Lecture

Neuroepigenetics: Molecular Mechanisms and Cognitive Implications

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In course

BIO-480: Neuroscience: from molecular mechanisms to disease

The goal of the course is to guide students through the essential aspects of molecular neuroscience and neurodegenerative diseases. The student will gain the ability to dissect the molecular basis of disease in the nervous system in order to begin to under ...

Description

This lecture explores the impact of maternal behavior on stress response through epigenetic modifications in rat pups. It delves into the genetic vs. epigenetic influence on various traits and explains euchromatin and heterochromatin separation mechanisms. The lecture also discusses DNA methylation and gene expression regulation in the brain, focusing on memory formation and synaptic plasticity.

Instructors (4)

Hilal Lashuel

2012-2013 Visiting Professor, Standford University. Stanford School of Medicine 2011- Associate Professor of Life Sciences-Brain Mind Institute-EPFL Dir. Laboratory of Chemical Biology of Neurodegeneration 2005-2011 Assistant Professor of Life Sciences-Brain Mind Institute-EPFL Dir. Laboratory of Molecular Neurobiology and Neuroproteomics 2005-2008 Director- EPFL Proteomic Core Facility 2002-2004 Instructor of Neurology- Harvard Medical School and Brigham and Women's Hospital 2001-2002 Sabbatical Fellow- Laboratory for Drug Discovery in Neurodegeneration Harvard Medical School, 2001-2002 Post-doctoral Fellow- Center for Neurologic Diseases Harvard Medical School and Brigham and Women's Hospital Advisor- Prof. Peter T. Lansbury 2000-2001 Research Scientist, The Picower Institute for Medical Research, Great Neck New York 1994-2000 PhD Student; Texas A&M University and the Scripps Research Institute Advisor- Prof. Jeffery W. Kelly 1990-1994 B.S. City University of New York, Brooklyn College Dr. Hilal A. Lashuel received his B.Sc. degree in chemistry from the City University of New York in 1994 and completed his doctoral studies at Texas A&M University and the Scripps Research Institute in 2000. After obtaining his doctoral degree, he became a research fellow at the Picower Institute for Medical Research in Long Island New York. In 2001, he moved to Harvard Medical School and the Brigham and Women's Hospital as a research fellow in the Center for Neurologic Diseases and was later promoted to an instructor in neurology at Harvard Medical School. During his tenure (2001-2004) at Harvard Medical School his work focused on understanding the mechanisms of protein misfolding and fibrillogenesis and the role of these processes in the pathogenesis of Parkinson's and Alzheimer's disease. In 2005 Dr. Lashuel moved Switzerland to join the Brain Mind Institute at the Swiss Federal Institute of Technology Lausanne as a tenure-track assistant professor in neurosciences. Currently, Dr. Lashuel is an associate professor of life sciences and the director of the laboratory of molecular and chemical biology of neurodegeneration. (http://lashuel-lab.epfl.ch/). Research efforts in the Lashuels laboratory focus on understanding the molecular mechanisms of neurodegeneration and developing novel strategies to diagnose and treat neurodegenerative diseases such as Alzheimers and Parkinsons disease. Research in the Lashuel lab is funded by several international funding agencies and foundations, including the Swiss National Science Foundation, European FP7 program (Marie Curie and ERC grants), Human Science Frontiers, Strauss Foundation, Cure the Huntingtons disease foundation and Michael J Fox foundation and is supported by collaborations with pharmaceutical and biotech companies (http://lashuel-lab.epfl.ch/page-50538-en.html), Nestle, Merck-Serono, AC Immune and Johnson and Johnson. Dr. Lashuels research has resulted in the characterization of novel quaternary structure intermediates on the amyloid pathway, identification of potential therapeutic targets, and new hypotheses concerning the mechanisms of pathogenesis in Alzheimers disease, Parkinsons disease and related disorders. Dr. Lashuel scientific contribution to this field includes i) more than100 publications in major peer reviewed journals including Nature journals, Cell, PNAS, JBC, J. Neuroscience JACS, and Angewandtie Chemie; ii) three patents on novel strategies for preventing protein aggregation and treating autoimmune and inflammatory diseases; iii) more than 150 invited lectures since 2002 and more than 5500 citations (7800 citation-Google Scholar) since 1996. Dr. Lashuel has received several pre-doctoral and post-doctoral awards and fellowships and was the recipient of two prestigious awards given to young investigators; Human Science Frontiers young investigator research award and the European Research Council (ERC) starting independent researcher grant and the ERC proof of concept award (2013) These awards provide more than $2.5 Million to Dr. Lashuel to translate some of his ideas and projects into novel strategies for diagnosing and treating neurodegenerative diseases such as Alzheimers and Parkinsons disease. Dr. Lashuel has chaired and co-organized several international conferences and serves as an academic editor for PLoS ONE, an associate editor for frontiers of molecular neuroscience, member of the Editorial advisory board of ChemBioChem and ad hoc reviewer for several international scientific journals and funding agencies.

Official source

Ontological neighbourhood

Biology

Genetics: Molecular genetics, Population genetics

Cell biology: Cell cycle

Related concepts (32)

Transgenerational epigenetic inheritance

Transgenerational epigenetic inheritance is the transmission of epigenetic markers and modifications from one generation to multiple subsequent generations without altering the primary structure of DNA. Thus, the regulation of genes via epigenetic mechanisms can be heritable; the amount of transcripts and proteins produced can be altered by inherited epigenetic changes. In order for epigenetic marks to be heritable, however, they must occur in the gametes in animals, but since plants lack a definitive germline and can propagate, epigenetic marks in any tissue can be heritable.

Slide show

A slide show (slideshow) is a presentation of a series of still images (slides) on a projection screen or electronic display device, typically in a prearranged sequence. The changes may be automatic and at regular intervals or they may be manually controlled by a presenter or the viewer. Slide shows originally consisted of a series of individual photographic slides projected onto a screen with a slide projector. When referring to the video or computer-based visual equivalent, in which the slides are not individual physical objects.

Slide projector

A slide projector is an opto-mechanical device for showing photographic slides. 35 mm slide projectors, direct descendants of the larger-format magic lantern, first came into widespread use during the 1950s as a form of occasional home entertainment; family members and friends would gather to view slide shows. Reversal film was much in use, and supplied slides snapped during vacations and at family events. Slide projectors were also widely used in educational and other institutional settings.

Presentation slide

A slide is a single page of a presentation. Collectively, a group of slides may be known as a slide deck. A slide show is an exposition of a series of slides or images in an electronic device or in a projection screen. Before the advent of the personal computer, a presentation slide could be a 35 mm slide viewed with a slide projector or a transparency viewed with an overhead projector. In the digital age, a slide most commonly refers to a single page developed using a presentation program such as MS PowerPoint, Apple Keynote, Google Slides, Apache OpenOffice or LibreOffice.

Histone deacetylase

Histone deacetylases (, HDAC) are a class of enzymes that remove acetyl groups (O=C-CH3) from an ε-N-acetyl lysine amino acid on both histone and non-histone proteins. HDACs allow histones to wrap the DNA more tightly. This is important because DNA is wrapped around histones, and DNA expression is regulated by acetylation and de-acetylation. HDAC's action is opposite to that of histone acetyltransferase. HDAC proteins are now also called lysine deacetylases (KDAC), to describe their function rather than their target, which also includes non-histone proteins.

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