Michal Schwartz | Neurodegenerative diseases | Best Researcher Award

Published on by Cognitive Scientist Awards

Prof Dr. Michal Schwartz | Neurodegenerative diseases | Best Researcher Award

Michal Schwartz (born 1 January 1950) is a professor of neuroimmunology at the Weizmann Institute of Science. She is active in the field of neurodegenerative diseases, particularly utilizing the immune system to help the brain fight terminal neurodegenerative brain diseases, such as Alzheimer’s disease and dementia.[3][1]

Schwartz’s studies have shown that the immune system supports a healthy brain’s function and is vital for healing and protecting the brain in case of injury or disease.[4]

Schwartz coined the term protective autoimmunity[5] and discovered roles for immune cells in repair and neurogenesis. She has been the elected chair of the International Society of Neuroimmunology (ISNI) since 2016.[6]

In 2023 Schwartz received the honorary Israel Prize for Life Sciences.

 

Profile

Education

Schwartz gained her Bachelor of Science in chemistry at the Hebrew University of Jerusalem in 1972. She received her Ph.D in Immunology in 1977 at the Weizmann Institute of Science, where she would later spend the majority of her career. She also spent time at the University of Michigan, Ann Arbor, researching nerve regeneration.[when?

 

Work experience

At the Weizmann Institute, she progressed from senior scientist in the Department of Neurobiology to full professor in 1998, and was then awarded the Maurice and Ilse Katz Professorial Chair in Neuroimmunology in 2016.[7] Schwartz’s work in neuroimmunology has encompassed a wide range of pathologies in the central nervous system (CNS), including injury, neurodegeneration, mental dysfunction, and aging. She coined the term protective autoimmunity and demonstrated the role of immune cells such as macrophages and T cells in spinal cord repair. She also identified specific brain areas for ‘cross talk’ between the CNS and the immune system. This cross-talk is important for recruiting immune cells and maintaining a healthy brain, and the disruption of this cross-talk can play a role in brain aging and neurodegenerative disease. She also showed this role in pregnancy and fetal brain development, where immune disruption in the mother can be linked to neurodevelopmental disorders in their children. Another focus of her work has been on repurposing cancer immunotherapies such as PD-1 blockers to treat neurodegenerative disorders, such as Alzheimer’s disease.

Macrophages

The Schwartz team discovered that bone marrow-derived macrophages are needed for central nervous system (CNS) repair. The brain-resident myeloid cells (the microglia), and infiltrating monocyte-derived macrophages are not redundant populations, despite their myeloid phenotype, and display distinct functions in resolution of brain inflammation.[8][9][10]

Autoimmunity

In her research, Schwartz discovered that the ability to cope with sterile CNS injuries requires support in the form of an adaptive immune response mediated by CD4+ T cells that recognize CNS antigens. She coined the concept of protective autoimmunity, to distinguish this response from autoimmune disease, in which the anti-self response escapes control. Over the years, it became clear that adaptive immunity is needed to facilitate the recruitment of immunoregulatory cells, including bone marrow-derived macrophages and FoxP3 regulatory T cells, though the balance between regulatory T cells and effector memory cells is different in the periphery versus the brain.[11][12][13]

Brain Homeostasis

Schwartz’s team discovered the role of adaptive systemic immune cells, and specifically T cells recognizing brain antigens (Protective autoimmune T cells), in supporting the cognitive capacity of the healthy brain, for lifelong neurogenesis, and functional brain plasticity. These observations paved the way for numerous additional discoveries in which the brain-immune axis was described.[14][15][16]

The Choroid Plexus

Schwartz’s team identified the brain’s choroid plexus (CP) within the blood-cerebrospinal fluid barrier as an immunological interface between the brain and the immune system. It serves as a niche that hosts immune cells, and as a physiological entry gate for leukocytes. Focusing on this unique niche within the brain led the Schwartz group to propose that IFN-γ holds the key to regulating CP gateway activity. Her team further showed that in brain aging and neurodegenerative diseases (studied using both mouse models and human samples), dysfunction of this interface is determined both by signals originating in the brain, and signals from the aged immune system, which led to the identification of Type-I Interferon (IFN-I) at the CP as a negative player, affecting the fate of the aging brain in general, and of microglia, in particular. A similar IFN-I signature at the CP was subsequently discovered by others in Alzheimer’s disease and in the postmortem brains of infected patients who died from COVID-19.[17][14][10]

