DOCSLIB.ORG

Transcriptionist

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Transcriptionist 00001 1 2 3 4 5 6 7 8 9 10 11 CENTERS FOR MEDICARE AND MEDICAID SERVICES 12 Medicare Evidence Development & Coverage 13 Advisory Committee 14 15 16 17 18 19 20 January 30, 2013 21 22 Centers for Medicare and Medicaid Services 23 7500 Security Boulevard 24 Baltimore, Maryland 25 00002 1 Panelists 2 Chairperson Rita Redberg, MD, MS 3 Vice-Chair 4 Art Sedrakyan, MD, PhD 5 Voting Members Jeffrey W. Cozzens, MD, FACS 6 Raymond E. Faught, Jr., MD A. Mark Fendrick, MD 7 Steven Gutman, MD Paula E. Hartman-Stein, PhD 8 Susan A. Levine, DVM, MS, PhD Theresa Miskimen, MD 9 Curtis Mock, MD, MBA Jerrold Rosenbaum, MD 10 Amy E. Sanders, MD, MS Robert K. Zeman, MD 11 CMS Liaison 12 Louis Jacques, MD 13 Industry Representative Brian Seal, RPh, MBA, PhD 14 Guest Panel Members 15 Peter Herscovitch, MD file:///F|/MEDCAC/PG013013-summation.txt[03/05/2013 7:18:14 AM] Constantine G. Lyketsos, MD, MHS 16 Invited Guest Speakers 17 Paul Aisen, MD Randall J. Bateman, MD 18 Mark Mintun, PhD Steven D. Pearson, MD, MSc, FRCP 19 William Thies, MD 20 Executive Secretary Maria Ellis 21 22 23 24 25 00003 1 TABLE OF CONTENTS 2 Page 3 Opening Remarks Maria Ellis/Louis Jacques, MD/ 4 Rita Redberg, MD 4 5 Introduction of Panel 7 6 CMS Presentation and Presentation of Voting Questions 7 Joseph Hutter, MD 10 Brijet Burton Coachman, MPP, MS, PA-C 13 8 Presentations by Invited Guest Speakers 9 Paul Aisen, MD 15 Randall Bateman, MD 32 10 Steven Pearson, MD, MSc 47 William Thies, MD 69 11 Mark Mintun, MD 82 12 Scheduled Public Comments Stephen Salloway, MD, MS 101 13 Howard Fillit, MD 106 Norman L. Foster, MD 111 14 Sam Gandy, MD, PhD 115 Carl Sadowsky, MD 118 15 Mykol Larvie, MD, PhD 122 Richard Wahl, MD 127 16 Richard Frank, MD, PhD 131 David Kuhlmann, MD 136 17 Michael D. Devous, Sr., MD 142 Teng J. Ong, MD 147 18 Open Public Comments 19 Rathan Subramaniam, MD 150 Lou Bordicco 151 20 Questions to Presenters 152 21 Panel Discussion, Final Remarks and Voting 22 Questions 248 file:///F|/MEDCAC/PG013013-summation.txt[03/05/2013 7:18:14 AM] 23 Closing Remarks and Adjournment 282 24 25 00004 1 PANEL PROCEEDINGS 2 (The meeting was called to order at 3 8:09 a.m., Wednesday, January 30, 2013.) 4 MS. ELLIS: Good morning, and welcome, 5 committee chairperson, vice chairperson, 6 members and guests. I am Maria Ellis, the 7 executive secretary for the Medicare Evidence 8 Development and Coverage Advisory Committee, 9 MedCAC. The committee is here today to discuss 10 beta amyloid positron emission tomography in 11 dementia and neurodegenerative disease. 12 The following announcement addresses 13 conflict of interest issues associated with 14 this meeting and is made part of the record. 15 The conflict of interest statutes 16 prohibit special government employees from 17 participating in matters that could affect 18 their or their employers' financial interests. 19 Each member will be asked to disclose any 20 financial conflicts of interest during their 21 introduction. We ask in the interest of 22 fairness that all persons making statements or 23 presentations disclose if you or any member of 24 your immediate family owns stock or has another 25 formal financial interest in any company, 00005 1 including Internet or e -commerce organizations, 2 that develops, manufactures, distributes and/or 3 markets consulting, evidence reviews or 4 analyses, or other services related to beta 5 amyloid positron emission tomography in 6 dementia. This includes direct financial 7 investments, consulting fees, and significant 8 institutional