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Missing Link Connects Diabetes and Alzheimer's Disease
Missing Link Connects Diabetes and Alzheimer’s Disease A gene called PGC-1! is associated with the onset of Type 2 diabetes, associated with dementia and but it has shown to decrease in Alzheimer’s disease dementia cases. an accumulation in the brain of The gene is a potential target for regulating glucose, according to an abnormal protein known as new research led by Giulio Maria Pasinetti, MD, PhD, the Aidekman "-amyloid. This abnormal protein Family Professor in Neurology, and Professor of Psychiatry and causes plaque buildup in the Geriatrics and Adult Development. The study was recently published brain, which is linked to cognitive in Archives of Neurology. deterioration in Alzheimer’s disease. The PGC-1! gene, which plays an important role in regulating We may be able to link a gene—whose glucose metabolism, is considered a potential target for treating alteration may lead to diabetes—to a Type 2 diabetes. Giulio Maria Pasinetti, MD, PhD mechanism that would promote conditions Using a mouse model of associated with Alzheimer’s disease. Alzheimer’s disease, Dr. Pasinetti and his team also found that promoting PGC-1! content in brain cells reduces the hyperglycemic- — GIULIO MARIA PASINETTI, MD, PHD mediated production of "-amyloid. The findings could help researchers identify potential pharmacological treatments that might promote PGC-1! expression Previous studies suggest that Type 2 diabetes is a risk factor for in the brain cells of Alzheimer’s patients. “We need to discover Alzheimer’s disease. The relationship between the two conditions is new therapeutic approaches for Alzheimer’s disease by looking at “a fascinating new area of research,” says Dr. -
The Evelyn F. and William L. Mcknight Brain Institute and the Cognitive Aging and Memory – Clinical Translational Research Program (CAM-CTRP) 2015 Annual Report
The Evelyn F. and William L. McKnight Brain Institute and the Cognitive Aging and Memory – Clinical Translational Research Program (CAM-CTRP) 2015 Annual Report Prepared for the McKnight Brain Research Foundation by the University of Florida McKnight Brain Institute and Institute on Aging Table of Contents Letter from UF Leadership ................................................................................................................................................................................................. 3 Age-related Memory Loss (ARML) Program and the Evelyn F. McKnight Chair for Brain Research in Memory Loss...... 4-19 Cognitive Aging and Memory Clinical Translational Research Program (CAM-CTRP) and the Evelyn F. McKnight Chair for Clinical Translational Research in Cognitive Aging and Memory ................................ 20-63 William G. Luttge Lectureship in Neuroscience ...............................................................................................................64-65 Program Financials .................................................................................................................................................................. 66 Age-related Memory Loss Program .............................................................................................................................................................................67 McKnight Endowed Chair for Brain Research in Memory Loss .........................................................................................................................68 -
Cytokine Gene Expression As a Function of the Clinical Progression of Alzheimer Disease Dementia
ORIGINAL CONTRIBUTION Cytokine Gene Expression as a Function of the Clinical Progression of Alzheimer Disease Dementia James D. Luterman, PhD; Vahram Haroutunian, PhD; Shrishailam Yemul, PhD; Lap Ho, PhD; Dushyant Purohit, MD; Paul S. Aisen, MD; Richard Mohs, MD; Giulio Maria Pasinetti, MD, PhD Background: Inflammatory cytokines have been linked gyrus (P,.01). When stratified by the Consortium to to Alzheimer disease (AD) neurodegeneration, but little Establish a Registry for Alzheimer’s Disease (CERAD) is known about the temporal control of their expression neuropathological criteria, IL-6 mRNA expression in in relationship to clinical measurements of AD demen- both the entorhinal cortex (P,.05) and superior tem- tia progression. poral gyrus (P,.01) correlated with the level of neuro- fibrillary tangles but not neuritic plaques. However, in