Using chimeric models to examine the impact of AD risk genes on human microglial function

May 21 @ 13:45

Mathew Blurton-Jones

University of California, Irvine (USA)

Matt Blurton-Jones, PhD, is an associate professor in the Department of Neurobiology and Behavior at the University of California, Irvine and director of the UCI ADRC iPS cell core. He earned his PhD in Neurosciences at UC San Diego and then completed postdoctoral studies at UC Irvine before starting his independent lab in 2011. His current research utilizes human induced pluripotent stem (iPS) cells and chimeric mouse models to examine the underlying molecular mechanisms that drive the development and progression of Alzheimer’s disease (AD). His earlier studies were among the first to show that neural stem cells can improve cognitive and motor function in transgenic models of Neurodegeneration by elevating levels of brain-derived neurotrophic factor (BDNF) and enhancing plasticity. His lab also demonstrated that the adaptive immune system can restrain the development of AD pathology by modulating microglial activation states.

More recently, his group developed one of the leading approaches to differentiate patient-derived iPS cells into microglia and generated chimeric models to study human microglial function in vivo. Ongoing work in the Blurton-Jones lab is now combining iPS cells, CRISPR gene editing, and chimeric modeling to examine the impact of AD-associated genes on human microglial function and the potential use of these microglial models for drug discovery.


Impact of vascular apoE isoforms on brain cognition and Alzheimer-related pathology

May 22 @ 8:30

Guojun Bu

Mayo Clinic (USA)

Dr. Guojun Bu is the Mary Lowell Leary Professor and Chair of the Department of Neuroscience at Mayo Clinic Jacksonville. He is also the Jorge and Leslie Bacardi Associate Director of the Mayo Clinic Center for Regenerative Medicine and an Associate Director for Mayo Clinic Alzheimer’s Disease Research Center. Prior to joining Mayo Clinic in 2010, he was a Professor of Cell Biology and Neuroscience at the Washington University School of Medicine in St. Louis. Dr. Bu received his B.S. degree in biology from Beijing Normal University, his Ph.D. degree in biochemistry from Virginia Tech, and completed his postdoctoral training in cell biology at the Washington University School of Medicine.

Dr. Bu is a world leader in the field of apoE and apoE receptors, which play critical roles in the pathogenesis of Alzheimer’s disease. His primary interest is to understand why APOE4 is a strong genetic risk factor for Alzheimer’s disease and how this pathway can be targeted for therapy by studying animal and stem cell-based cellular and organoid models. His research also includes interests in addressing the glial and vascular contributions to Alzheimer’s disease and related dementias. Dr. Bu has received numerous honors and awards including the Zenith Fellows Award from the Alzheimer’s Association, the Established Investigator Award from the American Heart Association, the Investigator of the Year award from the Mayo Clinic, and the MetLife Foundation Award for Medical Research in Alzheimer’s disease. He is an elected Fellow of the American Association for the Advancement of Science (AAAS), an Associate Editor for Science Advances, and a Co-Editor-in-Chief of Molecular Neurodegeneration.

Role of vasculature and glia in the pathogenesis of glaucoma, a leading neurodegenerative disease

May 22 @ 10:30

Abbot Clark

University of North Texas Health Science Center (USA)

Abbot (Abe) Clark, PhD, FARVO, is Regents Professor of Pharmacology & Neuroscience and Medical Education as well as Executive Director of the North Texas Eye Research Institute (NTERI) at the University of North Texas Health Science Center (UNTHSC) in Ft. Worth, Texas. Prior to joining UNTHSC 11 years ago, he worked at Alcon Laboratories for 23 years, retiring as Vice President of Discovery Research and Head of Glaucoma Research. The major focus of his research has been on the discovery of molecular pathogenic pathways for glaucomatous damage to the aqueous humor outflow pathway, retinal ganglion cells, the optic nerve head and optic nerve, as well as vision centers in the brain in order to develop novel disease modifying therapies for glaucoma. Glaucoma is a leading neurodegenerative disease and leading cause of visual impairment, affecting 80 million individuals worldwide. Dr. Clark’s laboratory has recently discovered both small molecule, gene therapies, and genome editing that prevent glaucoma-like damage to the eye and vision centers of the brain.

Dr. Clark collaborates with a number of other investigators around the world in order to perform interdisciplinary and translational research. His academic lab has been continuous funded by grants from the NEI, Department of Defense, and pharmaceutical/biotechnology companies. Dr. Clark has published more that 240 peer-reviewed scientific articles, 20 book chapters and is the editor of 2 ophthalmic textbooks. He is an inventor of more than 80 patents.

Dr. Clark has given 135 invited national and international presentations of his research and has organized and/or chaired sessions in 26 national and international scientific meetings. He serves on the editorial boards of 3 ophthalmic journals, Molecular Neurodegeneration, and Annals of Translational Medicine. He also has successfully trained 20 PhD students and 6 postdoctoral fellows. Under his leadership, NTERI has grown and is committed to improving vision health, discovering new ophthalmic therapies through interdisciplinary translational research, and training future eye care providers and researchers.

Neuropathology of common age-related neurodegenerative disorders

May 23 @ 8:55

Dennis Dickson

Mayo Clinic (USA)

Dr. Dennis Dickson’s professional career has been devoted to the neuropathology of disorders that produce dementia and Parkinsonism. He is the neuropathologist for the Mayo Clinic Alzheimer Disease Research Center, the State of Florida Alzheimer Disease Initiative and the Society for Progressive Supranuclear Palsy. His professional career began in the laboratory of Dr. Robert D. Terry at Albert Einstein College of Medicine in New York, where his studies led to recognition that some clinically normal individuals have as much amyloid deposition in their brains as patients with Alzheimer’s disease (AD), a process he termed “pathological aging.” His long-standing interest in tau and its role in dementia lead to research into other disorders where tau pathology is a prominent feature, including Pick’s disease, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD) and chronic traumatic encephalopathy (CTE). He was also one of the first to realize that Lewy body dementia (LBD) is a common cause of dementia in the elderly, and that LBD can be differentiated from AD clinically and pathologically.

