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1 of antibodies to PHF/tau, neurofilament, and beta-amyloid protein.
2                                              Beta amyloid protein (A beta) is the major extracellular
3                                              beta-amyloid protein (A beta) formation was reconstitute
4                                              Beta-amyloid protein (A beta) fragments have been shown
5 urs in association with elevation of soluble beta amyloid protein (Abeta), but before the appearance
6 ve agents that significantly reduced AD-type beta-amyloid protein (Abeta) accumulation.
7  the aggregation and deposition of misfolded beta-amyloid protein (Abeta) contribute to this progress
8 nuated in Tg mice at an age known to exhibit beta-amyloid protein (Abeta) deposition.
9                                              beta-Amyloid protein (Abeta) has been implicated as a ke
10 ease (AD) is an abnormal accumulation of the beta-amyloid protein (Abeta) in specific brain regions.
11                          The accumulation of beta-amyloid protein (Abeta) in the brain is thought to
12                              Accumulation of beta-amyloid protein (Abeta) in the extracellular space
13 ow that the Alzheimer's disease-linked human beta-amyloid protein (Abeta) synergistically enhances th
14 ether preoperative cerebrospinal fluid (CSF) beta-amyloid protein (Abeta) to tau ratio, an Alzheimer
15 finding that intracellular expression of the beta-amyloid protein (Abeta) under a neuron-specific pro
16 llular amyloid plaques formed by accumulated beta-amyloid protein (Abeta), a metabolic product of amy
17 characterized by extracellular deposition of beta-amyloid protein (Abeta), intracellular neurofibrill
18 its transmembrane domain to produce secreted beta-amyloid protein (Abeta).
19 e step in the formation of the C terminus of beta-amyloid protein (Abeta).
20 ces were examined by immunocytochemistry for beta-amyloid protein and abnormally phosphorylated tau p
21                         However, the role of beta-amyloid protein and abnormally phosphorylated tau p
22 Alzheimer-characteristic proteins" including beta-amyloid protein and beta-amyloid precursor protein,
23 siderable evidence exists demonstrating that beta-amyloid protein and its fragments 1-40 and 25-35 (b
24 l histological features are accumulations of beta-amyloid protein and the absence of inflammatory cel
25                                              beta-amyloid protein appears to be involved in the neura
26                  Increased levels of APP and beta-amyloid protein are also detected within dying moto
27                                          The beta-amyloid protein associated with Alzheimer's disease
28                                              beta-Amyloid protein (betaAP) deposition is a neuropatho
29 's disease (AD), affected neurons accumulate beta amyloid protein, components of which can induce mou
30 n, as well as with the extent of neocortical beta-amyloid protein deposition.
31  precursor protein (beta APP), including its beta-amyloid protein epitope, and increased beta APP-751
32       In Alzheimer's disease (AD), fibrillar beta-amyloid protein (fAbeta) accumulates in the walls o
33  a new strategy for detection and imaging of beta-amyloid protein in immunohistochemical sections fro
34                              The neocortical beta-amyloid protein load and the number of neurofibrill
35 eria and with an increase in the neocortical beta-amyloid protein load.
36  compatible with a sequence segment from the beta-amyloid protein of Alzheimer's disease.
37  reported that a variety of mutations in the beta-amyloid protein precursor gene and the Presenilin-1
38 bs genetically interacts with the Drosophila beta-amyloid protein precursor-like (Appl) protein, the
39                                              beta-Amyloid protein precursors (APPs, 695-770 amino aci
40 low molecular weight oligomeric cross-linked beta-amyloid protein species (CAPS).
41 optosis, which then leads to accumulation of beta-amyloid protein, the hallmark feature of Alzheimer
42 nd that nitric oxide produced in response to beta-amyloid protein, thought to be a key mediator of Al

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