Immunotherapy

The discovery that adaptive immunity plays a key role in brain function and repair, the need for bone marrow-derived macrophages to resolve local brain inflammation, the fact that Alzheimer’s disease (AD) and all forms of dementia are mainly age-related diseases, and the fact that the immune system is particularly affected by aging all led Schwartz to propose a new treatment for combating dementias. Schwartz suggested empowering systemic immunity, using a form of immunotherapy by modestly blocking the inhibitory immune checkpoint PD1/PD-L1 pathway.[citation needed] This treatment drives an immune-dependent cascade of events, that allows the harnessing of bone marrow-derived macrophages and regulatory T cells to help clear toxic factors from the diseased brain, and to arrest the local inflammation, thereby providing a comprehensive multi-factorial therapy through modification of multiple elements that go awry in AD. Schwartz’s patents for developing such immunotherapy for AD are licensed to a small Biopharma company, Immunobrain Checkpoint. The company is awaiting a clinical trial in AD patients, supported in part by the National Institute of Aging, the US National Institutes of Health, and The Alzheimer’s Association.[18][19][20][21][22][23]

Publication

1. Rachmian N, Medina S, Cherqui U, Akiva H, Deitch D, Edilbi D, Croese T, Salame T, Peralta Ramos
J, Cahalon L, Krizhanovsky V, Schwartz M. 2024. Senescent microglia conserved in aging and
Alzheimer’s disease exhibit elevated TREM2 protein levels. Nat Neurosci 27: 1116-24
2. Tsitsou-Kampeli A, Suzzi S, Kenigsbuch M, Satomi A, Strobelt R, Singer O, Feldmesser E, Purnapatre
M, Colaiuta SP, David E, Cahalon L, Hahn O, Wyss-Coray T, Shaul Y, Amit I, Schwartz M. 2023.
Cholesterol 24-hydroxylase at the choroid plexus contributes to brain immune homeostasis. Cell Rep
Med: 101278
3. Suzzi, S. Croese T., Ravid A., Gold O., Clark A., Medina A., Kitsberg D., Adam M., Vernon K., Kohnert
E., Shapira I., Malitsky S., Itkin M., Brandis A., Mehlman T., Salame T., Colaiuta S., Cahalon L.,Slyper
M., Greka A., Habib N., Schwartz M. 2023. N-acetylneuraminic acid links immune exhaustion and
accelerated memory deficit in diet-induced obese Alzheimer’s disease mouse model 2023. Nat. Commun.
14:1293.
4. Kenigsbuch M, Bost P, Halevi S, Chang Y, Chen S, Ma Q, Hajbi R, Schwikowski B, Bodenmiller B, Fu
H, Schwartz M*, Amit I* (equal contribution, and corresponding authors). 2022. A shared diseaseassociated oligodendrocyte signature among multiple CNS pathologies. Nat Neurosci 25: 876-86.
5. Dvir-Szternfeld R, Castellani G, Arad M, Cahalon L, Colaiuta SP, Keren-Shaul H, Croese T, Burgaletto
C, Baruch K, Ulland T, Colonna M, Weiner A, Amit I, Schwartz M. 2022. Alzheimer’s disease
modification mediated by bone marrow-derived macrophages via a TREM2-independent pathway in
mouse model of amyloidosis. Nature Aging 2: 60-73 (citations:17).
6. Ben-Yehuda H, Arad M, Peralta Ramos JM, Sharon E, Castellani G, Ferrera S, Cahalon L, Colaiuta SP,
Salame TM, Schwartz M. 2021. Key role of the CCR2-CCL2 axis in disease modification in a mouse
model of tauopathy. Mol Neurodegeneration 16: 39. (citations:20).
7. Cohen M, Giladi A, Raposo C, Zada M, Li B, Ruckh J, Deczkowska A, Mohar B, Shechter R, Lichtenstein
RG, Amit I, Schwartz M. 2021. Meningeal lymphoid structures are activated under acute and chronic
spinal cord pathologies. Life Sci Alliance 4: e202000907.
8. Habib N, McCabe C, Medina S, Varshavsky M, Kitsberg D, Dvir-Szternfeld R, Green G, Dionne D,
Nguyen L, Marshall JL, Chen F, Zhang F, Kaplan T, Regev A, Schwartz M. 2020. Disease- associated
astrocytes in Alzheimer’s disease and aging. Nat Neurosci 23: 701-6. (citations:617).
9. Ben-Yehuda H, Matcovitch-Natan O, Kertser A, Spinrad A, Prinz M, Amit I, Schwartz M. 2020.
Maternal Type-I interferon signaling adversely affects the microglia and the behavior of the offspring
accompanied by increased sensitivity to stress. Mol Psychiatry 25: 1050-67 (Cover page).
10. Kertser A,Baruch K, Deczkowska A,Weiner A,Croese T, Kenigsbuch M,CooperI, Tsoory M,Ben- Hamo
S, Amit I, Schwartz M. 2019. Corticosteroid signaling at the brain-immune interface impedes coping with
severe psychological stress. Sci Adv 5: eaav4111. (citations:32).
11. Rosenzweig N, Dvir-Sternfeld R, Tsitsou-Kampeli A, Keren-Shaul H, Ben-Yehuda H, Weill-Raynal P,
Cahalon L, Kertser A, Baruch K, Amit I, Weiner A, Schwartz M. 2019. PD-1/PD-L1 checkpoint blockade
harnesses monocyte-derived macrophages to combat cognitive impairment in a mouse model of tauassociated dementia. Nat Commun. 10: 465. (citations:141).
12. Deczkowska A, Matcovitch-Natan O, Tsitsou-Kampeli A, Ben-Hamo S, Dvir-Szternfeld R, Spinrad A,
Singer O, David E, Winter RD, Smith KL, Kertser A, Baruch K, Rosenzweig N, Terem A, Prinz M,
Villeda S, Citri A, Amit I, Schwartz M. 2017. Mef2C restrains the microglial inflammatory response and
is lost in brain ageing in an IFN-I-dependent manner. Nat Commun 8: 717. (citations:212).
13. Cohen M, Ben-Yehuda H, Porat Z, Raposo C, Gordon S, Schwartz M. 2017. Newly formed endothelial
2
cells regulate myeloid cell activity following spinal cord injury via expression of CD200 ligand. J
Neurosci 37: 972-85.