Dr. Dickson received his B.S. (Biochemistry) and M.D. degrees from the University of Iowa College of Medicine, where he was a member of the Alpha Omega Alpha Honor Medical Society. His awards include the Metropolitan Life Award in 2001, the Potamkin Prize in 2011, Robert E. Jacoby endowed professorship in Alzheimer’s Research in 2010, and Mayo Clinic Distinguished Investigator in 2015. He is past president of the American Association of Neuropathologists and was recognized for Meritorious Service to Neuropathology in 2016.

Genetic studies of Alzheimer’s disease implicate microglia in risk for disease

May 21 @ 9:10

Alison Goate

Icahn School of Medicine (USA)

Dr. Alison Goate has worked on Alzheimer’s disease genetics since 1987 as a postdoctoral fellow with Dr. John Hardy – at Imperial College, London. In 1992 she moved to Washington University in St. Louis, where she stayed until 2014, when she moved to the Icahn School of Medicine at Mount Sinai as the founding director of the Ronald M. Loeb Center for Alzheimer’s disease. She has been part of many gene finding teams that have successfully identified disease causing variants for both AD and FTD. Whilst working with Dr. Hardy she reported the first mutation to cause familial Alzheimer’s disease and early studies at Washington University identified the mutation in the Colombian families that are now part of the API clinical trial.

Dr. Goate is also a leader in the study of late onset AD genetics using both GWAS and sequencing approaches. She has demonstrated that LOAD families can carry PSEN mutations with reduced penetrance. Her team led the identification of rare variants in PLD3 as a risk factor for AD and collaborated with John Hardy in the identification of Trem2 as an AD risk factor. More recently her work on common variants has highlighted the importance of microglial expressed genes in AD risk, identifying SPI1/Pu.1 as an important regulator of AD risk genes. Fine mapping of AD risk loci has identified causal genes/variants in many loci and further emphasized the importance microglial gene expression and function to AD risk. Dr. Goate has received the Potamkin Award and the MetLife Award for her research on AD and was elected a fellow of AAAS in 2012 and a fellow of the National Academy of Medicine in 2016.

TREM2: from a loss-of-function to a novel target for disease modulation?

May 23 @ 10:30

Christian Haass

Ludwig-Maximilians University Munich (Germany)

Dr. Christian Haass graduated in Molecular Biology at the University of Heidelberg, Germany. He was a postdoc and assistant professor of Neurology at the Harvard Medical School in the institute of Dr. Dennis Selkoe. Since 1999 he is the head of the division of Biochemistry at the Ludwig-Maximilians University and since 2009 he is also the speaker of the German Center for Neurodegenerative Diseases (DZNE) in Munich. Dr. Haass received a number of prestigious awards, among them, the Gottfried Wilhelm Leibniz-Award of the Deutsche Forschungsgemeinschaft, the Potamkin Award of the American Academy of Neurology, an ERC advanced grant, and most recently the brain prize. Dr. Haass is the speaker of the Münich Cluster of Systems Neurology (SyNergy).

Pathways involving microglia and apoE in neurodegeneration

May 21 @ 11:10

David Holtzman

Washington University School of Medicine in St. Louis (USA)

Dr. David Holtzman received his BS (1983) and MD (1985) from Northwestern University followed by a Neurology residency at UCSF from 1985-1989. He did post-doctoral research at UCSF from 1989-1994. He moved to Washington University in 1994 as an Assistant Professor to both start his own lab as well as to get involved in clinical activities and teaching.

He is currently Professor and Chair of Neurology, scientific director of the Hope Center for Neurological Disorders, and Associate Director of the Knight ADRC. Some of his and his lab’s accomplishments include showing in part how apoE4 contributes to AD, development of a method to measure protein synthesis and clearance in the CNS of animals and humans, development of CSF biomarkers for AD, demonstration of how synaptic/neuronal activity and sleep affect amyloid-β (Aβ) and tau levels dynamically in vivo acutely and chronically, and development of an anti-Aβ and an anti-tau antibody now in clinical trials for AD. 

Dr. Holtzman has received a number of honors including being a recipient of a Paul Beeson Physician Faculty Scholar award in Aging research, the Potamkin prize from the American Academy of Neurology for research on Alzheimer’s disease, the MetLife award for Alzheimer’s disease research, a MERIT award from the NIA, election to the National Academy of Medicine of the National Academy of Sciences, election to the National Academy of Inventors, an alumni merit award from the Northwestern Feinberg School of Medicine, being appointed to the National Advisory council of the NINDS and NIA, the Chancellor’s award for innovation and entrepreneurship and the Carl and Gerty Cori award from Washington University, being elected Fellow of the AAAS, and being the current president of the American Neurological Association.

Holtzman has trained over 50 graduate students, post-doctoral fellows, and physician-scientists, many of whom have gone on to successful careers in academia and industry​.

A neuropathological perspective on neuroinflammation and microglia in Alzheimer’s disease

May 21 @ 9:35

Jeroen Hoozemans

VU University Medical Center Amsterdam (The Netherlands)

Jeroen Hoozemans, PhD, completed his undergraduate studies in Medical Biology at the Vrije Universiteit in Amsterdam. In 1998, he started his PhD training in the group of Dr. Piet Eikelenboom, on the role of inflammation in Alzheimer’s disease and especially on how non-steroidal anti-inflammatory drugs (NSAIDs) could lower the risk of developing Alzheimer’s disease. He was one of first to discover that the enzyme cyclooxygenase 1, a primary target of NSAIDs, is expressed in microglia in the human brain.