Design and Main Outcome Measures: We mea- the entorhinal cortex, TGF-b1 mRNA did not correlate sured inflammatory cytokine messenger RNA (mRNA) with the level of either neurofibrillary tangles or neu- expression in postmortem brain specimens of elderly sub- ritic plaques. Interestingly, in the superior temporal jects at different clinical stages of dementia and neuro- gyrus, TGF-b1 mRNA expression negatively correlated pathological dysfunction. with neurofibrillary tangles (P,.01) and showed no relationship to the pathological features of neuritic Setting and Patients: Postmortem study of nursing plaques. home patients. Conclusions: The data are consistent with the hypoth- Results: In brains of cognitively normal control sub- esis that cytokine expression may differentially contrib- jects, higher interleukin 6 (IL-6) and transforming ute to the vulnerability of independent cortical regions growth factor b1 (TGF-b1) mRNA expression was during the clinical progression of AD and suggest that observed in the entorhinal cortex and superior temporal an inflammatory cytokine response to the pathological gyrus compared with the occipital cortex. -
Neuroimaging Methods for Music Information Retrieval: Current Findings and Future Prospects
NEUROIMAGING METHODS FOR MUSIC INFORMATION RETRIEVAL: CURRENT FINDINGS AND FUTURE PROSPECTS Blair Kaneshiro Jacek P. Dmochowski Center for Computer Research in Music and Acoustics Department of Psychology Stanford University, Stanford, CA, USA Stanford University, Stanford, CA, USA [email protected] [email protected] ABSTRACT best a marginal or incidental role in that literature. The au- thors cite as a main obstacle a fundamental lack of interest, Over the past decade and a half, music information re- or understanding, from the cognitive science/neuroscience trieval (MIR) has grown into a robust, cross-disciplinary community. At the same time, the few brain-based MIR field spanning a variety of research domains. Collabo- studies published to date [16, 40, 52] have emphasized rations between MIR and neuroscience researchers, how- application over background, potentially leaving readers ever, are still rare, and to date only a few studies using lacking sufficient introduction to the imaging technique approaches from one domain have successfully reached and brain response of interest. As things currently stand, an audience in the other. In this paper, we take an initial the fields of MIR and neuroscience operate largely inde- step toward bridging these two fields by reviewing studies pendently, despite sharing approaches and questions that from the music neuroscience literature, with an emphasis might benefit from cross-disciplinary investigation. on imaging modalities and analysis techniques that might In an effort to begin reconciling these two fields, be of practical interest to the MIR community. We show the present authors—whose backgrounds collectively span that certain approaches currently used in a neuroscientific music, neuroscience, and engineering—present a review setting align with those used in MIR research, and discuss of studies drawn from the music neuroscience literature implications for potential areas of future research. -
The Brain That Changes Itself
The Brain That Changes Itself Stories of Personal Triumph from the Frontiers of Brain Science NORMAN DOIDGE, M.D. For Eugene L. Goldberg, M.D., because you said you might like to read it Contents 1 A Woman Perpetually Falling . Rescued by the Man Who Discovered the Plasticity of Our Senses 2 Building Herself a Better Brain A Woman Labeled "Retarded" Discovers How to Heal Herself 3 Redesigning the Brain A Scientist Changes Brains to Sharpen Perception and Memory, Increase Speed of Thought, and Heal Learning Problems 4 Acquiring Tastes and Loves What Neuroplasticity Teaches Us About Sexual Attraction and Love 5 Midnight Resurrections Stroke Victims Learn to Move and Speak Again 6 Brain Lock Unlocked Using Plasticity to Stop Worries, OPsessions, Compulsions, and Bad Habits 7 Pain The Dark Side of Plasticity 8 Imagination How Thinking Makes It So 9 Turning Our Ghosts into Ancestors Psychoanalysis as a Neuroplastic Therapy 10 Rejuvenation The Discovery of the Neuronal Stem Cell and Lessons for Preserving Our Brains 11 More than the Sum of Her Parts A Woman Shows Us How Radically Plastic the Brain Can Be Appendix 1 The Culturally Modified Brain Appendix 2 Plasticity and the Idea of Progress Note to the Reader All the names of people who have undergone neuroplastic transformations are real, except in the few places indicated, and in the cases of children and their families. The Notes and References section at the end of the book includes comments on both the chapters and the appendices. Preface This book is about the revolutionary discovery that the human brain can change itself, as told through the stories of the scientists, doctors, and patients who have together brought about these astonishing transformations. -