said Pournaghash-tehrani | Neuroscience | Best Faculty Award

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Dr. said Pournaghash-tehrani | Neuroscience | Best Faculty Award

 

Profile

  • Googlescholar
  • Researchgate

Education

Said Pournaghash-Tehrani earned his Doctor of Philosophy in Psychology in 1993 from The American University in Washington, D.C., where he also completed his Master of Arts in Psychology in 1990. He holds a Bachelor of Science in Distributive Science from the same institution, which he obtained in 1986. Fluent in English and German, he also has familiarity with French. He can be reached via email at spournaghash@yahoo.com or by telephone at 011-98-09122074388.

Work experience
  • Said Pournaghash-Tehrani has extensive academic and research experience in psychology. He served as a Research Associate in 2001 at the Department of Pharmacology and Experimental Therapeutics, Loyola University’s Stritch School of Medicine in Chicago, Illinois. In 2002, he took a sabbatical as a researcher at the Department of Psychology, Carleton University in Ottawa, Canada, focusing on cross-cultural studies related to Iranian attitudes towards the West. Since 2002, he has been an Assistant Professor in the Department of Psychology at Tehran University, having previously held the same position at Azzahra University in Tehran from 1996 to 2001. Additionally, he was a member of the Scientific Council on Energy and Economic Studies at the Institute for International and Political Studies (IPIS) from 1998 to 2000, where he also worked as a political researcher. His early academic career included serving as a Teaching and Research Assistant at The American University’s Department of Psychology from 1987 to 1990, where he contributed to courses such as Introduction to Psychology, Neuroscience Seminar, Psychopharmacology, Neuropsychology, Biological Basis of Behavior, and Learning and Behavior.

Books

–Fundamentals of Clinical Psychopharmacology, (2007); Samt Publications
-Drugs and Behavior, (2004); Samt Publications.
-Physiological Psychology, Tehran University Publication.
-Intimacy; Alzahra University Publication.
-Theories of Addiction, Alzahra University Publication.

Conference Presentations

Said Pournaghash-Tehrani has contributed extensively to neuroscience and psychology research, presenting his findings at prestigious conferences such as the Society for Neuroscience and the Eastern Psychological Association. His work has focused on drug discrimination learning, conditioned taste aversion, and the effects of opioids and their antagonists. In 1987, he co-authored studies assessing the discriminative stimulus properties of naloxone and the failure of cholecystokinin to counteract morphine sulfate’s effects. His later research explored the antagonism of morphine stimuli, the role of buprenorphine in opiate-naive and dependent animals, and the impact of RO15-4513 on ethanol-induced taste aversion. He has collaborated with notable researchers, including A.L. Riley, contributing to investigations on diazepam exposure and behavioral toxicology. His presentations in New Orleans, Washington, D.C., Boston, and other major research venues highlight his significant role in advancing psychopharmacology and behavioral neuroscience.