As postdoc researcher, he visited the lab of Dr. Thomas Arendt at the Paul Flechsig Institute for Brain Research in Leipzig where he was involved in several studies investigating the molecular mechanism of neurodegeneration in Alzheimer’s disease. Upon his return to Amsterdam in 2004, he got interested in the regulation of protein folding in neurodegenerative diseases. Using postmortem brain tissue, he was the first to show that the unfolded protein response (UPR) is activated in Alzheimer’s disease and Parkinson’s disease. In following studies, he was also able to show the connection between UPR activation and the accumulation of tau and alpha-synuclein in the human brain. Publications resulting from these studies are currently recognized as key papers subscribing the role of the UPR in neurodegeneration.

Since 2006, Dr. Hoozemans has been leading his own research group at the neuropathology research lab of the University Medical Centers in Amsterdam. His research projects mainly involve the use of post mortem brain tissue derived from donors. These projects are aimed to resolve the clinicopathological correlations in neurodegenerative diseases, identify new potential drug targets as well as early disease mechanisms in neurodegenerative diseases. Due to the close collaboration with the Netherlands Brain Bank, his lab is one of the few labs in the world being capable of isolating and culturing human primary adult microglia. Using the extensively characterized cohort of postmortem brain tissue and primary human microglia, he is currently investigating the role of microglia in the pathogeneses of Alzheimer’s disease. His lab is especially interested in how microglia respond to the presence of aggregated proteins during disease progression as well as during healthy aging.

Dr. Hoozemans has over 115 publications with an H-index of 40. He is a member of the scientific advisory board of the national public fund Alzheimer Nederland and since 2019, he is the Editor-in-Chief of Acta Neuropathologica Communications.

Immune-inflammatory modulation as a therapeutic strategy for neurodegenerative diseases

May 21 @ 12:00

Seung Hyun Kim

Hanyang University College of Medicine (Korea)

Dr. Seung Hyun Kim is currently professor of neurology, director of ALS clinic and Korean NIH sponsored Stem Cell Therapy Center at Hanyang University Hospital, Seoul. He also serves as President of the Korean Dementia Association.

Dr. Kim earned his MD degree in medicine and PhD in Neuroanatomy at Hanyang University.

He has worked in the field of ALS and neurodegenerative disorders where he developed JPI-289, novel PARP inhibitor, currently in Phase II clinical trial. Recently, his therapeutic strategy using autologous bone marrow originated Mesenchymal Stem Cell Therapy for ALS which was approved as an orphan drug. Dr. Kim is now conducting translational research in the field of rare neurodegenerative diseases for the development of personalized medicine based on unique genetic background of Korean and Asian population. With these works, Prof. Kim received “The Mystery of Life Award” from Catholic Foundation, and Award from Ministry of Science, ICT and Future Planning.

Currently, Dr. Kim serves as Member of National Academy of Medicine of Korea, National council member of dementia and editorial member of Molecular Neurodegeneration.

Mitochondrial and lysosomal dysfunction in Parkinson's disease: therapeutic implications in human neurons

May 22 @ 14:25

Dimitri Krainc

Northwestern University (USA)

Dimitri Krainc, MD, PhD, currently serves as the Aaron Montgomery Ward Professor and Chairman of the Department of Neurology and Director of the Simpson Querrey Center for Neurogenetics at Northwestern University, Feinberg School of Medicine in Chicago.  

Previously, Dr. Krainc spent more than 20 years at Harvard Medical School where he completed his research training followed by a neurology residency and fellowship in movement disorders at Massachusetts General Hospital. He then served on the neurology faculty at MGH and Harvard Medical School until 2013 when he relocated to Chicago.

The overarching goal of Dr. Krainc’s research is to study molecular mechanisms of neurodegeneration, focusing on Parkinson’s and Huntington’s disease, to facilitate the development of targeted therapies.  In the area of PD, his group identified a positive feedback loop between alpha-synuclein and glucocerebrosidase that after a threshold may lead to a self-propagating disease in sporadic and genetic forms of PD (Mazzulli et al, Cell, 2011).   They also described convergence of mitochondrial and lysosomal dysfunction in midbrain neurons from PD patients (Burbulla et al, Science, 2017), as well as direct contacts between lysosomes and mitochondria (Wong et al, Nature, 2018). More recently, they identified a small molecule activators of GCase that partially rescued pathogenic phenotypes observed in patient-derived dopaminergic neurons (Burbulla at al, Science Translational Medicine, 2019).

Targeting Aβ protofibrils with BAN2401 - from mutation to potential therapy for AD

May 23 @ 9:20

Lars Lannfelt

Uppsala University (Sweden)

Lars Lannfelt, MD, PhD, received his medical degree in 1978, becoming a specialist in psychiatry in 1987 and in geriatrics, in 2001.  He received his PhD from Karolinska Institute in 1990 and became an associate professor in neurodegeneration at Karolinska Institute in 1993. He went on to become Professor in Geriatrics at Uppsala University in 2001 and Senior Professor in 2016. He has been a member of the Royal Swedish Academy of Sciences since 2004.

Dr. Lannfelt’s first major scientific achievement was the detection of the “Swedish” mutation (Mullan et al. 1992). This genetic mutation causes Alzheimer’s disease in a large family. The Swedish mutation leads to 3-5 times increased production of amyloid β, and this feature has led to a widespread use of the mutation in transgenic mice. He also performed genetic counseling for family members, which was the first time this was done for Alzheimer’s disease (Lannfelt et al. 1995).

Another major scientific breakthrough was the detection of the “Arctic” mutation, found in a family from northern Sweden (Nilsbert et al. 2001). I realized in studying this mutation that the pathogenic effect is the generation of soluble Aβ protofibrils, and that these species of A are likely to be present and toxic in all Alzheimer’s disease cases. He decided to target these toxic, soluble Aβ aggregates with immunotherapy and developed a conformation-dependent antibody, able to recognize Aβ protofibrils. He succeeded in isolating such an antibody, mAb158 (Englund et al. 2007). The antibody was humanized, named BAN2401, and is now in phase 3 clinical development.

