|
|
|
|
|
| First Name: | Cynthia | | Last Name: | Lemere | | Title: | Associate Professor | | Advanced Degrees: | M.S., Ph.D. | | Affiliation: | Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School | | Department: | Neurology | | Street Address 1: | NRB 636F | | Street Address 2: | 77 Avenue Louis Pasteur | | City: | Boston | | State/Province: | MA | | Zip/Postal Code: | 02115 | Country/Territory: | U.S.A. | | Phone: | 617-525-5214 | | Fax: | 617-525-5252 | | Email Address: |  |
Disclosure:
(view policy)
|
Member reports the following financial or other potential conflicts of interest: [Last Modified: 19 May 2005]
ELAN-Wyeth-sponsored Aß vaccine study in primates from January 2005- January 2007.
|
|
|
View all comments by Cynthia Lemere
|
Aging Process, Neurodevelopmental Disorders (Down syndrome, etc.), Alzheimer Disease, Parkinson Disease
|
A-beta PP/A-beta, Neuropathology, Animal Models, Neuroimmunology
|
Medical hospital, medical school
|
Cynthia A. Lemere, Ph.D. Associate Professor of Neurology at Harvard Medical School and an Associate Neuroscientist at Brigham & Women’s Hospital in the Center for Neurologic Diseases (CND). She has been an active participant in the research field of Alzheimer's disease (AD) for more than sixteen years. Dr. Lemere received her B.A. from Mount Holyoke College, her M.S. in Neurobiology from State University of New York at Albany, and her Ph.D. in Pathology from Boston University School of Medicine. Her thesis research, conducted in the laboratory of Dr. Dennis Selkoe at the CND, focused on mechanisms of ß-amyloid generation and deposition in Alzheimer’s disease and models thereof, particularly in Down syndrome. During her years as Postdoctoral Fellow and Instructor at the CND, her research focused on the role of inflammation in Alzheimer’s disease. In particular, these studies involved examining brain tissue from APP transgenic mice, a transgenic or genetically-engineered mouse model of AD, and Down syndrome to examine the temporal accrual of amyloid-associated inflammatory proteins, such as complement protein, in relation to Aß deposition, gliosis and neuritic changes. In addition, she collaborated with scientists in Medellin, Colombia, to confirm in vivo that which was already known in vitro, that mutations in the presenilin 1 gene lead to overproduction of Aß42.
In 1997, she founded an independent laboratory at the CND and continued her research on the role of inflammation in AD by examining strategies for reducing amyloid ß-protein (Aß) protein, cerebral deposits of which are a key feature of AD, and its resultant inflammation in the AD brain. Her results showed that chronic nasal immunization with Aß peptide in APP transgenic mice led to anti-Aß antibody production and a lowering of the Aß burden in the brain. Dr. Lemere and her colleagues have optimized various treatment protocols in non-transgenic mice and then employed them to lower cerebral Aß levels in APP transgenic mice. In addition to pursuing the mechanism of these effects, much of her laboratory's work focuses on the humoral and cellular immune responses to Aß immunization in APP tg mice and in non-human primates. Recently, her lab completed a 10 month Aß immunization trial in Caribbean vervet monkeys and found a lowering of Aß protein in both CSF and brain.
Other projects in her laboratory have involved examining the temporal appearance of both intraneuronal Aß and P25 (the regulatory subunit for cdk5) in Down syndrome brain, characterization of a-synuclein following traumatic brain injury and characterization of sonic hedgehog in aged human control and AD brain.
|
|
|
|
|
|
|
Home