Superior Spider-Man: Necessary Evil (Marvel Now) Volume 4 Free
FREE SUPERIOR SPIDER-MAN: NECESSARY EVIL (MARVEL NOW) VOLUME 4 PDF Dan Slott,Ryan Stegman | 112 pages | 11 Feb 2014 | Marvel Comics | 9780785184737 | English | New York, United States Necessary Evil | Marvel Database | Fandom The storyline sees a dying Otto Octavius swapping bodies with Peter Parker and allowing Parker to die in his body. However, he later learns about responsibility Superior Spider-Man: Necessary Evil (Marvel Now) Volume 4 redeems himself. Adopting the alias "Superior Spider-Man", he becomes a superhero and is determined to prove himself as a better Spider-Man than Parker ever was, and a better man than Octavius. The series is a continuation of the " Dying Wish " storyline, which ended the long running series The Amazing Spider-Man. The series ended with issue 31, which determined the fate of Octavius's mind, and was followed up by a relaunch Superior Spider-Man: Necessary Evil (Marvel Now) Volume 4 The Amazing Spider-Man series, with the first volume depicting Parker regaining his body and the Spider-Man mantle. In Mayit was announced that the series would return for two additional issues 32 and 33 that fill a gap left by an earlier storyline, as well as lead into the " Spider-Verse " storyline. They were released in August It served as a continuation of the history of Otto Octavius after the events of "Go Down Swinging", and also serves as a tie-in to the "Spider-Geddon" storyline. Ina new volume of The Superior Spider-Man debuted as part of the " Spider-Geddon " storyline, with 12 new Superior Spider-Man: Necessary Evil (Marvel Now) Volume 4 written by Gage. -
(“Spider-Man”) Cr
PRIVILEGED ATTORNEY-CLIENT COMMUNICATION EXECUTIVE SUMMARY SECOND AMENDED AND RESTATED LICENSE AGREEMENT (“SPIDER-MAN”) CREATIVE ISSUES This memo summarizes certain terms of the Second Amended and Restated License Agreement (“Spider-Man”) between SPE and Marvel, effective September 15, 2011 (the “Agreement”). 1. CHARACTERS AND OTHER CREATIVE ELEMENTS: a. Exclusive to SPE: . The “Spider-Man” character, “Peter Parker” and essentially all existing and future alternate versions, iterations, and alter egos of the “Spider- Man” character. All fictional characters, places structures, businesses, groups, or other entities or elements (collectively, “Creative Elements”) that are listed on the attached Schedule 6. All existing (as of 9/15/11) characters and other Creative Elements that are “Primarily Associated With” Spider-Man but were “Inadvertently Omitted” from Schedule 6. The Agreement contains detailed definitions of these terms, but they basically conform to common-sense meanings. If SPE and Marvel cannot agree as to whether a character or other creative element is Primarily Associated With Spider-Man and/or were Inadvertently Omitted, the matter will be determined by expedited arbitration. All newly created (after 9/15/11) characters and other Creative Elements that first appear in a work that is titled or branded with “Spider-Man” or in which “Spider-Man” is the main protagonist (but not including any team- up work featuring both Spider-Man and another major Marvel character that isn’t part of the Spider-Man Property). The origin story, secret identities, alter egos, powers, costumes, equipment, and other elements of, or associated with, Spider-Man and the other Creative Elements covered above. The story lines of individual Marvel comic books and other works in which Spider-Man or other characters granted to SPE appear, subject to Marvel confirming ownership. -
View Final Program