In 2003, he co-founded BioArctic, based on the discovery of the Arctic mutation. The aim is to bring immunotherapy to patients with Alzheimer’s disease, targeting Aβ protofibrils. During 2018, results from a large phase 2b study with 856 patients were presented at international conferences.

Dr. Lannfelt has published approximately 300 papers and is the recipient of numerous awards (including the Khalid Iqbql Lifetime Achievement Award in Alzheimer’s Disease Research by Alzheimer’s Association 2019 and the Swedish Alzheimer’s Foundation (Alzheimerfonden) Grand Research Prize 2019).


MAOists join BAPtists and TAUists in Alzheimer's research: reactive astrocytes, MAO-B, GABA, H2O2, as a cause of Alzheimer’s disease

May 21 @ 10:00

C. Justin Lee

Institute for Basic Science (Korea)

Dr. C. Justin Lee is the co-director of the Center for Cognition and Sociality, established in July 2012. He earned his B.A. in Chemistry from The University of Chicago before getting his PhD from Columbia University in 2001, and later worked in Department of Pharmacology at Emory University as a postdoctoral fellow. In 2004 he joined KIST as a senior research scientist and later served as the Director of Center for Neuroscience.

In 2009, he founded the WCI Center for Functional Connectomics as a part of World Class Institute Program. In 2015 he became the recipient of Creative Research Investigator Award to establish the Center for Glia-Neuron Interaction at KIST to serve as the Director of the Center before taking up his position in IBS.

White matter mechanisms in neurodegeneration

May 21 @ 14:35

Francesca-Fang Liao

The University of Tennessee (USA)

Francesca-Fang Liao, PhD, is a Professor and Vice Chair in the department of Pharmacology at University Tennessee Health Science Center (UTHSC). Dr. Liao received her doctoral degree in 1993 from Albert Einstein College of Medicine in Molecular Immunology. She then completed her post-doctoral fellowship in 1998 at The Rockefeller University, New York, NY (Cell Physiology & Immunology).

Dr. Liao’s research interests focus on integrating genetic, neurological, molecular and cellular means to study the mechanisms underlying the pathogenesis of Alzheimer’s disease. The goal of her research is to identify and characterize early molecular events contributing to the emergence of cognitive decline and to discover information critical for the development of therapeutic strategies for the treatment of this devastating disorder.

More recently, her research interest has also included studying vascular dementia and white matter denegerative mechanisms using a spontaneous mouse model of chronic hypoperfusion due to eNOS deficiency, with special emphasis on early molecular signaling pathways initiated from brain microvessels. 

Mossy cell synaptic degeneration causes memory imprecision via miR-128 inhibition of STIM2 in Alzheimer’s disease

May 21 @ 15:00

Youming Lu

Tongji Medical School, Huazhong University of Science and Technology (China)



Tau protein & tau pathology: structure, aggregation, interaction partners and spreading

May 22 @ 10:55

Eckhard Mandelkow

DZNE (Germany)

Dr. Eckhard Mandelkow studied physics in Braunschweig, New Orleans, and Hamburg, and received his doctoral degree at the Max-Planck-Institute for Medical Research in Heidelberg for X-ray analysis of the structure of tobacco mosaic virus. This was followed by postdoctoral training at Brandeis University, Waltham MA (structure of cytoskeletal proteins). In 1986 he moved to the Deutsches Elektronensynchrotron (DESY) in Hamburg, Germany, and worked as director at the Max-Planck-Unit for Structural Molecular Biology, professor at Hamburg University, and scientific member of the Max-Planck-Society. His research focussed on structural molecular biology by X-rays using synchrotron radiation, image reconstruction in electron microscopy, cytoskeleton (microtubules, motor proteins), the structure, function, and aggregation of tau protein and protein kinases in Alzheimer disease, and the development of tau aggregation inhibitors. He is recipient of a 2010 Metlife Award, a 2011 Potamkin Award, and a 2013 Alzheimer’s Association Iqbal Life Time Achievement Award. In 2011 he joined the German Center for Neurodegenerative Diseases in Bonn (DZNE) as a Principal Investigator where his lab focusses on “Structural Principles of Neurodegeneration”.

Cell and animal models of tau pathology, modes of toxicity, and therapeutic approaches

May 23 @ 10:05

Eva-Maria Mandelkow

DZNE (Germany)

Dr. Eva-Maria Mandelkow studied human medicine in Heidelberg and Hamburg, followed by internships at university hospitals in Hamburg, Heidelberg, New Orleans, and then did her doctorate at the Max Planck Institute for Medical Research, Heidelberg, with research on enzyme kinetics of the motor protein myosin. She then performed postdoctoral research at Brandeis University, Waltham, MA and at the Scripps Research Institute in La Jolla, CA. She joined the Max Planck Institute in Heidelberg as research scientist where she studied the self-assembly of microtubules by cryo-electron microscopy. In 1986 she moved to the Max Planck Unit for Structural Molecular Biology at Deutsches Elektronen-Synchrotron (DESY), Hamburg. The research of her group focussed on the cell biology of tau protein and its role in Alzheimer disease, with emphasis on cell models, transgenic animal models of tau pathology (mouse, C. elegans), and development of therapeutic approaches.

She is recipient of a 2007 Breuer Award, a 2010 Metlife Award, a 2011 Potamkin Award, and a 2013 Alzheimer’s Association Iqbal Life Time Achievement Award. In 2011 she joined the German Center for Neurodegenerative Diseases in Bonn (DZNE) as a Principal Investigator where her lab focusses on “Cell and Animal Models of Neurodegeneration”.

The molecular origins of Alzheimer’s disease: when does it start and what strategies for primary prevention?

May 23 @ 8:30

Colin Masters

The University of Melbourne (Australia)

Dr. Colin Masters has focused his career on research in Alzheimer’s disease and other neurodegenerative diseases, including Creutzfeldt-Jakob disease. His work over the last 35 years is widely acknowledged as having had a major influence on Alzheimer’s disease research world-wide, particularly the collaborative studies conducted with Konrad Beyreuther in which they discovered the proteolytic neuronal origin of the Aβ amyloid protein which causes Alzheimer’s disease. This work has led to the continued development of diagnostics and therapeutic strategies. More recently, his focus has been on describing the natural history of Alzheimer’s disease as a necessary preparatory step for therapeutic disease modification.

