プロフィール詳細

プロジェクトを作成

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Dr. Madhusmita S.に依頼

Finland

Neuroscientist‑trained PMO leader applying brain‑based insights to decision‑making, performance, and leadership.

プロフィール概要

Freelance scientific write, Neuroscience specialist, helping teams cmmunicate complex ideas with clarity.

専門分野

• ☆ Zoology
• ☆ Cell Biology
• ☆ Cell-Based Assays
• ☆ Neuroscience
• ☆ Molecular Neuroscience
• ☆ Artificial Intelligence
• ☆ Primary Cells
• ☆ Excel
• ☆ Project Management

サービス

• Writing

Writing Medical Writing, Non-Medical Regulatory Writing, Creative Writing, Newswriting, Audio Transcription, General Proofreading & Editing

職務経験

Senior Project Manager, PMO team lead

Nanoform Finland Oyj

5月 2021 - 現在

University of Helsinki

- 12月 2020

学歴

PhD (Anatomy and Biomedicine, Faculty of medicine)

University of Helsinki

2月 2007 - 12月 2013

認定資格

• PMP

  PMI

  2月 2023 - 現在

出版物

JOURNAL ARTICLE

Fluoxetine and Ketamine Enhance Extinction Memory and Brain Plasticity by Triggering the p75 Neurotrophin Receptor Proteolytic Pathway @article{aa473af8f8c6469bbc2e456afa8a7e3f, title = "Fluoxetine and Ketamine Enhance Extinction Memory and Brain Plasticity by Triggering the p75 Neurotrophin Receptor Proteolytic Pathway", abstract = "BACKGROUND: Diverse antidepressants were recently described to bind to TrkB (tyrosine kinase B) and drive a positive allosteric modulation of endogenous BDNF (brain-derived neurotrophic factor). Although neurotrophins such as BDNF can bind to p75NTR (p75 neurotrophin receptor), their precursors are the high-affinity p75NTR ligands. While part of an unrelated receptor family capable of inducing completely opposite physiological changes, TrkB and p75NTR feature a crosslike conformation dimer and carry a cholesterol-recognition amino acid consensus in the transmembrane domain. As such qualities were found to be crucial for antidepressants to bind to TrkB and drive behavioral and neuroplasticity effects, we hypothesized that their effects might also depend on p75NTR. METHODS: Enzyme-linked immunosorbent assay-based binding and nuclear magnetic resonance spectroscopy were performed to assess whether antidepressants would bind to p75NTR. HEK293T cells and a variety of in vitro assays were used to investigate whether fluoxetine (FLX) or ketamine (KET) would trigger any a- and g-secretase- dependent p75NTR proteolysis and lead to p75NTR nuclear localization. Ocular dominance shift was performed with male and female p75NTR knockout mice to study the effects of KET and FLX on brain plasticity, in addition to pharmacological interventions to verify how p75NTR signaling is important for the effects of KET and FLX in enhancing extinction memory in male wild-type mice and rats. RESULTS: Antidepressants were found to bind to p75NTR. FLX and KET triggered the p75NTR proteolytic pathway and induced p75NTR-dependent behavioral/neuroplasticity changes. CONCLUSIONS: We hypothesize that antidepressants co-opt both BDNF/TrkB and proBDNF/p75NTR systems to induce a more efficient activity-dependent synaptic competition, thereby boosting the brain's ability for remodeling.", keywords = "Nuclear translocation, Antidepressant drugs, Synaptic plasticity, Fear extinction, Mature bdnf, Probdnf, Fluoxetine, Activation, Cleavage, Inhibition, 3112 Neurosciences, 3124 Neurology and psychiatry", author = "Diniz, \{Cassiano Ricardo Alves Faria\} and Crestani, \{Ana Paula\} and Casarotto, \{Plinio Cabrera\} and Caroline Biojone and Cecilia Cannarozzo and Frederike Winkel and Prozorov, \{Mikhail A.\} and Kot, \{Erik F.\} and Goncharuk, \{Sergey A.\} and Marques, \{Danilo Benette\} and Zacharias, \{Leonardo Rakauskas\} and Henri Autio and Sahu, \{Madhusmita Priyadarshini\} and Borges-Assis, \{Anna Barbara\} and Leite, \{Joao Pereira\} and Mineev, \{Konstantin S.\} and Eero Castren and Resstel, \{Leonardo Barbosa Moraes\}", year = "2025", month = feb, day = "1", doi = "10.1016/j.biopsych.2024.06.021", language = "English", volume = "97", pages = "248--260", journal = "Biological Psychiatry", issn = "0006-3223", publisher = "Elsevier Inc. ", number = "3", } . Biological Psychiatry.