support. If you haven't already 9 received a disclosure statement, they are 10 available on the table outside of the room. 11 We ask that all presenters please 12 adhere to their time limits. We have numerous 13 presenters to hear from today and a very tight 14 agenda, and therefore cannot allow extra time. 15 There is a timer at the podium that you should 16 follow. The light will begin flashing when you 17 have two minutes remaining and then turn red 18 when your time is up. Please note that there 19 is a chair for the next speaker, and please 20 proceed to that chair when it is your turn. We 21 ask that all speakers addressing the panel 22 please speak directly into the mic and state 23 your name. 24 For the record, voting members present file:///F|/MEDCAC/PG013013-summation.txt[03/05/2013 7:18:14 AM] 25 for today's meeting are Dr. Art Sedrakyan, 00006 1 Dr. Jeffrey Cozzens, Dr. Raymond Faught, Jr., 2 Dr. A. Mark Fendrick, Dr. Steven Gutman, 3 Dr. Paula Hartman-Stein, Dr. Susan Levine, 4 Dr. Theresa Miskimen, Dr. Curtis Mock, 5 Dr. Jerrold Rosenbaum, Dr. Amy Sanders and 6 Dr. Robert Zeman. A quorum is present and no 7 one has been recused because of conflicts of 8 interest. 9 The entire panel, including nonvoting 10 members, will participate in the voting. The 11 voting results will be available on our website 12 following the meeting. I ask that all panel 13 members, please speak directly into the mic, 14 and you may have to move the mic since we have 15 to share. 16 This meeting is being webcast via CMS 17 in addition to the transcriptionist. By your 18 attendance you are giving consent to the use 19 and distribution of your name, likeliness and 20 voice during this meeting. You are also giving 21 consent to the use and distribution of any 22 personal identifiable information that you or 23 others may disclose about you during today's 24 meeting. Please do not disclose personal 25 health information. 00007 1 If you require a taxicab, there are 2 telephone numbers to local cab companies at the 3 desk outside of the auditorium. Please 4 remember to discard your trash in the trash 5 cans located outside of this room. 6 And lastly, CMS guests attending 7 today's MedCAC meeting are only permitted in 8 the following areas of CMS single site, the 9 main lobby, the auditorium, the lower level 10 lobby, and the cafeteria. Any person found in 11 any area other than those mentioned will be 12 asked to leave the conference and will not be 13 allowed back on CMS property again. 14 And now, I would like to turn the 15 meeting over to Dr. Louis Jacques. 16 DR. JACQUES: Good morning. I'm Louis 17 Jacques, I'm the director of the Coverage and 18 Analysis Group and also the designated federal 19 official for this meeting. I have little to 20 say at this point other than to welcome you and 21 thank you for coming. We look forward to a 22 very interesting meeting. 23 DR. REDBERG: I am Rita Redberg, a 24 cardiologist at UCSF Medical Center and chair 25 for the MedCAC panel. I'm very pleased to be 00008 file:///F|/MEDCAC/PG013013-summation.txt[03/05/2013 7:18:14 AM] 1 here to consider all these questions along with 2 the help of the distinguished panel. 3 DR. SEDRAKYAN: Art Sedrakyan, from 4 Weill Cornell Medical College. I'm an 5 associate professor of cardiac surgery and 6 public health and direct the patient-centered 7 comparative effectiveness program, and have no 8 conflicts of interest to disclose. 9 DR. REDBERG: And I have no conflicts. 10 DR. COZZENS: I'm Jeff Cozzens, I'm 11 chief of neurosurgery at Southern Illinois 12 University Medical School. I have no 13 conflicts. 