142nd ANNUAL MEETING OF THE AMERICAN ANA2017 NEUROLOGICAL ASSOCIATION SAN DIEGO, CA • OCTOBER 15-17, 2017 SHERATON SAN DIEGO HOTEL & MARINA EXPLORE • EXAMINE • INVESTIGATE FINAL PROGRAM OCTOBER 14, 2017 | Pre-Meeting Symposium: Big Science and the BRAIN Initiative 2017.MYANA.org 142nd ANNUAL MEETING OF THE AMERICAN ANA2017 NEUROLOGICAL ASSOCIATION SAN DIEGO, CA • OCTOBER 15 -17, 2017 SHERATON SAN DIEGO HOTEL & MARINA ND Please note some session titles may have changed since this program was printed. Please refer THE 142 ANA to your Mobile app for the most current session updates. ANNUAL MEETING LETTER FROM THE CHAIR 3 Enjoy outstanding scientific SCHEDULE AT A GLANCE 4 symposia covering the latest HOTEL FLOOR PLANS 6 research in the fields of neurology and neuroscience GENERAL INFORMATION 7 while taking the opportunity WIRELESS CONNECTION 8 to network with leaders in the world of academic neurology CONTINUING MEDICAL EDUCATION 8 at the 142nd ANA Annual ANNUAL MEETING MOBILE APP 8 Meeting in San Diego, CA, October 15-17, 2017. PROGRAMS BY DAY 9 SATURDAY OCT 14 9 MEETING LOCATION SUNDAY OCT 15 9 Sheraton San Diego MONDAY OCT 16 17 Hotel & Marina 1380 Harbor Island Drive TUESDAY OCT 17 25 San Diego, California 92101 IN MEMORIAM 28 ONSITE MEETING CONTACTS SPEAKER ABSTRACTS 29 Registration and meeting questions: THANK YOU TO OUR SUPPORTERS & EXHIBITORS 42 [email protected] FUTURE MEETING DATES 42 OR visit the registration desk Bay View Foyer 2017 AWARDEES 43 (located in Marina Tower Lobby Level) ACADEMIC NEUROLOGY REPRESENTATIVES FROM JAPAN 47 Saturday, October 14 2017 ABSTRACT REVIEWERS 48 3:00 PM–7:00 PM BOARD OF DIRECTORS 49 Sunday, October 15 6:00 AM–5:45 PM ANA 2017 COMMITTEES, SUBCOMMITTEES & TASK FORCES 50 Monday, October 16 6:30 AM–5:45 PM Tuesday, October 17 6:30 AM–2:15 PM #ANAMTG2017 ANA 2017 FROM THE CHAIR Dear Colleagues, It is a pleasure to welcome you to the 142nd Annual Meeting of the American Neurological Association (ANA). -
Clausner-CV-2018 Without Lang
CURRICULUM VITAE TIMOTHY C. CLAUSNER University of Maryland, Institute for Advanced Computer Studies (UMIACS) A. V. Williams Building Room 3247 8223 Paint Branch Drive, College Park, Maryland 20742-3255 USA Email: [email protected] EDUCATION 1987-1993 Ph.D., Linguistics, University of Michigan, Ann Arbor. August 1993. Dissertation: Cognitive Structures in Metaphor Comprehension (W. Croft, principal advisor). 1982-1984 M.S., Computer Science, University of Maryland, College Park. May 1984. (S.K. Tripathi, principal advisor) 1976-1980 B.S., Applied Physics, Georgia Institute of Technology. June 1980. PROFESSIONAL EXPERIENCE 2007-present University of Maryland, College Park, Institute for Advanced Computer Studies. Visiting Research Scientist (2016-present). Affiliation: Dept. of Psychology: Cognitive Neuroscience Group. Human Computer Interaction Laboratory (2010-present). Senior Research Scientist/Associate, School of Information Studies Center for Advance Study of Language (2007-2009) 1997-2007 HRL Laboratories, Information and System Sciences Lab, Malibu, California. Senior Research Scientist (2001-2007). Human-Centered Systems Department Research Scientist (1999-2001), Member of Research Staff (1997). 1995-1997 Postdoctoral Fellow. University of Southern California, Language & Cognitive Neuroscience Lab. Program for Neural, Informational & Behavioral Sciences. 1995, Aug-Dec Lecturer. University of Southern California. Departments of Linguistics and Psychology. Linguistics/Psychology 586, Psycholinguistics: Aphasia (with M. MacDonald) 1993-1995 Postdoctoral Fellow. Johns Hopkins University, Cognitive Neurolinguistics/Neuropsychology Lab. Department of Cognitive Science. National Institutes of Health Cognitive Neuropsychology Training Grant (M. McCloskey and B. Rapp). 1 of 11 Timothy C. Clausner 1995, Jan-June Lecturer. Johns Hopkins University, Department of Cognitive Science. Designed and instructed a new course, Cognitive Science 126 Meanings in the Mind: Introduction to Semantics. -
Spring 2006 Exciting Advances in 2005 Neuroergonomics
!uman Fac"rs / Applied Cogni#on Newsle$e% Spring 2006 Neuroergonomics an Interview with Dr. Raja Parasuraman pg 3 Exciting Advances in 2005 in Human Factors and Applied Cognition pg 6 Designs We Love To Hate! Students Speak Out pg 5 Departments Welcome - Carl Smith (pg 2) Contact Information The Next Wave (pg 8) Student activities and new graduate profiles The Beat (pg 10) GMU Publications, Presentations and Awards A Moment With...