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1 ergic hypofunction in patients with advanced Alzheimer's disease.
2 y amyloid-beta proteotoxic diseases, such as Alzheimer's disease.
3 n-specific manner to cognitive impairment in Alzheimer's disease.
4 esent a new therapeutic avenue for combating Alzheimer's disease.
5 led states is central to the pathogenesis of Alzheimer's disease.
6 xic effect of Abeta(1-40) and Abeta(1-42) in Alzheimer's disease.
7 degenerative neurological illnesses, such as Alzheimer's disease.
8 s the risk for the development of late-onset Alzheimer's disease.
9 cated in reducing the severity of stroke and Alzheimer's disease.
10 ing TLR4-TLR6 dimerization as a treatment of Alzheimer's disease.
11 as autism spectrum disorder, depression and Alzheimer's disease.
12 Ser367 should be useful in the treatment of Alzheimer's disease.
13 a with Lewy bodies, Parkinson's disease, and Alzheimer's disease.
14 d individuals at early symptomatic stages of Alzheimer's disease.
15 ntribute to the loss of synaptic function in Alzheimer's disease.
16 umerous neuropsychiatric disorders including Alzheimer's disease.
17 t target for developing therapeutics against Alzheimer's disease.
18 sion is associated with an increased risk of Alzheimer's disease.
19 plays a central role in the pathogenesis of Alzheimer's disease.
20 id and fcMRI in individuals with preclinical Alzheimer's disease.
21 e contributes directly to the development of Alzheimer's disease.
22 regates in the brain tissue of patients with Alzheimer's disease.
23 ein 43 (TDP-43) is another protein linked to Alzheimer's disease.
24 higher in dementia with Lewy bodies than in Alzheimer's disease.
25 r of neural circuit defects in patients with Alzheimer's disease.
26 oup of community-dwelling veterans with mild Alzheimer's disease.
27 community-dwelling veterans (N=60) with mild Alzheimer's disease.
28 isk of side effects including angioedema and Alzheimer's disease.
29 BChE as a promising drug target in advanced Alzheimer's disease.
30 ggests a new link between RBFOX proteins and Alzheimer's disease.
31 treat psychosis, agitation and aggression in Alzheimer's disease.
32 portant contributors to neurodegeneration in Alzheimer's disease.
33 w in brain regions susceptible to ageing and Alzheimer's disease.
34 loid fibrils is a defining characteristic of Alzheimer's disease.
35 ting with the aggregation of beta-amyloid in Alzheimer's disease.
36 hat are able to slow down the progression of Alzheimer's disease.
37 logical disorders, such as schizophrenia and Alzheimer's disease.
38 ousal and in pathological conditions such as Alzheimer's disease.
39 is, amyotrophic lateral sclerosis (ALS), and Alzheimer's disease.
40 ant for managing diseases such as cancer and Alzheimer's disease.
41 in other neurodegenerative disorders such as Alzheimer's disease.
42 cluding multiple sclerosis (MS), stroke, and Alzheimer's disease.
43 nd aging and in models of brain ischemia and Alzheimer's disease.
44 on is an important modifiable risk factor in Alzheimer's disease.
45 well-known amyloid-beta peptide involved in Alzheimer's disease.
46 tiple neurodegenerative disorders, including Alzheimer's disease.
47 upancy for optimal treatment of psychosis in Alzheimer's disease.
48 eper understanding of the molecular basis of Alzheimer's disease.
49 autism spectrum disorder, schizophrenia, and Alzheimer's disease.
50 re common disorders, such as Parkinson's and Alzheimer's diseases.
51 suggesting a link between mRNA stability and Alzheimer's disease."