14 DR. FAUGHT: I'm Ed Faught, I'm a 15 professor of neurology at Emory University, and 16 I have no conflicts. 17 DR. FENDRICK: Mark Fendrick, 18 University of Michigan. No conflicts. 19 DR. GUTMAN: I'm Steve Gutman, I work 20 for a regulatory consulting firm, Myraqa, and I 21 have no conflicts. 22 DR. HARTMAN-STEIN: Paula 23 Hartman-Stein, in northeast Ohio, and I'm a 24 clinical geropsychologist. I have no 25 conflicts. 00009 1 DR. LEVINE: I'm Susan Levine, senior 2 vice president of Hayes, Incorporated, which is 3 a health technology assessment company, and I 4 have no conflicts of interest. 5 DR. MISKIMEN: Theresa Miskimen, 6 professor of psychiatry, University Behavioral 7 Health Care, and I have no conflicts. 8 DR. MOCK: Curtis Mock, family 9 medicine geriatrics, medical director, United 10 Healthcare, I have no conflicts. 11 DR. ROSENBAUM: I'm Jerry Rosenbaum, 12 chief of psychiatry at Mass General Hospital 13 and professor of psychiatry at Harvard Medical 14 School. I have no conflicts. 15 DR. SANDERS: I'm Amy Sanders, an 16 assistant professor of neurology at the Albert 17 Einstein College of Medicine, and I have no 18 conflicts. 19 DR. ZEMAN: Hi, I'm Bob Zeman, I'm 20 chair and professor of radiology at George 21 Washington University, and I have no conflicts. 22 DR. SEAL: Brian Seal, director of 23 health outcomes research for Bayer HealthCare. 24 No conflicts. 25 DR. HERSCOVITCH: I'm Peter 00010 1 Herscovitch, director of the positron emission 2 tomography department at the NIH Clinical file:///F|/MEDCAC/PG013013-summation.txt[03/05/2013 7:18:14 AM] 3 Center. I am not representing the NIH here. I 4 have no financial conflicts. 5 DR. LYKETSOS: Good morning, I am 6 Constantine Lyketsos, I'm a professor of 7 psychiatry at Johns Hopkins, chair of 8 psychiatry at Hopkins Bayview, and I also 9 direct the Hopkins Memory and Alzheimer's 10 Treatment Center.
Load more

Recommended publications
  • Brain Scan-Blood Test Panel Promises Improved Diagnosis Of
    Medical Center 130 W. Kingsbridge Rd Bronx, NY 10468 (718) 741-4273 Fax (718) 741-4269 Department of Veterans Affairs Health Headlines For Immediate Release February 28, 2020 Sam Gandy, MD, PhD Gregory Elder, MD Brain Scan-Blood Test Panel Promises Improved Diagnosis of Brain Trauma Following Battlefield Blast Exposure New brain scans and blood tests move researchers towards more sensitive diagnosis of battlefield brain trauma and evaluation of new drugs BRONX, NY – An array of tests that combines functional assessment with blood tests and brain scans promises more sensitive and objective estimation of brain degeneration in human veterans exposed to battlefield improvised explosive device (IED) blasts, according to research led by doctors at the Icahn School of Medicine at Mount Sinai and the James J. Peters VA Medical Center. The study was published in Molecular Psychiatry on Tuesday, February 25, and featured on the journal’s cover. Traumatic brain injury (TBI) is associated with acute brain destruction at the time of the injury and is also a risk factor for developing neurodegenerative diseases later in life. It is estimated that 10 to 20 percent of veterans returning from the conflicts in Iraq and Afghanistan sustained mild TBI resulting from IED and other blast exposures. The true prevalence may be even higher, given that many blast- related injuries go undocumented. Symptoms of mild TBI frequently resolve in days to months following injury, but in a subset of patients, symptoms persist and evolve into a chronic syndrome. Veterans who had sustained TBIs may suffer subtle, yet important, endocrine and neuropsychiatric dysfunction.