Publication

Marcelo Luis Berthier | Neuroscience| Best Researcher Award

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Prof. Marcelo Luis Berthier | Neuroscience| Best Researcher Award

 

Unversidad de Málaga, Spain

Profile

Education

Marcelo Luis Berthier obtained his degree in Medicine (1972-1976) and completed residency training in Neurosurgery (1977-1980), later specializing in Neurology (1980). He served as a staff neurologist at the Institute of Neurological Research, FLENI, Buenos Aires, Argentina (1980-1989), before becoming a research fellow in the Department of Neurology at Clinic Hospital of Barcelona, Spain (1989-1990). From 1991 to 2000, he was a staff neurologist and physician in charge of the Behavioural Neurology Unit at the Clinic University Hospital of Malaga. He earned a PhD in Neuroscience (cum laude) from the University of Malaga and coordinated the Group of Behavioural Neurology and Dementia of the Spanish Neurological Society (2004-2006). In 2004, he founded and directed the Unit of Cognitive Neurology and Aphasia at the Centro de Investigaciones Médico-Sanitarias, University of Malaga, leading it until 2023. Additionally, he served as the director of the Consolidated Research Group on Cognitive Neuroscience: Aphasia and Related Disorders (UNCA, C-12) at the Instituto de Investigación Biomédica de Málaga (IBIMA – Plataforma BIONAND).

Work experience

Dr. Marcelo L. Berthier Torres has led and contributed to several groundbreaking research projects in cognitive neurology and aphasia. As a co-investigator, he participated in the Telerehabilitation in Aphasia project (2021-2023), which evaluated the effectiveness of telerehabilitation compared to face-to-face therapy and identified predictive biomarkers of response, funded by the Junta de Andalucía. He also served as the principal investigator for a study on the efficacy of combined treatment with donepezil, intensive rehabilitation, and transcranial direct current stimulation in chronic post-stroke aphasia (2016-2019), funded by the Instituto de Salud Carlos III. Additionally, he has contributed to the Proyectos de Generación de Conocimiento “Frontera”, an initiative under the FEDER Andalucía 2014-2020 program, which investigates brain biomarkers for individualized treatment approaches in chronic post-stroke aphasia

Areas of Research

Dr. Marcelo L. Berthier Torres has made significant contributions to the treatment of post-stroke aphasia and speech-language disorders. He conducted the first open-label and randomized, placebo-controlled, double-blind trials investigating the use of cognitive-enhancing drugs (donepezil and memantine) alone and in combination with standard aphasia therapy or intensive language-action therapy (ILAT) in chronic post-stroke aphasia. His pioneering studies stimulated international research on aphasia pharmacotherapy, leading to clinical translation. Today, donepezil and memantine, alone or combined with therapy, are widely used off-label for post-stroke aphasia and language disturbances associated with neurodegenerative disorders like Alzheimer’s disease and primary progressive aphasia.

Publication

  • Revisiting the boundaries of different altered accents profiles

    Cortex
    2025-03 | Journal article
    DOI: 10.1016/j.cortex.2025.01.001
    CONTRIBUTORS: Marcelo L. Berthier; Ignacio Moreno-Torres; Jo Verhoeven; Guadalupe Dávila

  • Turning the Spotlight to Cholinergic Pharmacotherapy of the Human Language System

    CNS Drugs
    2023-07 | Journal article
    DOI: 10.1007/s40263-023-01017-4
    CONTRIBUTORS: Guadalupe Dávila; María José Torres-Prioris; Diana López-Barroso; Marcelo L. Berthier

  • Pharmacotherapy for post-stroke aphasia: what are the options?