53 upranuclear palsy, relative to patients with Alzheimer's disease, 18F-AV-1451 binding was elevated in
54 d be categorised as stage 2 or 3 preclinical Alzheimer's disease (A+T+N-, A+T-N+, and A+T+N+; 86% at
56 STATEMENT Understanding how risk factors for Alzheimer's disease (AD) affect brain function and cogni
60 nosis of neurodegenerative disorders such as Alzheimer's disease (AD) and related Dementias has been
62 l destruction methods.SIGNIFICANCE STATEMENT Alzheimer's disease (AD) and similar dementias are commo
63 ingulate cortex (PCC) predicts conversion to Alzheimer's disease (AD) and tracks disease progression,
67 splant (KT) may develop post-KT dementia and Alzheimer's disease (AD) associated with their long-stan
68 laques, a potential biomarker present in the Alzheimer's disease (AD) brain is crucial for both clini
69 a-amyloid (Abeta) plaques are key lesions in Alzheimer's disease (AD) but both pathologies also occur
70 pse degeneration and cognitive impairment in Alzheimer's disease (AD) by reactivating expression of t
71 A genome-wide survival analysis of 14,406 Alzheimer's disease (AD) cases and 25,849 controls ident
74 lot study on differentiating early stages of Alzheimer's disease (AD) from Dementia with Lewy Bodies
88 ein E-epsilon4 carriers, is a major risk for Alzheimer's disease (AD) is increasing steadily, with ov
91 current frontline symptomatic treatment for Alzheimer's disease (AD) is whole-body upregulation of c
92 y-Camacho et al. (2017) generate a humanized Alzheimer's disease (AD) model that reveals species-spec
93 FASS-LTP analysis in two well-characterized Alzheimer's disease (AD) mouse models (3xTg and Tg2576)
94 oinflammation is an important contributor to Alzheimer's disease (AD) pathogenesis, as underscored by
100 protein (oAbeta) isolated from the brains of Alzheimer's disease (AD) patients have been shown experi
103 al, and symptomatic heterogeneity underlying Alzheimer's disease (AD) requires a deep understanding o
106 myloid-beta pathology early in the course of Alzheimer's disease (AD) with high sensitivity and speci
107 with frontotemporal dementia (FTD-ALS), and Alzheimer's disease (AD), and found profound apical dend
108 s upregulated in the brains of patients with Alzheimer's disease (AD), and its expression levels infl
109 ques are a key histopathological hallmark of Alzheimer's disease (AD), and soluble Abeta species are
110 s the most important genetic risk factor for Alzheimer's disease (AD), ApoE3 is neutral, and ApoE2 is
111 gate the effect of a genetic risk factor for Alzheimer's disease (AD), ApolipoproteinE epsilon4 (APOE
113 at the intermediate and late Braak stages of Alzheimer's disease (AD), as well as in other neurodegen
114 eta) plays a key role in the pathogenesis of Alzheimer's disease (AD), but little is known about the
115 ne loss is recognized as an early feature of Alzheimer's disease (AD), but the underlying mechanisms
116 gomers is one of the earliest impairments in Alzheimer's Disease (AD), driving initial cognitive defi
117 of tau proteins, termed tauopathies, include Alzheimer's disease (AD), frontotemporal lobar degenerat
119 While SMD might be the earliest sign of Alzheimer's disease (AD), it also occurs in aging and va
120 been the central dogma in drug discovery for Alzheimer's disease (AD), leading to many small-molecule
121 rophy in seven neurodegenerative conditions (Alzheimer's disease (AD), Parkinson's disease (PD) and H
122 ques is one of the pathological hallmarks of Alzheimer's disease (AD), soluble oligomeric Abeta has b
124 Age is, by far, the greatest risk factor for Alzheimer's disease (AD), yet few AD drug candidates hav
163 ociated with type 2 diabetes (T2D), with the Alzheimer's disease amyloid-beta (Abeta) peptide modulat
164 unity on neurodegenerative disorders such as Alzheimer's disease, amyotrophic lateral sclerosis, Park
165 onstitute the histopathological hallmarks of Alzheimer's disease and are prominent targets for novel
166 ed the relationship between genetic risk for Alzheimer's disease and cortical thickness, such that in
167 e more clearly detected by PBB3 in brains of Alzheimer's disease and diffuse neurofibrillary tangles
168 ementia with Lewy bodies, five patients with Alzheimer's disease and five healthy control subjects to
169 to investigate pathological states including Alzheimer's disease and HIV-associated neurocognitive di
170 participants, but not those of patients with Alzheimer's disease and MCI, possess effective phagocyto
171 The innate immune system of patients with Alzheimer's disease and mild cognitive impairment (MCI)
173 unction ranging from severe loss, as seen in Alzheimer's disease and Parkinson's disease, to relative
176 eases associated with hippocampal pathology (Alzheimer's disease and schizophrenia) are more enriched
178 Alzheimer's Disease trial, 180 patients with Alzheimer's disease and symptoms of agitation or psychos
181 (Abeta) plays a crucial synaptotoxic role in Alzheimer's disease, and hyperphosphorylated tau facilit
182 ain regions previously associated with early Alzheimer's disease, and their relationship with episodi
183 he second most common form of dementia after Alzheimer's disease, and there is increasing awareness t
185 e decline (greater impairment on the 11-item Alzheimer's Disease Assessment Scale cognitive subscale
187 ipants who received IVIG performed better on Alzheimer's Disease Assessment Scale-cognitive subscale
189 N = 14), controls (N = 14) and "asymptomatic Alzheimer's disease" (ASYMAD), i.e., individuals with si
190 oid precursor protein (APP), a key player in Alzheimer's disease, belongs to the family of synaptic a
192 relevance not only to the pathophysiology of Alzheimer's disease but also diet-associated obesity.
193 ds have a greater role for AMD compared with Alzheimer's disease, but a lesser role than for CAD.