    [Show full text]
  • Departments of Neurology and Neurosurgery
    FEATURED STORY Studying Fluorescence- Guided Surgery www.mountsinai.org See Page 3 SPECIALTY REPORT | WINTER 2017 Departments of Neurology and Neurosurgery IN THIS ISSUE 2 Message From the Chairs 2 Treating Seizure Disorders 3 Studying Fluorescence-Guided Surgery 4 Integrated Neurosurgical Tools, 3D Printing 6 Studying a New Imaging Agent 7 Advancing Intracerebral Hemorrhage Care (Top) Intraoperative detection of residual tumor at the glioblastoma margin with protoporphyrin IX (PPIX) fluorescence during 5-ALA fluorescence- guided surgery. (Bottom) MRI neuronavigation confirms that the location of the tumor fluorescence is outside the gadolinium contrast-enhancing border. MESSAGE FROM THE CHAIRS Treating Seizure Disorders Combining the Minimally Invasive Stereo-EEG Technique With Awake Language Mapping The patient is a 15-year-old right-handed young man, diagnosed at age six in his home country with a le temporoparietal and insular dysembryoplastic neuroepithelial tumor (DNET). The tumor was diagnosed aer the patient presented with seizures consisting of liing his right hand above his head and lauhing for a few seconds. These seizures occurred approximately every 10 days. His other seizure type consisted of a sensation of an electrical current traveling up through his le leg, which frequently resulted in falls Barbara G. Vickrey, MD, MPH that caused multiple so-tissue injuries. He was deemed to have Joshua B. Bederson, MD gelastic as well as focal seizures without loss of consciousness. Over the years, in his home country, he tried 15 anti-seizure Mount Sinai continues to use the most advanced technology medications and underwent placement of a vagus nerve stimulator to make a lasting, global impact on patient care, research, implant—without benefit.
    [Show full text]
  • Mount Sinai Leads Global Program Using Stem Cells, Collaborates with the New York Stem Cell Foundation to Accelerate Cures for Alzheimer’S Disease
    FOR IMMEDIATE RELEASE Contact: Contact: Mount Sinai Press Office David McKeon 212-241-9200 212-365-7440 [email protected] [email protected] Mount Sinai Leads Global Program Using Stem Cells, Collaborates with The New York Stem Cell Foundation to Accelerate Cures for Alzheimer’s Disease Researchers Using Skin Samples and Brain Imaging to Identify Causes and Cures (New York—March 26, 2013) —Sam Gandy, MD, PhD, of the Icahn School of Medicine at Mount Sinai is leading an international team of researchers working to reprogram skin cells into brain cells to gain a better understanding of Alzheimer’s disease (AD). As part of the Consortium, Dr. Gandy is collaborating with Scott Noggle, PhD, the NYSCF – Charles Evans Senior Research Fellow for Alzheimer’s Disease and Director of the New York Stem Cell Foundation (NYSCF)’s laboratory in Manhattan. Dr. Gandy heads the Stem Cell Research Consortium funded by the Cure Alzheimer’s Fund (CAF). The Consortium consists of six institutions that plan to directly investigate, for the first time, brain cells in petri dishes from individual patients who have the common form of AD. Dr. Gandy is working with Dr. Noggle’s team to reprogram skin cells from AD patients into brain cells using stem-cell technology. The research team will obtain and monitor adult AD brain cells, providing not only a way to study the causes of the disease but also a system for discovering potentially effective drugs. The strategy has been nicknamed “the patient- specific disease in a dish” and enables studies on a time scale of minutes or hours, compared with mouse model testing, which routinely requires nine months to one year.
    [Show full text]
  • B87118dcd374d4040914d63600
    F1000Research 2017, 6:413 Last updated: 19 APR 2017 OPINION ARTICLE Midlife interventions are critical in prevention, delay, or improvement of Alzheimer’s disease and vascular cognitive impairment and dementia [version 1; referees: 2 approved] Sam Gandy 1,2, Tamas Bartfai3, Graham V. Lees4, Mary Sano2 1Department of Neurology and NFL Neurological Center, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA 2Department of Psychiatry and Alzheimer’s Disease Research Center, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA 3Department of Neurochemistry, Stockholm University, Stockholm, 114 18, Sweden 4Corpus Alienum Oy, Kirkkonummi, 02400, Finland v1 First published: 03 Apr 2017, 6:413 (doi: 10.12688/f1000research.11140.1) Open Peer Review Latest published: 03 Apr 2017, 6:413 (doi: 10.12688/f1000research.11140.1) Referee Status: Abstract The basic strategy for focusing exclusively on genetically identified targets for intervening in late life dementias was formulated 30 years ago. Three decades Invited Referees and billions of dollars later, all efforts at disease-modifying interventions have 1 2 failed. Over that same period, evidence has accrued pointing to dementias as late-life clinical phenotypes that begin as midlife pathologies. Effective version 1 prevention therefore may need to begin in midlife, in order to succeed. No published report report current interventions are sufficiently safe to justify their use in midlife dementia 03 Apr 2017 prevention trials. Observational studies could be informative in testing the proposal that amyloid imaging and APOEε4 genotype can predict those who W.Sue T Griffin, University of Arkansas for are highly likely to develop Alzheimer’s disease and in whom higher risk 1 interventions might be justifiable.