Depletion of TrkB Receptors From Adult Serotonergic Neurons Increases Brain Serotonin Levels, Enhances Energy Metabolism and Impairs Learning and Memory @article{eb5f7add93db4f5492fa2553f5f3a817, title = "Depletion of TrkB Receptors From Adult Serotonergic Neurons Increases Brain Serotonin Levels, Enhances Energy Metabolism and Impairs Learning and Memory", abstract = "Neurotrophin brain-derived neurotrophic factor (BDNF) and neurotransmitter serotonin (5-HT) regulate each other and have been implicated in several neuronal mechanisms, including neuroplasticity. We have investigated the effects of BDNF on serotonergic neurons by deleting BDNF receptor TrkB from serotonergic neurons in the adult brain. The transgenic mice show increased 5-HT and Tph2 levels with abnormal behavioral phenotype. In spite of increased food intake, the transgenic mice are significantly leaner than their wildtype littermates, which may be due to increased metabolic activity. Consistent with increased 5-HT, the proliferation of hippocampal progenitors is significantly increased, however, long-term survival of newborn cells is unchanged. Our data indicates that BDNF-TrkB signaling regulates the functional phenotype of 5-HT neurons with long-term behavioral consequences.", keywords = "serotonin, TrkB, BDNF, neuronal plasticity, neurotrophic factor, 3112 Neurosciences", author = "Sahu, \{Madhusmita P.\} and Yago Pazos-Boubeta and Anna Steinzeig and Katja Kaurinkoski and Michela Palmisano and Olgierd Borowecki and Piepponen, \{Timo Petteri\} and Eero Castren", year = "2021", month = apr, day = "15", doi = "10.3389/fnmol.2021.616178", language = "English", volume = "14", journal = "Frontiers in Molecular Neuroscience", issn = "1662-5099", publisher = "Frontiers Media SA", } . Frontiers in Molecular Neuroscience.

Antidepressant drugs act by directly binding to TRKB neurotrophin receptors @article{742b75a6d0924b2581c85410ca808bbe, title = "Antidepressant drugs act by directly binding to TRKB neurotrophin receptors", abstract = "It is unclear how binding of antidepressant drugs to their targets gives rise to the clinical antidepressant effect. We discovered that the transmembrane domain of tyrosine kinase receptor 2 (TRKB), the brain-derived neurotrophic factor (BDNF) receptor that promotes neuronal plasticity and antidepressant responses, has a cholesterol-sensing function that mediates synaptic effects of cholesterol. We then found that both typical and fast-acting antidepressants directly bind to TRKB, thereby facilitating synaptic localization of TRKB and its activation by BDNF. Extensive computational approaches including atomistic molecular dynamics simulations revealed a binding site at the transmembrane region of TRKB dimers. Mutation of the TRKB antidepressant-binding motif impaired cellular, behavioral, and plasticity-promoting responses to antidepressants in vitro and in vivo. We suggest that binding to TRKB and allosteric facilitation of BDNF signaling is the common mechanism for antidepressant action, which may explain why typical antidepressants act slowly and how molecular effects of antidepressants are translated into clinical mood recovery.", keywords = "1182 Biochemistry, cell and molecular biology", author = "Casarotto, \{Plinio C.\} and Mykhailo Girych and Fred, \{Senem M.\} and Vera Kovaleva and Rafael Moliner and Giray Enkavi and Caroline Biojone and Cecilia Cannarozzo and Sahu, \{Madhusmita Pryiadrashini\} and Katja Kaurinkoski and Brunello, \{Cecilia A.\} and Anna Steinzeig and Frederike Winkel and Sudarshan Patil and Stefan Vestring and Tsvetan Serchov and Diniz, \{Cassiano R. A. F.\} and Liina Laukkanen and Iseline Cardon and Hanna Antila and Tomasz Rog and Piepponen, \{Timo Petteri\} and Bramham, \{Clive R.\} and Claus Normann and Lauri, \{Sari E.\} and Mart Saarma and Ilpo Vattulainen and Eero Castren", year = "2021", month = mar, day = "4", doi = "10.1016/j.cell.2021.01.034", language = "English", volume = "184", pages = "1299--+", journal = "Cell", issn = "0092-8674", publisher = "Elsevier B.V.", number = "5", } . Cell.