Professor Masters is a Laureate Professor of Dementia Research at the Florey Institute, University of Melbourne and a consultant at the Royal Melbourne Hospital. His achievements have been recognised by the receipt of many international awards.

Therapeutic strategies targeting alpha-synuclein in AD-related dementia

May 23 @ 10:55

Pamela McLean

Mayo Clinic (USA)

Dr. Pamela McLean is a Professor of Neuroscience at the Mayo Clinic Jacksonville.

Research in the laboratory of Dr. McLean focuses on understanding the cellular and molecular mechanisms underlying neurodegeneration in Parkinson’s disease, dementia with Lewy bodies and related neurodegenerative disorders In particular, her research group studies the role of alpha-synuclein, a protein that misfolds and aggregates in the brain regions that are critically involved in these diseases.
Dr. McLean’s lab uses in vitro cellular models of alpha-synuclein aggregation and toxicity as well as in vivo targeted gene transfer with adeno-associated virus (AAV) to understand the molecular pathogenesis of these diseases with special emphasis on developing novel therapeutic approaches. Specific areas of interest include mechanisms of protein degradation, disease spreading, and mitochondrial dysfunction. In addition to the models described above, Dr. McLean’s research uses patient-derived material such as post-mortem brain tissue from the Mayo Clinic Brain Bank and skin-derived induced pluripotent stem cell-derived neurons in her studies.

Dr. McLean received her Bachelor of Science in biochemistry from the University of Glasgow in Scotland, and her PhD in Pharmacology from Boston University. She received post-doctoral training in the lab of Dr. Bradley Hyman at Massachusetts General Hospital and Harvard Medical School. She has been at Mayo Clinic in Jacksonville since 2012.

Relevance of a liver APOE4 phenotype and plasma apolipoprotein E levels to pathological processes in the brain

May 22 @ 9:20

Henrietta Nielsen

Stockholm University (Sweden)

Dr. Henrietta Nielsen earned her PhD from Lund University, Sweden, and thereafter further trained as a postdoctoral researcher at the VU Medical Center Amsterdam, the Netherlands, and at the Mayo Clinic in Jacksonville, Florida USA.

During her training in the Netherlands she focused on amyloid-beta clearance and the influence of amyloid-associated-proteins like apolipoproteins E and J in primary cultures of post-mortem isolated human astrocytes and microglia. Further work of hers at Lund University in Sweden entailed biomarker discovery efforts focusing on CSF alpha-synuclein levels and various inflammatory markers in patients with Alzheimer’s disease and synucleinopathies like Parkinson’s disease and dementia with Lewy bodies.

More recently and together with colleagues at the Mayo Clinic, Dr. Nielsen studied individual apolipoprotein E isoform levels in plasma and CSF from Alzheimer’s patients and controls, by use of mass-spectrometry. Since 2015 Dr. Nielsen heads the Translational Neurodegeneration Research Team at Stockholm University, Sweden, with major efforts invested in assessing the role of alpha-synuclein in Alzheimer’s disease pathophysiology, and potential links between liver-derived apolipoprotein E and neurodegeneration of the brain.

Dr. Nielsen is a senior editor of Molecular Neurodegeneration, an associate editor of the Journal for Alzheimer’s Disease (JAD) and a frequent reviewer for numerous journals and grant agencies.


Understanding the mechanistic link between C9orf72 and TDP-43

May 22 @ 14:50

Leonard Petrucelli

Mayo Clinic (USA)

Leonard Petrucelli, PhD, is a Ralph B. and Ruth K. Abrams Professor and enterprise chair of the Department of Neuroscience at Mayo.

Dr. Petrucelli earned his Bachelor of Science degree at Barry University, Miami, and his Ph.D. degree in molecular and cellular biochemistry at Loyola University and Stritch School of Medicine, Chicago. He came to Mayo Clinic’s Florida campus as a research fellow in 2000 and joined the neurosciences research staff two years later.

Dr. Petrucelli and his research team are at the forefront of their field, researching the cellular mechanisms that cause neurodegeneration in Alzheimer’s disease, amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease, and frontotemporal dementia (FTD) and more recent movement disorders and stroke. By combining expertise in drug discovery, cell biology and induced pluripotent stem cell (iPSC) modeling, his lab aims to develop therapies and biomarkers for the treatment of diseases characterized by abnormal protein aggregation.  Dr. Petrucelli’s team recently discovered a new therapeutic target and biomarker with the aim of improving the diagnosis and prognosis for patients suffering from FTD and ALS. His team’s research has been published in top tier journals including Science, Nature Medicine, Nature Neuroscience, Neuron, Journal of Clinical Investigation and Annals of Neurology.

Dr. Petrucelli is principal investigator for several grants funded by the National Institutes of Health (NIH) including R35 and is director of two funded NIH programs focused on c9orf72 and Tau Center without Walls.  He serves on the Scientific Advisory Board of Science Translational Medicine. He is also the Chief Scientific Advisor to Target ALS Foundation. Lastly, he was recently appointed as vice-chair to the Florida Alzheimer’s Disease Research Grant Advisory Board.

Endosomal cargo sorting dysfunction in Alzheimer's disease pathogenesis: therapeutic implications

May 23 @ 9:20

Domenico Praticò

Temple University, Lewis Katz School of Medicine (USA)

Domenico Praticò, MD, graduated from the University of Rome “La Sapienza”, School of Medicine, where he also completed a residency program in Internal Medicine. He continued his post-graduate training as a Research Fellow at the University of Pennsylvania, where two years later he was appointed Assistant Professor. In 2007, he joined Temple University, School of Medicine, as Associate Professor of Pharmacology and Director of the Neurodegenerative Diseases Research Laboratory. Since 2011, he is Professor of Pharmacology, Microbiology and Immunology at the Lewis Katz School of Medicine. In March 2018, he was awarded the Scott Richards North Star Foundation Chair in Alzheimer’s research, and nominated the Founding Director of the Alzheimer’s Center at Temple.