    [Show full text]
  • A Workshop on Cognitive Aging and Impairment in the 9/11-Exposed Population
    International Journal of Environmental Research and Public Health Review A Workshop on Cognitive Aging and Impairment in the 9/11-Exposed Population Robert D. Daniels 1,* , Sean A. P. Clouston 2 , Charles B. Hall 3 , Kristi R. Anderson 1 , David A. Bennett 4, Evelyn J. Bromet 2, Geoffrey M. Calvert 1, Tania Carreón 1 , Steven T. DeKosky 5, Erica D. Diminich 2, Caleb E. Finch 6, Sam Gandy 7, William C. Kreisl 8, Minos Kritikos 2 , Travis L. Kubale 1, Michelle M. Mielke 9 , Elaine R. Peskind 10, Murray A. Raskind 11, Marcus Richards 12, Mary Sano 7, Albeliz Santiago-Colón 1 , Richard P. Sloan 13, Avron Spiro III 14 , Neil Vasdev 15 , Benjamin J. Luft 2 and Dori B. Reissman 1 1 World Trade Center Health Program, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, Washington, DC 20201, USA; [email protected] (K.R.A.); [email protected] (G.M.C.); [email protected] (T.C.); [email protected] (T.L.K.); [email protected] (A.S.-C.); [email protected] (D.B.R.) 2 Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11794, USA; [email protected] (S.A.P.C.); [email protected] (E.J.B.); [email protected] (E.D.D.); [email protected] (M.K.); [email protected] (B.J.L.) 3 Department of Epidemiology & Population Health (Biostatistics), Albert Einstein College of Medicine, Bronx, NY 10461, USA; [email protected] 4 Department of Neurological Sciences, Rush Medical College, Rush University, Chicago, IL 60612,
    [Show full text]
  • Relationship of Traumatic Brain Injury to Chronic Mental Health Problems and Dementia in Military Veterans
    Accepted Manuscript Title: Relationship of traumatic brain injury to chronic mental health problems and dementia in military veterans Authors: Gregory A. Elder, Michelle E. Ehrlich, Sam Gandy PII: S0304-3940(19)30367-2 DOI: https://doi.org/10.1016/j.neulet.2019.134294 Article Number: 134294 Reference: NSL 134294 To appear in: Neuroscience Letters Received date: 22 February 2019 Revised date: 25 April 2019 Accepted date: 24 May 2019 Please cite this article as: Elder GA, Ehrlich ME, Gandy S, Relationship of traumatic brain injury to chronic mental health problems and dementia in military veterans, Neuroscience Letters (2019), https://doi.org/10.1016/j.neulet.2019.134294 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Relationship of traumatic brain injury to chronic mental health problems and dementia in military veterans Gregory A. Eldera,b,c,d, Michelle E. Ehrlichb,d,f, and Sam Gandyb,c,d,e,g aNeurology Service, James J. Peters Department of Veterans Affairs Medical Center, 130 West Kingsbridge Road, Bronx, New York 10468, USA bDepartment of Neurology, Icahn School of Medicine at Mount Sinai, One Gustave Levy Place, New York, New York 10029, USA cDepartment of Psychiatry, Icahn School of Medicine at Mount Sinai, One Gustave Levy Place, New York, New York 10029, USA dMount Sinai Alzheimer’s Disease Research Center and the Ronald M.
