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1 of antibodies to PHF/tau, neurofilament, and beta-amyloid protein.
5 lation of both brain plaques [(consisting of beta-amyloid protein (AB) 1-42)] and neurofibrillary tan
6 urs in association with elevation of soluble beta amyloid protein (Abeta), but before the appearance
8 the aggregation and deposition of misfolded beta-amyloid protein (Abeta) contribute to this progress
11 ease (AD) is an abnormal accumulation of the beta-amyloid protein (Abeta) in specific brain regions.
14 ow that the Alzheimer's disease-linked human beta-amyloid protein (Abeta) synergistically enhances th
15 ether preoperative cerebrospinal fluid (CSF) beta-amyloid protein (Abeta) to tau ratio, an Alzheimer
16 finding that intracellular expression of the beta-amyloid protein (Abeta) under a neuron-specific pro
17 llular amyloid plaques formed by accumulated beta-amyloid protein (Abeta), a metabolic product of amy
18 characterized by extracellular deposition of beta-amyloid protein (Abeta), intracellular neurofibrill
22 ces were examined by immunocytochemistry for beta-amyloid protein and abnormally phosphorylated tau p
24 Alzheimer-characteristic proteins" including beta-amyloid protein and beta-amyloid precursor protein,
25 siderable evidence exists demonstrating that beta-amyloid protein and its fragments 1-40 and 25-35 (b
26 l histological features are accumulations of beta-amyloid protein and the absence of inflammatory cel
31 's disease (AD), affected neurons accumulate beta amyloid protein, components of which can induce mou
32 disease both demonstrate the accumulation of beta-amyloid protein containing "plaques" and tau protei
34 precursor protein (beta APP), including its beta-amyloid protein epitope, and increased beta APP-751
36 a new strategy for detection and imaging of beta-amyloid protein in immunohistochemical sections fro
40 reported that a variety of mutations in the beta-amyloid protein precursor gene and the Presenilin-1
41 bs genetically interacts with the Drosophila beta-amyloid protein precursor-like (Appl) protein, the
44 ally, S100 protein, neuron-specific enolase, beta-amyloid protein, tau protein and phospho-tau were d
45 optosis, which then leads to accumulation of beta-amyloid protein, the hallmark feature of Alzheimer
46 nd that nitric oxide produced in response to beta-amyloid protein, thought to be a key mediator of Al