His main area of investigation is clinical pharmacology and oxidative biology with a special focus on cellular and molecular mechanisms involved in brain health, and the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease and Frontotemporal dementia.  Dr. Pratico has authored over 260 original articles in high impact journals, and more than 25 chapters in thematic books.  He has served and still serves as PI in grants from the private sector, Foundations and NIH.

During his career, he has received many awards for his research accomplishments including the Irvine H. Page Award, Zenith Award from the Alzheimer’s Association, and Dorothy Dillon Eweson Lectureship from the American Federation for Aging Research, and the Paul W. Eberman Faculty Research Award​.

Modulation of amyloid deposition and neuroinflammation by the microbiome

May 21 @ 14:10

Sangram Sisodia

The University of Chicago (USA)

Dr. Sangram (Sam) Sisodia’s research has focused on understanding the cellular and molecular biology of the amyloid precursor protein (APP) and presenilins (PS1 and PS2), polypeptides that are mutated in pedigrees with familial Alzheimer’s Disease (FAD). His most notable contributions include the generation and characterization of mouse models that exhibit amyloid plaques in the brain. These models have been invaluable for understanding the impact of environmental enrichment and exercise in modulating amyloid deposition and adult neurogenesis. More recent studies have focused on the impact of the microbiome on modulation of Abeta amyloidosis in mouse models. He has published 178 peer-reviewed manuscripts.

Dr. Sisodia has received several awards, including: the Potamkin Prize for Alzheimer’s Disease Research from the American Academy of Neurology and the Metropolitan Life Foundation Award for Medical Research. He was inducted as a Fellow of AAAS, and Foreign Fellow of the National Academy of Sciences, India and the Spanish Royal Academy of Sciences. In addition, he has served as: Member, NLS1 (NIH) Study Section; Member, NIA Board of Scientific Counselors; Scientific Advisory Boards of Autism Speaks; the Packard Center for ALS Research; Chair, Scientific Advisory Committee of the Brain Research Foundation; and Advisory Committee of the MetLife Foundation. He has also organized, or co-organized several Adler Symposia on Alzheimer’s Disease at the Salk Institute, two Keystone Symposia, and was the co-director of the Cold Spring Harbor Neurobiology of Disease course. Dr.Sisodia has served on the Editorial Boards of eight journals, including Neuron and Cell (10 year term expired in 2009), and is a member of the Dana Alliance for Brain Initiatives.

The roles of genes and innate immunity in Alzheimer’s disease

May 21 @ 8:45

Rudy Tanzi

Massachusetts General Hospital/Harvard Medical School (USA)

Dr. Rudolph Tanzi is the Vice-Chair of Neurology, Director of the Genetics and Aging Research Unit, Co-Director of the Henry and Allison McCance Center for Brain Health, and Co-Director of the MassGeneral Institute for Neurodegenerative Disease at Massachusetts General Hospital. He also serves as the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard Medical School. Dr. Tanzi received his B.S. (microbiology) and B.A. (history) at the University of Rochester in 1980 and his Ph.D. (neurobiology) at Harvard Medical School in 1990.

Early in his career, Dr. Tanzi worked with Dr. James Gusella to discover the first human genetic markers and use them to find a disease gene (Huntington’s disease). He went on to first discover the amyloid precursor protein (APP) gene, the first Alzheimer’s disease (AD) gene and he co-discovered the two other early-onset familial AD genes, known as the presenilins (PSEN1 and PSEN2) As leader of the Cure Alzheimer’s Fund Alzheimer’s Genome Project, Dr. Tanzi identified several other AD genes, including ADAM10, ATXN1, and CD33, the first AD gene directly modulating neuroinflammation. He also discovered the Wilson’s disease gene and contributed to the discovery of several other neurological disease genes.

Dr. Tanzi and his team were the first to use human stem cells to create a human brain organoid model of AD, dubbed “Alzheimer’s-in-a-Dish”, a three-dimensional human stem cell-derived neural culture system, which was the first to recapitulate the key AD pathological hallmarks. This system was also used to definitively show for the first time that amyloid plaques cause neurofibrillary tangles. This model has made drug screening for AD much faster and more effective. Using this system, Dr. Tanzi has developed several novel therapies for AD including gamma secretase modulators aimed at plaque pathology, and other drugs, including repurposing of cromolyn for targerting neuroinflammation. Dr. Tanzi and his team also discovered that beta-amyloid, the main component of senile plaques, plays a key role in the innate immune system of the brain operating as an anti-microbial peptide, suggesting a possible role for infection in driving AD pathology.

Dr. Tanzi serves as Chair of the Cure Alzheimer’s Fund Research Leadership Group and numerous advisory and editorial boards, He has published over 550 research papers and has received the highest awards in his field, including the Metropolitan Life Foundation Award, Potamkin Prize, Ronald Reagan Award, Silver Innovator Award, the Smithsonian American Ingenuity Award, and the Brain Research Foundation Award. He serves on dozens of editorial boards and scientific advisory boards and was named to TIME magazine’s list of TIME100 Most Influential People in the World. He co-authored the books Decoding Darkness, and the three international bestsellers, Super Brain, Super Genes, and The Healing Self. In his spare time, he plays keyboards with Joe Perry and Aerosmith.

