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1 yloid precursor protein (APP) gene can cause familial Alzheimer disease.
2 2 (PS1 and PS2) are the most common cause of familial Alzheimer disease.
3 ause the most aggressive form of early-onset familial Alzheimer disease.
4 that shows evidence of linkage to late-onset familial Alzheimer disease.
5 ciated with approximately 50% of early-onset familial Alzheimer disease.
6 n the gene STM2 result in autosomal dominant familial Alzheimer disease.
7 myloid precursor protein (APP) identified in familial Alzheimer disease.
8 enilin 2 (PS2) proteins are a major cause of familial Alzheimer disease.
9 that may delay or accelerate age at onset of familial Alzheimer disease (AD) by examining age at onse
10                             Most early-onset familial Alzheimer disease (AD) cases are caused by muta
11                Linkage to chromosome 12p for familial Alzheimer disease (AD) has been inconsistent.
12 red PS1 gene are responsible for early-onset familial Alzheimer disease (AD), and PS1 is abnormally a
13 e brains of patients with autosomal dominant familial Alzheimer disease (AD).
14 e have been described as causing early onset familial Alzheimer disease (AD).
15                           Further studies of familial Alzheimer diseases and diabetes show that the a
16  homodimerization, or of the presence of the familial Alzheimer disease Arctic mutation (APP E693G).
17 S1 in two affected siblings with early-onset familial Alzheimer disease characterized by deposition o
18 erved in individuals affected by early-onset familial Alzheimer disease (FAD) associated with mutatio
19 ble for approximately 40% of all early-onset familial Alzheimer disease (FAD) cases in which a geneti
20 eta and in particular Abeta42 is enhanced by familial Alzheimer disease (FAD) causing mutations in AP
21                                              Familial Alzheimer disease (FAD) is linked to mutations
22                                              Familial Alzheimer disease (FAD) mutations suppress the
23                               hiN cells from familial Alzheimer disease (FAD) patients with presenili
24          Furthermore, in contrast to WT PS1, familial Alzheimer disease (FAD) PS1 mutants expressed i
25  lead to dominant inheritance of early onset familial Alzheimer disease (FAD).
26 in 1 gene on chromosome 14 cause early onset familial Alzheimer disease (FAD).
27 cretase, and mutations in this protein cause familial Alzheimer Disease (FAD).
28 (PS1) and -2 (PS2), which when mutated cause familial Alzheimer disease, have been localized to numer
29 sing an inherited form of Alzheimer disease (familial Alzheimer disease) in the PS1 motif suggested t
30  1, a protein involved in the development of familial Alzheimer disease, is an important functional c
31                             In addition, six familial Alzheimer disease-linked mutant human presenili
32                                   Late-onset familial Alzheimer disease (LOFAD) is a genetically hete
33                              Remarkably, PS1 familial Alzheimer disease mutant DeltaE9 increased neit
34 e to Abetao as well as chronic expression of familial Alzheimer disease mutant transgenes in model mi
35 s nor cell aggregation, suggesting that this familial Alzheimer disease mutation interferes with cadh
36                                  Early onset familial Alzheimer disease mutations in presenilin (PS),
37 d that PS1 positively regulates, whereas PS1 familial Alzheimer disease mutations suppress, phosphati
38   This cleavage is inhibited by presenilin 1 familial Alzheimer disease mutations.
39 ic function associated with the presenilin-1 familial Alzheimer disease mutations.
40 mic reticulum Ca(2+) leak function, and many familial Alzheimer disease presenilin mutations impair t
41 senilin-1 (PS1), the major causative gene of familial Alzheimer disease, regulates neuronal different
42 hologic changes in the retina of carriers of familial Alzheimer disease who are cognitively unimpaire