TY - JOUR
T1 - Emerging Alzheimer's disease therapies
T2 - Focusing on the future
AU - Trojanowski, John Q.
AU - Lieberburg, Ivan
AU - Lemere, Cynthia
AU - Gandy, Sam
AU - Bush, Ashley
AU - Frangione, Blas
AU - Citron, Martin
AU - Li, Yue Ming
AU - Lee, Virginia M.Y.
AU - Sisodia, Sangram
AU - Clark, Christopher
AU - Karlawish, Jason
PY - 2002/11
Y1 - 2002/11
N2 - The Center for Neurodegenerative Disease Research (CNDR) organized a 1 day symposium entitled "Emerging Alzheimer's disease Therapies: Focusing On The Future" on November 7th, 2001 at the University of Pennsylvania in Philadelphia, PA. The agenda (Fig. 1 Emerging Alzheimer's disease therapies: focusing on the future.) focused on novel therapies for Alzheimer's disease (AD) designed to prevent/eliminate Aβ deposits in the brains of AD patients. While fibrillar Aβ deposits known as senile plaques (SPs) and intraneuronal tau fibrils known as neurofibrillary tangles (NFTs) are diagnostic of AD, >50% of patients with familial or sporadic AD as well as elderly Down's syndrome patients with AD harbor a third type of brain amyloid known as Lewy bodies formed by intraneuronal alpha-synuclein fibrils [1,6]. Thus, AD is a "triple brain amyloidosis" since three different proteins (tau, alpha-synuclein) or peptide fragments (Aβ) of a larger Aβ precursor protein (APP) fibrillize and aggregate into pathological deposits of amyloid within (NFTs, LBs) and outside (SPs) neurons in AD brains. The symposium is summarized here followed by reviews from symposium speakers who describe potential anti-Aβ therapies some of which are in clinical trials [2,3].
AB - The Center for Neurodegenerative Disease Research (CNDR) organized a 1 day symposium entitled "Emerging Alzheimer's disease Therapies: Focusing On The Future" on November 7th, 2001 at the University of Pennsylvania in Philadelphia, PA. The agenda (Fig. 1 Emerging Alzheimer's disease therapies: focusing on the future.) focused on novel therapies for Alzheimer's disease (AD) designed to prevent/eliminate Aβ deposits in the brains of AD patients. While fibrillar Aβ deposits known as senile plaques (SPs) and intraneuronal tau fibrils known as neurofibrillary tangles (NFTs) are diagnostic of AD, >50% of patients with familial or sporadic AD as well as elderly Down's syndrome patients with AD harbor a third type of brain amyloid known as Lewy bodies formed by intraneuronal alpha-synuclein fibrils [1,6]. Thus, AD is a "triple brain amyloidosis" since three different proteins (tau, alpha-synuclein) or peptide fragments (Aβ) of a larger Aβ precursor protein (APP) fibrillize and aggregate into pathological deposits of amyloid within (NFTs, LBs) and outside (SPs) neurons in AD brains. The symposium is summarized here followed by reviews from symposium speakers who describe potential anti-Aβ therapies some of which are in clinical trials [2,3].
KW - Aβ
KW - Brain amyloidosis
KW - Drug discovery
KW - Neurodegenerative diseases
UR - http://www.scopus.com/inward/record.url?scp=0036827419&partnerID=8YFLogxK
U2 - 10.1016/S0197-4580(02)00123-9
DO - 10.1016/S0197-4580(02)00123-9
M3 - Article
C2 - 12470793
AN - SCOPUS:0036827419
SN - 0197-4580
VL - 23
SP - 985
EP - 990
JO - Neurobiology of Aging
JF - Neurobiology of Aging
IS - 6
ER -