Neuronal and non-neuronal functions of Alzheimer’s disease GWAS risk factor BIN1

May 22 @ 12:10

Gopal Thinakaran

USF Morsani College of Medicine (USA)

Gopal Thinakaran, PhD, is a Professor in the Department of Molecular Medicine at the University of South Florida Morsani College of Medicine. Dr. Thinakaran graduated in 1992 with a PhD degree in Molecular Biology and Genetics from the University of Guelph, Canada. He then trained as a post-doctoral fellow in the Division of Neuropathology, The Johns Hopkins University School of Medicine, and in 1997 rose to the rank of Assistant Professor in the Department of Pathology. In 1999, he moved to the Department of Neurobiology at the University of Chicago and was promoted to a Full Professor in 2010. He moved to USF in 2019 to become the Associate Director of the Neuroscience Institute and Associate Dean for Neuroscience Research at the College of Medicine. Dr. Thinakaran enjoys International recognition as an excellent cell biologist in the field of Alzheimer’s disease. He was the recipient of a Zenith Fellows Award in 2002 (Alzheimer’s Association) and gave a Plenary Lecture at the International Conference on Alzheimer’s Disease and Related Disorders in 2008.

Research in Thinakaran lab focuses on the cellular and cellular mechanisms that are central to Alzheimer’s disease neuropathology – the characterization of proteins and enzymes responsible for beta-amyloid production and investigation of the late-onset Alzheimer’s disease risk factor BIN1. Dr. Thinakaran’s lab uses an integrated approach that combines hypothesis driven mutagenesis, biochemical characterization, detailed subcellular localization, and advanced live cell imaging to accomplish their goals. Cultured non-neuronal cells, primary hippocampal neurons, transgenic, knock-out, and gene-targeted mice serve as experimental models in Dr. Thinakaran’s investigation. His research has been funded by the National Institutes of Health, Cure Alzheimer’s Fund, BrightFocus Foundation, Alzheimer’s Association, Illinois Public Department of Health, and National Multiple Sclerosis Society.

The role of angiotensin converting enzyme in Alzheimer’s disease pathogenesis

May 22 @ 9:45

Robert Vassar

Northwestern University (USA)

Dr. Robert Vassar’s research focuses on molecular and cellular mechanisms of Alzheimer’s disease. In particular, he investigate the beta-secretase enzyme BACE1, which initiates the production of the beta-amyloid peptide that plays a central early role in the pathogenesis of Alzheimer’s.

He uses a combination of biochemical, cell culture and animal model approaches to investigate the role of BACE1 in health and disease.


New insights into the role of lipoproteins in Alzheimer’s disease

May 22 @ 8:55

Cheryl Wellington

University of British Columbia (Canada)

Dr. Cheryl Wellington is a Professor in the Department of Pathology and Laboratory Medicine at the University of British Columbia. Dr. Wellington’s research interests focus on dementia, traumatic brain injury, cerebrovascular dysfunction, and lipoprotein metabolism, in humans, animal models, and engineered human tissues.

Dr. Wellington developed the first perfusible bioengineered model of the human blood brain barrier and large cerebral vessels. She also co-founded the CHIMERA (Closed Head Impact Model of Engineered Rotational Acceleration) platform of TBI animal modeling, which a unique system that uses non-surgical methods to deliver precise mechanical inputs to an unconstrained head and is now recognized as an excellent model of mild TBI and concussion.

Dr. Wellington has published over 120 papers, trained over 35 junior scientists in a dynamic multidisciplinary environment, and has contributed to workshops held by National Institutes of Neurological Disorders and Stroke, National Heart Lung and Blood Institute, Alzheimer’s Association, and the Canadian Institutes of Health Research on dementia. She is a Team Leader within the Canadian Consortium for Neurodegeneration in Aging, Canada’s lead basic scientist in the Biomarkers Working Group of the International Traumatic Brain Injury Research Consortium, and Co-Principal Investigator in the Canadian Traumatic Brain Injury Research Consortium. Her studies have supported by the Canadian Institutes of Health Research, Weston Brain Institute, BrightFocus, Alzheimer Society of Canada, the Heart and Stroke Foundation of Canada, Alzheimer’s Drug Discovery Foundation, Pfizer, and AstraZeneca.

Targeting TDP-43 splicing repression for neurodegenerative disease

May 22 @ 15:15

Philip Wong

Johns Hopkins University (USA)

Over the past 25 years, Dr. Philip Wong has developed two major programs in the field of neurodegenerative diseases, focused on molecular mechanisms of Alzheimer’s disease (AD) and Frontotemporal Dementia-Amyotrophic Lateral Sclerosis (FTD-ALS) and on defining the molecular pathways potentially amenable to therapeutic interventions using molecular cellular and biological approaches. His work on AD has been recognized by a “MetLife Foundation Award for Medical Research”.

Dr. Wong has developed novel tools, including mouse models of AD and ALS to examine the pathophysiology of these diseases with the goal of identifying targets that would ultimately lead to effective therapies. His lab recently showed that TDP-43 – an RNA binding protein (RBP) implicated in ADRD, including FTD-ALS and AD with TDP-43 pathology – functions to repress transcriptome-wide splicing of non-conserved cryptic exons. TDP-43 is recognized as a founding member of a family of RBPs that protects the transcriptome from deleterious splicing events to ensure a normal proteome (dubbed “guardians” of the transcriptome). His team’s discovery that such guardian role of TDP-43 is compromised in FTD-ALS and AD provides the opportunity to identify potential therapeutic strategy of these human diseases. Using in vivo models, Dr. Wong and team validated TDP-43 splicing repression as a therapeutic target for FTD-ALS, providing the opportunity to translate this idea to the clinic for these devastating diseases of the elderly.

Multiomic landscape and functional analysis of Alzheimer’s disease-associated gene variants in human ESC-derived microglia

May 21 @ 11:35

Huaxi Xu

Sanford Burnham Prebys Medical Discovery Institute (USA)

Dr. Huaxi Xu, Jeanne & Gary Herberger Leadership Chair in Neuroscience at Sanford Burnham Prebys Medical Discovery Institute, earned his doctorate in Anatomy and Cell Biology from Albert Einstein College of Medicine in New York, NY. He completed his postgraduate studies with a fellowship from the Albert Einstein College of Medicine and at The Rockefeller University (with Nobel Laureate Paul Greengard). In 1998 Dr. Xu became an Assistant Professor at the Fisher Center for Research on Alzheimer Disease, Rockefeller University. In 2003 Dr. Xu joined the Neurodegenerative Disease Program at the Burnham Institute for Medical Research as Associate Professor and in 2008 as a Professor. During this time he was Acting Director (2007-2011) of the Neurodegenerative Disease Program. In 2016 Dr. Xu was appointed Director of the Neuroscience Initiative.

