Carmela Conte | Neurodegenerative diseases | Best Researcher Award

Posted on by sciencefather

Prof Dr. Carmela Conte | Neurodegenerative diseases | Best Researcher Award

 

Profile

Education

Carmela Conte obtained her Master’s degree in Biological Sciences from the University of Perugia on November 3, 1994. She then pursued a Ph.D. in Medical Embryology through a joint program between the Universities of Perugia and Ferrara, completing it between December 30, 1996, and January 19, 2000. Following this, she specialized in Chemistry and Food Technology at the University of Perugia, earning her specialization between November 1, 2000, and November 1, 2002. Most recently, on September 29, 2023, she received National Habilitation as an Associate Professor in Biochemistry. She currently serves as an Aggregate Professor in her field.

Work experience

Since September 7, 2007, Carmela Conte has been serving as an Aggregate Professor in Biochemistry at the University of Perugia, where she teaches courses in General and Systematic Biochemistry, Medical Applied Biochemistry, and Molecular Biology. In addition to her teaching responsibilities, she participated in a Teaching and Training Mobility Program at VUMC Medical University of Amsterdam from June 24 to July 5, 2019, where she worked on a research project investigating the role of Toll-like receptors in Parkinson’s disease. She has been a member of the European Society for Neurochemistry since 2007 and, since March 17, 2022, has also been affiliated with the International Parkinson and Movement Disorder Society.

Research Activity

Carmela Conte’s research focuses on neurodegenerative diseases, with particular emphasis on animal models, signal transduction, molecular biology, and cell biology. Her specific research topics include the role of Toll-like receptors in Parkinson’s disease, neuroinflammation, synucleinopathies, oxidative stress, and Parkinson’s disease. Since September 7, 2007, she has been actively involved in editorial work, serving as a Reviewer Editor for Frontiers in Neuroscience (Neurodegeneration section) and as an ad hoc reviewer for several journals, including Amino Acids, The Cerebellum, Free Radical Research, Biomolecules, PLOS One, Experimental Gerontology, Molecules, Cells, Neurochemical Research, Neuroscience, Pharmacological Reports, International Journal of Molecular Sciences, Viruses, and the Journal of Biotechnology. Additionally, she has been a Guest Editor for Molecules and Cells, overseeing special issues and topic collections on neurodegenerative diseases. She has presented her research at numerous scientific meetings and conferences, including the 2009 Meeting of the European Society for Neurochemistry in Leipzig, the 2019 European Biotechnology Congress in Valencia, the 2021 European Biotechnology Congress in Sofia, the 2022 National Meeting of the Sphingolipid Club, and the 2023 Meeting of Parkinson’s Disease and Movement Disorders, where she discussed findings related to Toll-like receptor 4, alpha-synuclein accumulation, and sphingomyelinase activity in Parkinson’s disease models.

Publication

Suleyman Yildizdal | Craniosynostosis | Best Researcher Award

Posted on by sciencefather

Dr. Suleyman Yildizdal | Craniosynostosis | Best Researcher Award

 

 

Profile

Education

He completed his education at Org. Kenan Evren School from 2000 to 2008, followed by Gaziantep Anadolu High School from 2008 to 2012. He then pursued his medical training at Hacettepe University Faculty of Medicine from 2012 to 2018. After earning his medical degree, he continued his specialization in Plastic, Reconstructive, and Aesthetic Surgery as a resident at Hacettepe University Faculty of Medicine from November 2018 to February 2024. In April 2024, he joined Ankara Research and Training Hospital, where he continues to work in the Department of Plastic, Reconstructive, and Aesthetic Surgery.

 

Work experience

He has participated in various courses and workshops to enhance his expertise in plastic, reconstructive, and aesthetic surgery. He attended the Resident Ethics Course at Hacettepe University’s Department of History of Medicine and Medical Ethics on January 10-11, 2019. He also completed the 5th Basic Residency School organized by the Turkish Society of Plastic, Reconstructive, and Aesthetic Surgery in Bolu, Turkey, from January 22-25, 2020. Further advancing his skills, he took part in the 15th Advanced Residency School in Antalya, Turkey, from April 20-24, 2023. Additionally, he attended the 1st Cadaver Course of Craniofacial Anomaly and Maxillofacial Surgery at Hacettepe University on September 3-4, 2022, and the 1st Cadaver Course of Orthognathic Surgery at Koc University Hospital in Istanbul, Turkey, on September 7-8, 2022.

In addition to his clinical and surgical training, he has contributed to academic literature by co-authoring book chapters. He co-wrote Age-Related Changes in Trunk Aesthetics in Beauty, Aging, and Anti-Aging (1st ed., Elsevier, 2022) alongside G. G. Üstün and S. Yıldızdal. He also contributed to Dudak ve Damak Yarıkları Hacettepe Ekip Yaklaşım, co-authoring “Apert and Crouzon Syndrome” with İbrahim Vargel.

Awards

He has achieved remarkable academic success, securing 16th place in the National Examination for Specialty in Medicine among over 18,000 participants. Additionally, he ranked 571st in the National Student Selection and Placement Examination out of more than 2 million candidates.

He has actively participated in national meetings within his field, contributing to discussions and advancements in plastic, reconstructive, and aesthetic surgery. He attended the 41st National Turkish Plastic Reconstructive and Aesthetic Surgery Meeting in Samsun, Turkey, from October 26-30, 2019. He also participated in the National Turkish Plastic Reconstructive and Aesthetic Surgery Eastern Mediterranean Meeting on Cleft Lip and Palate, held in Gaziantep, Turkey, from February 7-9, 2020. Furthermore, he attended the 43rd National Turkish Plastic Reconstructive and Aesthetic Surgery Meeting in Antalya, Turkey, from November 10-14, 2021.

 

Publication

Michal Schwartz | Neurodegenerative diseases | Best Researcher Award

Posted on by sciencefather

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.