    Expert Opinion on Pharmacotherapy
    2023-07-24 | Journal article
    DOI: 10.1080/14656566.2023.2221382
    CONTRIBUTORS: Marcelo L. Berthier; Guadalupe Dávila

  • Brain structural and functional correlates of the heterogenous progression of mixed transcortical aphasia

    Brain Structure and Function
    2023-05-31 | Journal article
    DOI: 10.1007/s00429-023-02655-6
    CONTRIBUTORS: Diana López-Barroso; José Paredes-Pacheco; María José Torres-Prioris; Guadalupe Dávila; Marcelo L. Berthier

  • Controlling the past, owning the present, and future: cholinergic modulation decreases semantic perseverations in a person with post-stroke aphasia

    Aphasiology
    2022-11-02 | Journal article
    DOI: 10.1080/02687038.2021.1957082
    CONTRIBUTORS: Marcelo L. Berthier; Daniel Santana-Moreno; Álvaro Beltrán-Corbellini; Juan C. Criado-Álamo; Lisa Edelkraut; Diana López-Barroso; Guadalupe Dávila; María José Torres-Prioris

Hongjun JIN | Nuclear Medicine Molecular Imaging | Interdisciplinary Innovation Prize

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Prof Dr.  Hongjun JIN | Nuclear Medicine Molecular Imaging | Interdisciplinary Innovation Prize

: Sun Yat-sen University Fifth Affiliated Hospital, china

Profile

Education

Dr. Hongjun Jin is a Principal Investigator in Nuclear Medicine and a Doctoral Supervisor of Molecular Medicine at Sun Yat-sen University. He earned his PhD in Biochemistry from Texas A&M University in 2007, following a BS in Radiochemistry from Lanzhou University in 1994 and a BMed in Chinese Medicine from Beijing University of Chinese Medicine in 1997. He completed his postdoctoral training at PNNL from 2008 to 2012 and served as a radiology instructor at Washington University in St. Louis from 2012 to 2017. Since 2017, he has led the PET and radiochemical laboratory at his institute, having been recruited through Sun Yat-sen University’s “Hundred Talents Program.”

Research and Innovations:

1) General Research Fund for National Sciences Foundation of China (NSFC), 82372004,
“F-18 labelled PET probe targeting P2X7 receptor for Evaluation of Treatment for AD”
01/01/2024-12/31/2027￥480,000,
2) Key R&D project, 0007/2022/AKP, Macao S&T Fund (FDCT),“R&D of an Integrated
Molecular probe for Targeted TNFR2 New Tumor Diagnosis and
Treatment”,01/01/2024-12/31/2027,￥2,400,000 (out of ￥120,000,000)
3) Guangdong Provincial Enterprise Joint Fund, 2021A1515220004, Guangdong Province
“PET/MRI Neuromolecular Imaging Quantitative Study of New Drug Targeting Sigma1

Research Project

  • 1) Outstanding Foreign Young Scientist Talent Program, RFIS, 82150610508 NSF-CN，
    “ Establishment and drug evaluation of acetylcholinergic and dopaminergic
    neuromolecular probes (18F VAT and 18F-DTBZ) PET brain imaging quantitative
    system for Parkinson’s disease” 2022/01-2022/12，￥400,000
  • General Research Fund for NSFC, 81871382, “F-18 labelled PET probe targeting P2X7
    receptor for early detection of AD”01/01/2019-12/31/2022￥570,000
  • SYSU “Hundred Talent “Starting Fund (Period I)” SYSU-FA10/01/2017-09/30/2022
    ￥2,500,000
  • National Key R&D Program for Precision Medicine, 2018YFC0910601 Real-time, highdimensional, multi-modality imaging co-registration and theronoastic strategies for
    oesophageal squamous-cell carcinomas10/01/2018-12/31/2020￥1,272,500 (out of
    ￥19,230,000)
  • Sun Yat-sen University Military Industry Cultivation Project, 89000-18843403 SYSU
    “Key Technologies of Molecular Imaging of Immune Dysfunction in Microgravity
    Environment”, 2019/08-2021/12￥1,890,00
  • Researchers Initiate Clinical Research Project (IIT) Award, SYSU-FAH”A single-center,
    open, prospective assessment of the diagnostic significance of 18F-FDG PET/CT
    dynamic imaging and gene sequencing in detecting metastatic lesions of non-small cell
    lung cancer”,2020/10-2021/09￥50,000
  • COVID-19 infection prevention and control emergency S&T, ZH22036302200036PWC,
    Zhuhai City”Specific Targeting S- protein of SARS-CoV-2 PET molecular imaging
    probe”2020/08-2021/09,￥70,000

Citation Index:

Google Scholar Citations: 8684 (total) 7943 (since 2020)
h-index 26(total) 20 (since 2020)
i10-index 52(total) 39(since 2020)

Publications