Dr. Xu is an expert specialized in the molecular mechanisms of Alzheimer’s disease (AD). His research is focused on the regulation of APP processing and trafficking, and mechanisms of synaptic dysfunction and neurotoxicity induced by proteotoxic beta amyloid and neurofibrillary tangle (NFT) tau components. Dr. Xu’s laboratory has also engaged in pioneering research in investigating novel genes and pathways involved in neuronal function/dysfunction and cell death, and integrating their cellular function to the pathogenesis of neurodegenerative diseases such as AD, Down syndrome, ALS and Progressive Supranuclear Palsy. To this end, his laboratory is also developing animal models to study neuronal and microglial function in relation to neurodegenerative dysfunction.

As an independent PI with over 20 years’ experience, Dr. Xu has continuously received funding of multiple grants from the NIH and many private foundations, and published over 150 papers with a total impact factor of ~1200 (with ~16,900 citations and h-index 61).

Enhancing neurogenesis by CX3CL1 back signals reverses neuronal loss and reduces amyloid deposition in AD mouse models

May 22 @ 11:45

Riqiang Yan

University of Connecticut Health (USA)

Dr. Riqiang Yan discovered BACE1 and published this study in Nature in 1999. He is recognized as the leading investigator in the functional study of BACE1, and reported their findings in Nature Medicine, Nature Neuroscience, Journal of Experimental Medicine, and etc.

Dr. Yan received his BS from Shanghai Medical University, his PhD from University of Kentucky, and postdoctoral training in the laboratory of Dr. James Darnell at the Rockefeller University. He was a principal investigator at Pharmacia and Upjohn Company and Pfizer between 1997 and 2003. He then became an Associate Professor, Professor, Morris R and Ruth V. Graham Endowed Professor and Vice Chair of Neuroscience Department at Cleveland Clinic Lerner Research Institute.

In 2018, he became the Chair of Department of Neuroscience and Scoville Endowed Professor at the University of Connecticut School of Medicine. He is the recipient of 2014 MetLife Award in Medical Research.

Multiscale gene network analysis identifies novel pathways and key regulators of Parkinson’s disease

May 22 @ 14:00

Bin Zhang

Icahn School of Medicine at Mount Sinai (USA)

Dr. Bin Zhang is a professor in the Department of Genetics and Genomic Sciences and the Director of the Mount Sinai Center for Transformative Disease Modeling at the Icahn School of Medicine at Mount Sinai. His expertise lies in machine learning, pattern recognition, bioinformatics, systems biology and with applications to disease modeling and drug discovery.

In the past 15 years, he has developed a series of influential gene network inference and analysis algorithms which have been extensively used for identification of novel pathways and gene targets, as well as development of drugs for a variety of human diseases such as cancer, atherosclerosis, Alzheimer’s, obesity and diabetes.

Currently his research is focused on integration of large scale bulk and single cell RNA-seq data as well as other Omics data into multiscale network models for discovering novel mechanisms of human diseases and developing novel therapeutics.

An astrocyte-microglia lipid signaling pathway in Alzheimer’s disease

May 21 @ 10:45

Hui Zheng

Baylor College of Medicine (USA)

Dr. Hui Zheng obtained her PhD degree from Baylor College of Medicine in 1990. After a brief postdoctoral training at Baylor, she joined Merck & Co. where she began her research on Alzheimer’s disease and continued after her return to Baylor in 1999. Dr. Zheng’s expertise is mouse genetics and she is a pioneer in utilizing sophisticated mouse models to probe the biology and pathophysiology of Alzheimer’s disease. Through her long-standing effort, she revealed the amyloid precursor protein as a synaptic adhesion protein mediating synaptic and cognitive function. Her studies on the presenilins offered critical clinical insights. Dr. Zheng’s current research focus are in the investigation of the autophagy-lysosomal pathway and neuron-immune interaction in AD.

Dr. Zheng is Huffington Foundation Endowed Chair and Director of the Huffington Center on Aging at Baylor College of Medicine. She serves on the Alzheimer’s Association Medical & Scientific Advisory Council, is a member of the Tau Consortium Scientific Advisory Board, and co-Chair of the Scientific Advisory Committee of the BrightFocus Foundation.

DJ-1 regulates the integrity and function of ER-mitochondria association: Implications in Parkinson’s disease

May 22 @ 11:20

Xiongwei Zhu

Case Western Reserve University (USA)

Dr. Xiongwei Zhu is a Professor of Pathology and Neurology at Case Western Reserve University.

He received his B.S. in 1995 and M.S. in 1998 from the Department of Biochemistry at Wuhan University in China. He received his Ph.D. in 2002 from the Department of Pathology at Case Western Reserve University. He joined faculty of Case Western Reserve University in 2004 and became full professor in 2015. His research focuses on the neurodegenerative mechanisms underlying Alzheimer’s disease, Parkinson’s disease and other neurodegenerative diseases with a focus on mitochondrial dysfunction and oxidative stress.

Dr. Zhu’s research is continuously funded by NIH, NASA and/or Alzheimer’s Association. He routinely serves as a review for NIH and other federal funding agencies such as Department of Defense, VA and NASA as well as a number of national/international private funding agencies.

He is deputy chief Editor of the Journal of Neurochemistry and Journal of Alzheimer’s Disease and a member of the editorial board of more than a dozen reputable international journals.

Abstract submission ends FEBRUARY 7, 2020.


Early bird registration ends February 28, 2020.