(pg 12) Patrick McKnight Parting Thoughts (pg 13) Dr. Boehm-Davis &elcom' This year has seen big changes and huge progress from the HFES student group! In just over two years, we have grown from a small group of dedicated students to a large, active student group striving to make a name for George Mason University both locally and nationally. The growth of the student group has led to several activities over the course of this year. In the 2005-2006 academic year, the GMU HFES Student Chapter will have hosted 8 speakers at GMU, participated in 6 community presentations to increase human factors awareness, and participated in a joint symposium with the Virginia Tech Human Factors Student Chapter. While the actions of our group are certainly noteworthy, we must be cognizant that our student chapter will only persevere through the energetic and continuous development of an active chapter membership. For our student group to continue to grow in size Carl Smith and prestige, it is critical that new and continuing students be GMU HFES Student Board President brought into the fold. For those students who are currently attend- ing GMU, take notice of the many HFES opportunities for students to become involved. -
The Dichotomous Role of Inflammation in The
biomolecules Review The Dichotomous Role of Inflammation in the CNS: A Mitochondrial Point of View Bianca Vezzani 1,2 , Marianna Carinci 1,2 , Simone Patergnani 1,2 , Matteo P. Pasquin 1,2, Annunziata Guarino 2,3, Nimra Aziz 2,3, Paolo Pinton 1,2,4, Michele Simonato 2,3,5 and Carlotta Giorgi 1,2,* 1 Department of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy; [email protected] (B.V.); [email protected] (M.C.); [email protected] (S.P.); [email protected] (M.P.P.); [email protected] (P.P.) 2 Laboratory of Technologies for Advanced Therapy (LTTA), Technopole of Ferrara, 44121 Ferrara, Italy; [email protected] (A.G.); [email protected] (N.A.); [email protected] (M.S.) 3 Department of BioMedical and Specialist Surgical Sciences, University of Ferrara, 44121 Ferrara, Italy 4 Maria Cecilia Hospital, GVM Care & Research, 48033 Cotignola (RA), Italy 5 School of Medicine, University Vita-Salute San Raffaele, 20132 Milan, Italy * Correspondence: [email protected]; Tel.: +39-0532-455803 Received: 28 August 2020; Accepted: 10 October 2020; Published: 13 October 2020 Abstract: Innate immune response is one of our primary defenses against pathogens infection, although, if dysregulated, it represents the leading cause of chronic tissue inflammation. This dualism is even more present in the central nervous system, where neuroinflammation is both important for the activation of reparatory mechanisms and, at the same time, leads to the release of detrimental factors that induce neurons loss. Key players in modulating the neuroinflammatory response are mitochondria. Indeed, they are responsible for a variety of cell mechanisms that control tissue homeostasis, such as autophagy, apoptosis, energy production, and also inflammation. -
Obesity & Weight Management
Giulio Maria Pasinetti, J Obes Wt Loss Ther 2012, 2:9 http://dx.doi.org/10.4172/2165-7904.S1.003 International Conference and Exhibition on Obesity & Weight Management December 3-5, 2012 DoubleTree by Hilton Philadelphia, USA HDAC IIa-specific inhibitors as a potential novel therapy for type 2 diabetes-mediated cognitive deterioration in alzheimer’s disease Giulio Maria Pasinetti Mount Sinai School of Medicine, USA ur laboratory recently demonstrated that epigenetic chromatin modifications associated with type-2 diabetes (T2DM) may Oplay a role in brain pathophysiology in neurodegenerative disorders. We previously discovered that there are significant changes in the expression of select chromatin modification enzymes, such as histone deacetylases (HDACs), in the brains of T2DM subjects compared to control subjects, and that these changes coincide with altered expression of proteins involved in synaptic function, such as PSD95 and synaptophysin. We hypothesized that T2DM may induce epigenetic modifications associated with increased susceptibility to Alzheimer’s disease (AD)-type neurodegeneration. Using a mouse model of diet- induced T2DM, we found that, similar to humans, T2DM mice showed differential expression of epigenetic-modifying enzymes in the brain compared to controls. In particular, we found significant up-regulation of HDAC class IIa, including HDACs 4, 5, and 9, in the brains of diabetic mice. These alterations coincided with increased susceptibility to oligomeric Aβ (oAβ) induced synaptic toxicity and oAβ-induced synaptic dysfunction, as assessed by long term potentiation (LTP). Most interestingly, we found that inhibition of class IIa HDACs using an HDAC IIa-specific inhibitor, MC1568, increased transcription levels of PSD95 and synaptophysin in primary neuron cultures from C57Bl6/J mice and prevented LTP deficits found in old-T2DM mouse ex vivo hippocampal slices.