Madhusmita Priyadarshini Sahu, Outi Nikkilä, Seija Lågas, Sulo Kolehmainen, Eero Castrén(2019). Culturing primary neurons from rat hippocampus and cortex . Neuronal Signaling. 3. (2). Portland Press Ltd.

Neurotrophin receptor Ntrk2b function in the maintenance of dopamine and serotonin neurons in zebrafish @article{cd1af9dc8d3a4a2ead3b913e64374ef6, title = "Neurotrophin receptor Ntrk2b function in the maintenance of dopamine and serotonin neurons in zebrafish", abstract = "Neurotrophins and their receptors have highly conserved evolutionary lineage in vertebrates including zebrafish. The NTRK2 receptor has two isoforms in zebrafish, Ntrk2a and Ntrk2b. The spatio-temporal expression pattern of bdnf and ntrk2b in the zebrafish brain was studied using in situ hybridization. The robust and corresponding expression pattern of ntrk2b to bdnf suggests that ntrk2b is the key receptor for bdnf in the zebrafish brain, unlike its duplicate isoform ntrk2a. To study ntrk2b function, two different genetic strategies, the TILLING mutant and morpholino oligonucleotides (MO), were used. Specific subsets of the dopaminergic and serotonergic neuronal populations were affected in the mutants and morphants. The mutant showed anxiety-like behavior both in larval and adult stages. Our results consistently indicate that BDNF/NTRK2 signaling has a significant role in the development and maintenance of aminergic neuronal populations. Therefore, the ntrk2b-deficient zebrafish is well suited to study mechanisms relevant for psychiatric disorders attributed to a dysfunctional monoaminergic system.", keywords = "ADULT ZEBRAFISH, BRAIN, BDNF, TRKB, EXPRESSION, SYSTEM, ACTIVATION, LOCALIZATION, PLASTICITY, PHENOTYPE, 3112 Neurosciences, 3111 Biomedicine", author = "Sahu, \{Madhusmita Priyadarshini\} and Yago Pazos-Boubeta and Ceren Pajanoja and Stanislav Rozov and Pertti Panula and Eero Castren", year = "2019", month = feb, day = "14", doi = "10.1038/s41598-019-39347-3", language = "English", volume = "9", journal = "Scientific Reports", issn = "2045-2322", publisher = "Nature Research ", } . Scientific Reports.

Madhusmita Priyadarshini Sahu, Yago Pazos-Boubeta, Ceren Pajanoja, Stanislav Rozov, Pertti Panula, Eero Castrén (2019). Neurotrophin receptor Ntrk2b function in the maintenance of dopamine and serotonin neurons in zebrafish . Scientific Reports.

Madhusmita Priyadarshini Sahu, Outi Nikkilä, Seija Lågas, Sulo Kolehmainen, Eero Castrén(2019). Culturing primary neurons from rat hippocampus and cortex . Neuronal signaling. 3. (2). Portland Press Ltd.

