical characteristics, detailing important functional consequences of the mutant K+ channel along with examining its structure in great detail.

More specifically, in Prof. Ikrar’s study, cardiac diseases were found to have the same amino acid substitution at residue 313 of KCNQ1, resulting from a double-point mutation at nucleotide positions 938 (T-to-A) and 939 (C-to-A) in the gene, as determined by sequence analysis of all exons; these scientific results have since been published (Biochemical and Biophysical Research Communications 2009; 378: 589–594).

In addition to his discovery concerning the prolonged QT interval and its role in the growth of cardiac disease, Prof. Ikrar also conducted electrophysiological experiments showing that I313K mutation resulted in loss of channel function, therefore leading to dominant negative suppression.

Prof. Ikrar concluded that the I313K mutations must be related to the prolongated QT interval and syncope found in patients within the study, even finding that all patients with an I313K mutation in KCNQ1 had been diagnosed with the dominantly inherited Romano-Ward long QT syndrome (RWS). This finding indeed suggests that the mutation is a primary cause of the syndrome, a disorder associated with characteristic cardiac abnormalities, such as a prolonged QTc interval and T-wave alterations.

Prof. Ikrar's discoveries in this discipline of cardiac diseases have been published (Journal Cardiovascular Electrophysiology 2008; 19: 541-549). [1,2,3,4,5,6,7,8]

Prof. Ikrar has continued to make breakthroughs in the fields of cardiovascular and vital control electrophysiology research. By exploring the effects of the charge and the size of the amino acid residue at the pore center of KCNQ1, with advanced biotechnology techniques and studying the mutant channels, Dr. Ikrar shows the effects of the charge and the size of the amino acid residue at the pore center of KCNQ1.

These discoveries are a basis for gene therapy for cardiac arrhythmia.

Prof. Ikrar’s extraordinary works were published in the most prestigious of scientific journals: Nature, Neuron, Cell, Molecular Biology, Journal Physiology, International Journal of Cardiology, The Journal of Comparative Neurology, Lab on a Chip, Frontiers in Neural Circuits, PLoS ONE, Journal of Neurophysiology, Biochemical and Biophysical Research Communications, Journal of Cardiovascular Electrophysiology, and Circulation Journal.

Because of his groundbreaking research, Prof. Ikrar has earned worldwide scientific acclaim. [1,2,3,4,5,6,7,8]

Prof. Ikrar’s important findings provide the basis of the hypothesis of many other researchers and have led to numerous remarkable follow-up studies in the field, such as Hedley et al., Human Mutation, 2009; Peroz et al., JBC, 2008; and Burgess et al., Biochemistry 2012, that would ultimately lead to new development of novel, effective cardiac arrhythmias disorders therapeutics.

Since 2008, Prof. Ikrar's has focused his research on inhibitory neurons in the somato-sensory cortex. The inhibitory neurons in this area have projections to the thalamus and autonomic nervous system including signaling to the heart, lung, and digestive system, with particular evidence showing that the heart’s complex intrinsic nervous system qualified as a “brain”.

The heart and the brain are an intricate network with several types of neurons, neurotransmitters, proteins, and support cells. Research has shown that the heart communicates to the brain in four major ways: neurologically (through the transmission of nerve impulses), biochemically (via hormones and neurotransmitters), biophysically (through pressure waves), and energetically (through electromagnetic field interactions).

The heart’s elaborate circuitry enables it to act independently of the cranial brain - to learn, remember, and even feel and sense. The heart’s intrinsic nervous system consists of ganglia, which contain local circuit neurons of several types, and sensory neurites, which are distributed throughout the heart.

The intrinsic ganglia process and integrate inflowing information from the extrinsic nervous system and from the sensory neurites within the heart.

The extrinsic cardiac ganglia, located in the thoracic cavity, have direct connections to organs such as the lungs and esophagus and are also indirectly connected via the spinal cord to many other organs, including the skin and arteries.

The “afferent” (flowing to the brain) parasympathetic information travels from the heart to the brain through the vagus nerve to the medulla, after passing through the nodose ganglion. The sympathetic afferent nerves first connect to the extrinsic cardiac ganglia (also a processing center), then to the dorsal root ganglion and the spinal cord.

Once afferent signals reach the medulla, they travel to the subcortical areas (thalamus, amygdala, etc.) and then to the cortical areas.

“Communication along all these conduits significantly affects the brain’s activity,” Science of the Heart says, “Moreover, research shows that messages the heart sends the brain can also affect performance.”

Prof. Ikrar’s abilities show he is a both cardio-scientist and neuroscientist. As a neuroscientist, Prof. Ikrar also studies inhibitory neurons which prove to be crucial to cortical function.