    [Show full text]
  • NYSCF PR 2014-01-08 Alzheimers PLOS
    Contact: David McKeon Contact: Mount Sinai Press Office 212-365-7440 212-241-9200 [email protected] [email protected] STEM CELL RESEARCH IDENTIFIES NEW GENE TARGETS IN PATIENTS WITH EARLY-ONSET ALZHEIMER’S DISEASE Scientists provide new insight into cause of Alzheimer’s disease NEW YORK, NY (January 8, 2014) – Scientists at The New York Stem Cell Foundation (NYSCF) Research Institute in collaboration with scientists at the Icahn School of Medicine at Mount Sinai (ISMMS) successfully generated a stem cell model of familial Alzheimer’s disease (FAD). Using this stem cell model, researchers identified fourteen genes that may be implicated in the disease and one gene in particular that shows the importance that inflammation may play in the brain of Alzheimer’s patients. In this study, published today in PLOS ONE, the team of scientists produced stem cells and neural precursor cells (NPCs), representing early neural progenitor cells that build the brain, from patients with severe early-onset AD with mutations in the Presenilin 1 (PSEN1) gene. These NPCs had elevated Abeta42/Abeta40 ratios, indicating elevation of the form of amyloid found in the brains of Alzheimer’s patients. These levels were greater than those in adult cells that did not have the PSEN1mutation. This elevated ratio showed that these NPCs grown in the petri dish were accurately reflecting the cells in the brains of FAD patients. “Our ability to accurately recapitulate the disease in the petri dish is an important advance for this disease. These genes provide us with new targets to help elucidate the cause of sporadic forms of the disease as well provide targets for the discovery of new drugs,” said Susan L.
    [Show full text]
  • United States District Court Eastern District of Pennsylvania in Re: National Football League Players' Concussion Injury Litig
    Case 2:12-md-02323-AB Document 7070-1 Filed 01/11/17 Page 1 of 55 UNITED STATES DISTRICT COURT EASTERN DISTRICT OF PENNSYLVANIA IN RE: NATIONAL FOOTBALL LEAGUE PLAYERS’ CONCUSSION No. 2:12-md-02323-AB INJURY LITIGATION MDL No. 2323 Kevin Turner and Shawn Wooden, Civil Action No. 2:14-cv-00029-AB on behalf of themselves and others similarly situated, Plaintiffs, v. National Football League and NFL Properties, LLC, successor-in-interest to NFL Properties, Inc., Defendants. THIS DOCUMENT RELATES TO: ALL ACTIONS FANECA OBJECTORS’ MEMORANDUM OF LAW IN SUPPORT OF PETITION FOR AN AWARD OF ATTORNEYS’ FEES AND EXPENSES Case 2:12-md-02323-AB Document 7070-1 Filed 01/11/17 Page 2 of 55 TABLE OF CONTENTS Page I. INTRODUCTION ................................................................................................................. 1 II. BACKGROUND ................................................................................................................... 2 III. PROCEDURAL HISTORY .................................................................................................. 5 A. The Precursor Lawsuits and the Initial Settlement ....................................................... 5 B. The Faneca Objectors’ Efforts To Improve the Settlement .......................................... 8 1. The Motion To Intervene ..................................................................................... 8 2. The Opposition to Preliminary Approval ............................................................ 9 3. The Rule 23(f) Petition to
    [Show full text]
  • Effective Anti-Alzheimer Ab Therapy Involves Depletion of Specific Ab Oligomer Subtypes
    Effective anti-Alzheimer Ab therapy involves depletion of specific Ab oligomer subtypes Elysse M. Knight, PhD ABSTRACT Soong Ho Kim, PhD Background: Recent studies have implicated specific assembly subtypes of b-amyloid (Ab)pep- Jessica C. Kottwitz, BS tide, specifically soluble oligomers (soAb) as disease-relevant structures that may underlie mem- Asa Hatami, PhD ory loss in Alzheimer disease. Removing existing soluble and insoluble Ab assemblies is thought to Ricardo Albay, BS be essential for any attempt at stabilizing brain function and slowing cognitive decline in Akinobu Suzuki, PhD Alzheimer disease. IV immunoglobulin (IVIg) therapies have been shown to contain naturally Alex Lublin, PhD occurring polyclonal antibodies that recognize conformational neoepitopes of soluble or insoluble Cristina M. Alberini, PhD Ab assemblies including soAb. These naturally occurring polyclonal antibodies have been sug- William L. Klein, PhD gested to underlie the apparent clinical benefits of IVIg. However, direct evidence linking anti-Ab Paul Szabo, PhD antibodies to the clinical bioactivity of IVIg has been lacking. Norman R. Relkin, MD, Methods: Five-month-old female Dutch APP E693Q mice were treated for 3 months with neat PhD IVIg or with IVIg that had been affinity-depleted over immobilized Ab conformers in 1 of 2 assem- Michelle Ehrlich, MD bly states. Memory was assessed in a battery of tests followed by quantification of brain soAb Charles G. Glabe, PhD levels using standard anti-soAb antibodies. Sam Gandy, MD, PhD John W. Steele, PhD Results: We provide evidence that NU4-type soAb (NU4-soAb) assemblies accumulate in the brains of Dutch APP E693Q mice and are associated with defects in memory, even in the absence of insoluble Ab plaques.