Oxidative Stress and Regulation of Pink1 in Zebrafish (Danio rerio) @article{4980e0f0bbca4d9ab9eb9b593aea5c5c, title = "Oxidative Stress and Regulation of Pink1 in Zebrafish (Danio rerio)", keywords = "PARKINSONS-DISEASE, TYROSINE-HYDROXYLASE, MITOCHONDRIAL DYNAMICS, TRANSGENE EXPRESSION, MESSENGER-RNA, GENES, BRAIN, TOL2, SYSTEMS, GLUTATHIONE, 3111 Biomedicine", author = "Madhusmita Priyadarshini and Orosco, \{Lori A.\} and Panula, \{Pertti J.\}", year = "2013", month = nov, day = "26", doi = "10.1371/journal.pone.0081851", language = "English", volume = "8", journal = "PLoS One", issn = "1932-6203", publisher = "Public Library of Science", number = "11", } . PLoS One.

A zebrafish model of PINK1 deficiency reveals key pathway dysfunction including HIF signaling @article{2e1e462384b8426fb4e1ebff3ddac821, title = "A zebrafish model of PINK1 deficiency reveals key pathway dysfunction including HIF signaling", keywords = "PINK1, HIF, ROS, notch1a, vegf, Parkinson's disease, ONSET PARKINSONS-DISEASE, NEURODEGENERATIVE DISEASES, HYPOXIA, SYSTEMS, NEURONS, BRAIN, ANTIOXIDANTS, ACTIVATION, EXPRESSION, MUTATIONS, 3111 Biomedicine, 3112 Neurosciences", author = "M. Priyadarshini and J. Tuimala and Chen, \{Y. C.\} and P. Panula", year = "2013", month = jun, doi = "10.1016/j.nbd.2013.02.002", language = "English", volume = "54", pages = "127--138", journal = "Neurobiology of Disease", issn = "0969-9961", publisher = "Academic Press Inc.", } . Neurobiology of Disease.

MANF regulates dopaminergic neuron development in larval zebrafish @article{32cdb5493b1d4e3e96d5cae565e47f88, title = "MANF regulates dopaminergic neuron development in larval zebrafish", keywords = "3112 Neurosciences", author = "Chen, \{Y. -C.\} and M. Sundvik and S. Rozov and M. Priyadarshini and P. Panula", year = "2012", month = oct, day = "15", doi = "10.1016/j.ydbio.2012.07.030", language = "English", volume = "370", pages = "237--249", journal = "Developmental Biology", issn = "0012-1606", publisher = "Elsevier Inc. ", number = "2", } . Developmental Biology.

P. Panula, Y. -C. Chen, M. Priyadarshini, H. Kudo, S. Semenova, M. Sundvik, V. Sallinen(2010). The comparative neuroanatomy and neurochemistry of zebrafish CNS systems of relevance to human neuropsychiatric diseases . Neurobiology of Disease. 40. Microsoft.AspNetCore.Mvc.Localization.LocalizedHtmlString 46--57. Academic Press Inc.

Ville Sallinen, Juha Kolehmainen, Madhusmita Priyadarshini, Gabija Toleikyte, Yu-Chia Chen, Pertti Panula(2010). Dopaminergic cell damage and vulnerability to MPTP in Pink1 knockdown zebrafish . Neurobiology of Disease. 40. Microsoft.AspNetCore.Mvc.Localization.LocalizedHtmlString 93--101. Academic Press Inc.

OTHER

Plinio C Casarotto, Mykhailo Girych, Senem M Fred, Vera Kovaleva, Rafael Moliner, Giray Enkavi, Caroline Biojone, Cecilia Cannarozzo, Madhusmita Pryiadrashini Sahu, Katja Kaurinkoski, et al.(2019). Antidepressant drugs act by directly binding to TRKB neurotrophin receptors . Cold Spring Harbor Laboratory

Madhusmita Priyadarshini Sahu, Outi Nikkilä, Seija Lågas, Sulo Kolehmainen, Eero Castrén(2018). Culturing primary neurons from rat hippocampus and cortex . Cold Spring Harbor Laboratory

DISSERTATION THESIS

Madhusmita Priyadarshini(2013). Neurobiology of Parkinson’s disease gene Pink1 in Danio rerio (Zebrafish) . Helsinki University Biomedical dissertations. (190). University of Helsinki