Inhibitory neurons comprise about 20% of the entire cortical neuronal population and can be further subdivided into diverse subtypes based on their immunochemical, morphological, and physiological properties.

Although previous research has revealed much about intrinsic properties of individual types of inhibitory neurons, knowledge about their local circuit connections is still relatively limited.

Given that each individual neuron's function is shaped by its excitatory and inhibitory synaptic input within cortical circuits, Dr. Ikrar has been using laser scanning photostimulation (LSPS) to map local circuit connections to specific inhibitory cell types.

Compared to conventional electrical stimulation or glutamate puff stimulation, LSPS has unique advantages which allow for extensive mapping and quantitative analysis of local functional inputs to individually recorded neurons.

Laser photostimulation via glutamate uncaging selectively activates neurons perisomatically, without activating axons of passage or distal dendrites, which ensures a sub-laminar mapping resolution.

The sensitivity and efficiency of LSPS for mapping inputs from many stimulation sites over a large region are well suited for cortical circuit analysis.

Here, Prof. Ikrar introduces the technique of LSPS combined with whole-cell patch clamping for local inhibitory circuit mapping, namely injecting mice with green fluorescent proteins (GFP) in limited inhibitory neuron populations in the cortex, which enable consistent sampling of the targeted cell types. [1,2,3,4,5,6,7,8]

As for LSPS mapping, Prof. Ikrar continues to outline the system's instrumentation, describing the experimental procedures and data acquisition, and making sense of such implementations by presenting examples of circuit mappings in primary somatosensory cortex of the mouse.

As illustrated in Prof. Ikrar's experiments, caged glutamate is activated in a spatially restricted region of the brain slice by UV laser photolysis; simultaneous voltage-clamp recordings allow detection of photostimulation evoked synaptic responses.

Maps of either excitatory or inhibitory synaptic input to the targeted neuron are generated by scanning the laser beam to stimulate hundreds of potential presynaptic sites.

Thus, LSPS enables the construction of detailed maps of synaptic inputs impinging onto specific types of inhibitory neurons through repeated experiments.

Taken together, the photostimulation-based technique offers neuroscientists a powerful and useful tool for determining the functional organization of local cortical circuits, opening a new era in understanding functional neuron circuitry.

Recent progress of Prof. Ikrar’s research has presented technical advances to the field of neuroscience, all of which study the regulation of neuronal circuit activity with high spatial and temporal resolution.

Among them, the allatostatin receptor (AlstR)/ligand system has been developed for selective and quick reversible silencing of mammalian neurons.

However, targeted AlstR-mediated inactivation of specific neuronal types, particularly diverse types of inhibitory interneurons, remains to be established.

In the present study, he achieved Cre-directed expression of AlstRs to excitatory and inhibitory cell-types in the cortex and found that the AlstR-mediated inactivation was specific and robust at single-cell and neuronal population levels.

Both application of the allatostatin peptide markedly reduced spiking activity of AlstR expressing excitatory and inhibitory neurons in response to intrasomatic current injections and laser photostimulation via glutamate uncaging, but control neurons without AlstR expression were not affected.

As for the cortical network activity, the peptide application constrained photostimulation-evoked excitatory activity propagation detected by fast voltage-sensitive dye (VSD) imaging of the slices expressing AlstRs selectively in excitatory neurons, while it augmented excitatory activity in those slices with inhibitory neurons expressing AlstRs. Additionally, AlstR-mediated inactivation effectively suppressed pharmacologically induced seizure activity in the slices targeting AlstRs to excitatory neurons.

Taken together, Prof. Ikrar’s work demonstrated that the genetic delivery of AlstRs can be used for regulation of cortical excitability in a cell-type specific manner and suggested that the AlstR system can be potentially used for fast seizure control.

He is an expert in performing experiments with combined whole cell recording, electrophysiology, laser scanning photostimulation, fast voltage-sensitive dye (VSD) imaging, and optogenetics, which very few scientists can do well due to the difficulty of such advanced techniques.

The power of these combined advanced techniques is demonstrated in published data in international journals.

His study demonstrates that the AlstR/AL system has appropriate merit and features as a potent molecular tool for regulating cortical brain excitability.

Optical inactivation of neurons can be effectively achieved by using the halorhodopsin or Arch system, which activates chloride or proton pumps and offers high temporal precision.

Therefore, the study may help to design drug ligands that can be administered in the periphery and cross the blood-brain barrier, in order to access receptors within deep brain structures and/or widely distributed neuronal populations. [1,2,3,4,5,6,7,8]

A major focus of Prof. Ikrar's study is to examine whether the AlstR system can regulate the activity of diverse types of inhibitory cortical interneurons.

