Zobrazeno 1 - 10
of 29
pro vyhledávání: '"Edward T. Spooner"'
Autor:
Cynthia A Lemere, Edward T Spooner, John LaFrancois, Brian Malester, Chica Mori, Jodi F Leverone, Yasuji Matsuoka, Jennie W Taylor, Ronald B DeMattos, David M Holtzman, John D Clements, Dennis J Selkoe, Karen E Duff
Publikováno v:
Neurobiology of Disease, Vol 14, Iss 1, Pp 10-18 (2003)
Immunization with amyloid-β (Aβ) peptide in mouse models of Alzheimer’s disease has been reported to decrease cerebral Aβ levels and improve behavioral deficits. Several mechanisms have been proposed, including antibody-induced phagocytosis of A
Externí odkaz:
https://doaj.org/article/4f47f1c3bb8b443086efd9bb58489f0a
Autor:
Chica Mori, Dennis J. Selkoe, Howard L. Weiner, R. Desai, Edward T. Spooner, Trelawney J. Grenfell, Ruth Maron, Cynthia A. Lemere, Wayne W. Hancock
Publikováno v:
Annals of the New York Academy of Sciences. 920:328-331
Autor:
Vicki Betts, Dennis J. Selkoe, Michael J. Rowan, Dominic M. Walsh, Igor Klyubin, William K. Cullen, Cynthia A. Lemere, Liying Jiang, Ganesh M. Shankar, Roger Anwyl, Edward T. Spooner
Publikováno v:
Nature Medicine. 11:556-561
One of the most clinically advanced forms of experimental disease-modifying treatment for Alzheimer disease is immunization against the amyloid β protein (Aβ)1,2,3,4,5,6,7, but how this may prevent cognitive impairment is unclear8,9,10,11,12,13. We
Autor:
Jeanne K. Bloom, Timothy J. Seabrook, Melitza Iglesias, Cynthia A. Lemere, Edward T. Spooner, Dominic M. Walsh
Publikováno v:
Neurobiology of Aging. 25:1141-1151
Amyloid beta (A beta) immunization of amyloid precursor protein (APP)-transgenic (tg) mice with human A beta induces humoral immunity, however, the immune response to endogenous rodent A beta is unknown. Fourteen-month J20 APP-tg mice and non-tg litt
Publikováno v:
Vaccine. 22:4075-4083
The cerebral accumulation of beta-amyloid (Abeta) is a pathological hallmark of Alzheimer's disease (AD). Abeta vaccination or anti-Abeta specific antibodies may be a possible therapeutic option for AD. Previously, we demonstrated variation in the hu
Autor:
John LaFrancois, Yasuji Matsuoka, Jodi F. Leverone, Karen Duff, Chica Mori, John D. Clements, Brian Malester, Cynthia A. Lemere, Edward T. Spooner, David M. Holtzman, Dennis J. Selkoe, Jennie W. Taylor, Ronald Demattos
Publikováno v:
Neurobiology of Disease, Vol 14, Iss 1, Pp 10-18 (2003)
Immunization with amyloid-beta (Abeta) peptide in mouse models of Alzheimer's disease has been reported to decrease cerebral Abeta levels and improve behavioral deficits. Several mechanisms have been proposed, including antibody-induced phagocytosis
Publikováno v:
Vaccine. 21:2197-2206
Immunizing mouse models of Alzheimer's disease (AD) against beta-amyloid (Abeta) leads to a decrease in cerebral Abeta burden as well as an improvement in behavioral deficits. Circulating Abeta-antibodies may be responsible for interfering with Abeta
Autor:
Edward T. Spooner, Timothy J. Seabrook, Jeanne K. Bloom, Jodi F. Leverone, Chica Mori, Melitza Iglesias, Cynthia A. Lemere
Publikováno v:
Neurochemical Research. 28:1017-1027
Alzheimer's disease is the most prevalent form of dementia worldwide. Therapies are desperately needed to prevent and cure the disease. Mouse models of amyloid-β deposition [APP and PSAPP transgenic (tg) mice] have been useful in determining the rol
Autor:
Chica Mori, Krystyna E. Wisniewski, Dean R. Tolan, Dennis J. Selkoe, Thomas Wisniewski, Takaomi C. Saido, Cynthia A. Lemere, Haruyasu Yamaguchi, Edward T. Spooner
Publikováno v:
Amyloid. 9:88-102
Alzheimer's disease (AD) brains display A beta (Aβ) plaques, inflammatory changes and neurofibrillary tangles (NFTs). Converging evidence suggests a neuronal origin of Aβ. We performed a temporal s...
Autor:
Dennis J. Selkoe, Shohreh Issazadeh, Chica Mori, Howard L. Weiner, Wayne W. Hancock, Edward T. Spooner, Trelawney J. Grenfell, Ruth Maron, Cynthia A. Lemere
Publikováno v:
Annals of Neurology. 48:567-579
Progressive cerebral deposition of amyloid-beta (Abeta) peptide, an early and essential feature of Alzheimer's disease (AD), is accompanied by an inflammatory reaction marked by microgliosis, astrocytosis, and the release of proinflammatory cytokines