    [Show full text]
  • The Friedman Brain Institute
    Advancing the Understanding New Collaboration Multiplexing of Cognitive Loss and Dementia Collaborative Drives Dementia Alison M. Goate, Immunofluorescence in at Mount Sinai’s Alzheimer’s Programs Science and DPhil, Joins the Neocortex in Severe Disease Research Center Awarded Care Delivery Mount Sinai Alzheimer’s Disease The Friedman SPRING 2015 Brain Institute www.mountsinai.org/fbi Compassionate Care, Pioneering Research Alzheimer’s disease and related dementias are among the top 10 causes of recently established Ronald M. Loeb Center for death and debility in the United States, and the number of deaths attributed Alzheimer’s Disease joins Mount Sinai’s long- standing National Institute on Aging-funded to Alzheimer’s disease is expected to triple by 2050, when it is estimated Alzheimer’s Disease Research Center and our that more than 135 million people worldwide will be afflicted. Center for Cognitive Health in driving efforts to better understand dementing illnesses, Without dramatic improvements in our Institutes of Health provides manyfold fewer developing better ways at diagnosing and ability to treat or prevent these illnesses, dollars for dementia. treating them, and working toward ultimate dementia will likely overwhelm health care cures and preventive measures. budgets worldwide. Still, research into the Mount Sinai is leading efforts to study causes and treatment of these dementias Alzheimer’s disease and other dementias, as Eric J. Nestler, MD, PhD does not receive support commensurate with well as chronic traumatic encephalopathies, Nash Family Professor and Chair, Department of Neuroscience; their devastating impact. For example, when which are caused by repeated traumas—even Director, The Friedman Brain Institute compared to the health and economic costs concussions—resulting in similar syndromes [email protected] of cancer and heart disease, the National with shared pathological mechanisms.
    [Show full text]
  • Amyloid Plaques Are Surprisingly Dynamic Predicting Recovery
    From the publishers of The New England Journal of Medicine July 2008 Vol. 10 No. 7 Amyloid Plaques Are reinforce the notion that amyloid plaques the 40-odor University of Pennsylvania are dynamic, again suggesting that Smell Identification Test (UPSIT) and Surprisingly Dynamic they do not result from an unstoppable an average of 2.9 years later (range, 3 he amyloid hypothesis of Alzheimer march of amyloid accretion but, rather, months to 24 years) with the 40-odor T disease predicts that amyloid plaques from a process wherein plaques may UPSIT or a 12-odor version. (One of the are a precursor of neuronal damage. come and (with manipulation) go. Un- study authors is a shareholder in the However, researchers recently proposed doubtedly, the kinetics are different in company that manufactures the smell that neuronal damage may precede humans, but again, overturning conven- test used.) plaque formation. In this study, the tional wisdom enables the contemplation From baseline to follow-up, 11.3% of authors used a novel imaging technique of therapeutic opportunities that might anosmic and 23.3% of hyposmic patients to provide insights into the chronology heretofore have been discarded out regained their age-adjusted sense of of amyloid deposition in the brains of of hand. smell (although significant improvement transgenic mice bred to overexpress — Sam Gandy, MD, PhD occurred in 56.7% and 42.7%, respec- human amyloid precursor protein. Meyer-Luehmann M et al. Rapid appear- tively). Age, initial severity of smell loss, The authors monitored brain paren- ance and local toxicity of amyloid-β and time from onset to baseline signifi- chyma of these transgenic mice weekly plaques in a mouse model of Alzheimer’s cantly predicted the degree of recovery; disease.
    [Show full text]