His study shows that the AlstR approach represents an important advancement for genetic manipulation of neuronal activity and can be valuable for many basic applications. Prof. Ikrar believes that the AlstR system can also be potentially useful in translational applications, such as seizure control and epilepsy treatment, whose dangers are previously detailed in this exposition.

Despite the progress in antiepileptic drug development and surgical management, anywhere from 30–40% of cases, epileptic seizures do not respond well to conventional therapeutic methods, presenting a wide danger for individuals suffering such diseases.

Based on Prof. Ikrar’s specificity and effectiveness of the AlstR system, this genetic inactivation system can be potentially developed as a molecular anticonvulsant with few side effects. Prof. Ikrar's most recent work was published in Frontiers in Neural Circuits, 2013, under the title: Adult neurogenesis modifies excitability of the dentate gyrus. Adult-born dentate granule neurons contribute to memory encoding functions of the dentate gyrus (DG) such as pattern separation.

However, local circuit-mechanisms in which adult-born neurons partake in this process are still poorly understood.

Computational, neuroanatomical, and electrophysiological studies suggest that sparseness of activation in the granule cell layer (GCL) is conducive for pattern separation.

A sparse coding scheme is thought to facilitate the distribution of similar entorhinal inputs across the GCL to de-correlate overlapping representations and minimize interference.

Here, Prof. Ikrar used fast voltage-sensitive dye (VSD) imaging combined with laser photostimulation and electrical stimulation to examine how selectively increasing adult DG neurogenesis influences local circuit activity and excitability.

Prof. Ikrar data shows that DG in mice with more adult-born neurons exhibits decreased strength of neuronal activation and more restricted excitation spread in GCL while maintaining effective output to CA3c.

Conversely, blockage of adult hippocampal neurogenesis changed excitability of the DG in the opposite direction.

Analysis of GABAergic inhibition onto mature dentate granule neurons in the DG of mice with more adult-born neurons shows a modest readjustment of perisomatic inhibitory synaptic gain without changes in overall inhibitory tone, presynaptic properties or GABAergic innervation pattern.

Retroviral labeling of connectivity in mice with more adult-born neurons showed increased number of excitatory synaptic contacts of adult-born neurons onto hilar interneurons.

Together, these studies demonstrate that adult hippocampal neurogenesis modifies excitability of mature dentate granule neurons and that this non-cell autonomous effect may be mediated by local circuit mechanisms, such as excitatory drive onto hilar interneurons.

Modulation of DG excitability by adult-born dentate granule neurons may enhance sparse coding in the GCL to influence pattern separation. His discovery explains important regeneration of the brain. [1,2,3,4,5,6,7,8]

Prof. Ikrar’s discovery that experience alters cortical networks through neural plasticity mechanisms. During a developmental critical period, the most dramatic consequence of occluding vision through one eye (monocular deprivation) is a rapid loss of excitatory synaptic inputs to parvalbumin-expressing (PV) inhibitory neurons in visual cortex.

Subsequent cortical disinhibition by reduced PV cell activity allows for excitatory ocular dominance plasticity.

However, the molecular mechanisms underlying critical period synaptic plasticity are unclear.

Here we show that brief monocular deprivation during the critical period downregulates neuregulin-1(NRG1)/ErbB4 signaling in PV neurons, causing retraction of excitatory inputs to PV neurons.

Exogenous NRG1 rapidly restores excitatory inputs onto deprived PV cells through downstream PKC-dependent activation and AMPA receptor exocytosis, thus enhancing PV neuronal inhibition to excitatory neurons. NRG1 treatment prevents the loss of deprived eye visual cortical responsiveness in vivo.

Our findings reveal molecular, cellular, and circuit mechanisms of NRG1/ErbB4 in regulating the initiation of critical period visual cortical plasticity. His work was published at Neuron (2016). [17,18,19,20]

Prof. Ikrar continues to contribute to the medical field, pursuing collaborative work with the University of California, Irvine and the University of California, Los Angeles neurobiologists, revealing a new approach to correcting visual disorders in children who suffer from early cataracts or amblyopia, also known as lazy eye.

Such youngsters can have permanent defects in vision, even after surgery, which tries to remove cataracts or correct lazy eye.

These flaws are often a result of improper brain development due to visual deprivation during childhood.

In contrast, when cataracts in adults are surgically corrected, normal vision is usually restored. Prof. Ikrar and his team found that this phenomenon is caused by a specific class of inhibitory neurons that control the time window, or “critical period,” in early vision development, generally before age 7.

The researchers discovered that improper functioning of these key neurons during the critical period of development is responsible for these vision defects. Additionally, in tests on mice, they used an experimental drug compound to reopen this critical-period window and treat the neuronal defects associated with temporary loss of vision in one eye during early development (2013, 2020).

Also, Prof. Ikrar discovered ALS (Amyotrophic Lateral Sclerosis) etiology, pathophysiology, and new treatment. (2018, 2019). [1,2,3,4,5,6,7,8]

Prof. Ikrar's discoveries in this discipline of neurosciences disorder have been published in One’s of the highest impact papers (Nature, 2013; 501:543-6).

His work suggests that drugs targeted to the critical period-regulating neurons can correct central vision disorders in children who’ve suffered from amblyopia or early cataracts.

The specific types of neurons that mediate the critical-period window during childhood development have not been well understood until now.

The breakthrough outlines a new path for treatments that can restore normal vision in children who have had early vision disorders.

The study received support from the National Eye Institute (grant EY016052) and the National Institute for Neurological Disorders & Stroke (grant NS078434): “In addition, Prof. Ikrar’s work has been supported by grants from the National Institute of Health (project number: RO1-NS078434), the National Alliance for Research on Schizophrenia and Depression (NARSAD), the National Institute for Neurological Disorders and Stroke (grant EY016052),"

"He also is supported by collaboration through funding by National Eye Institute (Grant EY016052), the US National Institute of Health grant RO1-EY014882 (Hey-Kyoung Lee), the Bettencourt Schueller Foundation and Philippe Foundation (Antonie Bernard), NARSAD, the New York Stem Cell Initiative, the US National Institute of Health grant RO1- MH068542, the (HDRF) Hope for Depression Foundation grants (Rene Hen), the US National Institutes of Health grant 4R00MH086615-03, the Ellison Medical Foundation New Scholar Aging and the Whitehall Foundation grant (Amar Sahay), and the Mombukagakusho award (Ministry of Education, Sciences, and Technology of Japan).” Prof. Ikrar’s publications also reflect his achievements. [12,13,14,15,16]

He has more than 100 publications in peer reviewed journals, conference publications, 25 of which he acted as first author, in prestigious journals such as Nature, a top number 1-ranked journal in broad and inter-discipliners science research and authored a book.

Prof. Ikrar’s publication record has had profound effect; many papers have cited his published work, and his research has been cited thousands of times by researchers all over the world. Moreover, Prof. Ikrar has other achievements.

He has extensive services as a Co-editor in Chief of a scientific international journal, Progress and Communication in Sciences, Malaysian Journal of Health Sciences, Makara Journal of Health Sciences, Periodical of Dermatology and Venereology Journal, and the Multidisciplinary Journal of Dental, Jaw, and Face Development and Sciences. [1,2,3,4,5,6,7,8]

Prof. Ikrar has been featured in several media reports as well. He is a member of several prominent organizations, including the prestigious Society for Neuroscience (SFN), and the Asia Pacific Heart Rhythm Society (APHRS).

SFN is an outstanding organization of scientists and physicians who are devoted to advance research on the brain and nervous system.

SFN is also devoted to education of the latest advances in brain research and raising awareness of the need to make neuroscience research a funding priority. The Society's annual meeting is the premier venue for neuroscientists from around the world to debut cutting-edge research.

Membership in SFN is by recommendation, i.e., the candidate has to do research relating to neurosciences, and must be sponsored by two full members of SFN. Thus, being a member in SFN means that Prof. Ikrar has received recognition as a valuable member of his scientific community.

Prof. Ikrar has established himself as a top scientist in his field and will undoubtedly continue to make significant contributions. He is an internationally recognized molecular geneticist, cardiologist, and neuroscientist.

In summary, Prof. Ikrar is an excellent and internationally recognized scientist. Prof. Ikrar’s research has focused on understanding the mechanisms underlying several neurological and mental disorders such as epilepsy, schizophrenia, and attention disorders.

Prof. Ikrar has made many seminal contributions including his pioneering work on functional imaging techniques, gene, and cell therapy for rare diseases. [29,30,31,32, 33,34,35,36, 37]

He and his family hold Green Cards as Permanent Residents in the USA, and they are living in Irvine. Irvine is one of the safest and one of the best places to live in the USA. In his happy family, Prof. Ikrar is married with Dr. Elfi Wardaningsih and has three healthy kids: Aqilla S. Ikrar, Athallah R. Ikrar, Alaric K. Ikrar. [38,39]