195 polyneuropathy, and Abeta42 associated with Alzheimer's disease by stabilizing their respective prot
199 ocortical, limbic and subcortical areas from Alzheimer's disease cases (n = 19), neurologically norma
200 d the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) battery (Word List Learning,
201 dividuals with mild cognitive impairment and Alzheimer's disease clinical diagnoses can display signi
203 We applied this tool to the analysis of Alzheimer's disease data from three datasets CHS, FHS an
205 s, with known revised diagnosis in over 25% (Alzheimer's disease, dementia with Lewy bodies, and prog
207 re achieved at very low amisulpride doses in Alzheimer's disease due to higher than anticipated occup
208 o be actively involved in the development of Alzheimer's disease due to its ability to seed the aggre
209 k1A might be an ideal therapeutic target for Alzheimer's disease, especially for Down syndrome and EG
212 8F-AV-1451) associated with well-established Alzheimer's disease factors in a cohort including cognit
213 mation of amyloid beta fibrils implicated in Alzheimer's disease, gamma-secretase is an important tar
214 duals (5,728 AD, 5,653 CN controls) from the Alzheimer's Disease Genetics Consortium (ADGC), a Nation
215 and 9,386 older controls from Phase 1 of the Alzheimer's Disease Genetics Consortium (ADGC), providin
217 ed using summary statistics from the largest Alzheimer's disease genome-wide association study to dat
218 or protein, BACE1 is a therapeutic target in Alzheimer's disease, however, consistent with its role i
219 is a dominant feature in the pathogenesis of Alzheimer's disease; however, it is not clear how indivi
220 and PTEN dysregulation and suggest that, in Alzheimer's disease, impairment of brain insulin signali
221 ntified rare coding variants associated with Alzheimer's disease in a three-stage case-control study
222 tor for frontotemporal dementia spectrum and Alzheimer's disease in an initial case-control study.
223 on of induced neuron-based model of sporadic Alzheimer's disease in mice and humans, and used this sy
224 ith an increased risk of dementia, including Alzheimer's disease, in patients with prostate cancer.
225 l features of neurodegeneration occurring in Alzheimer's disease including age-dependent cortical atr
227 tion of AbetaOs in AD.SIGNIFICANCE STATEMENT Alzheimer's disease is characterized by progressive cogn
230 One of the main research topics related to Alzheimer's disease is the aggregation of the amyloid-be
231 n are associated with the pathophysiology of Alzheimer's disease, it is clear that amyloid precursor
234 on as seen in neurological disorders such as Alzheimer's disease may contribute to neurovascular dysf
236 th mitochondrial dysfunction in the brain of Alzheimer's disease mouse model CRND8 as early as 3 mont
238 g follow-up; (ii) individuals with classical Alzheimer's disease neuroanatomical, cognitive, cerebros
239 individuals with a low likelihood of having Alzheimer's disease (neurofibrillary tangle stage B1; n=
240 aximum follow-up, 10.3 years) as part of the Alzheimer's Disease Neuroimaging Initiative (ADNI).
243 ease neuropathology, 56 (26%) with low-level Alzheimer's disease neuropathology, 45 (21%) with interm
244 thy, we identified 49 (23%) patients with no Alzheimer's disease neuropathology, 56 (26%) with low-le
245 opathology, 45 (21%) with intermediate-level Alzheimer's disease neuropathology, and 63 (30%) with hi
248 alogs for the management of type 2 diabetes, Alzheimer's disease, or other diseases related to IAPP d
249 hology in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington
250 such as anxiety, depression, schizophrenia, Alzheimer's disease, Parkinson's disease, and pain, prov
251 y of developing age-related diseases such as Alzheimer's disease, Parkinson's disease, multiple scler
252 al in groups with varying levels of comorbid Alzheimer's disease pathology according to US National I
253 's component features.SIGNIFICANCE STATEMENT Alzheimer's disease pathology appears earliest in brain
254 ociated with dementia that is independent of Alzheimer's disease pathology or larger infarcts (ie, la
258 ure in vivo may correlate with variations in Alzheimer's disease phenotype, in analogy to distinct pr
260 litating protein deposition diseases such as Alzheimer's disease, prion diseases, and type II diabete
262 various neurodegenerative diseases including Alzheimer's disease, progressive supranuclear palsy and
263 ought to result in neurodegeneration causing Alzheimer's disease, progressive supranuclear palsy, chr
264 Cog]) and self-reported QoL (Quality of Life Alzheimer's Disease [QoL-AD]) for the person with dement
266 d BACE1 is accumulated in the distal axon of Alzheimer's disease-related mutant human APP transgenic
268 pt of cognitive aging to include evidence of Alzheimer's disease-related protein aggregation as an un
270 genic mechanisms resulting from the sporadic Alzheimer's disease risk factor apolipoprotein E (APOE)
271 ction between APOE varepsilon3/4 and another Alzheimer's disease risk factor, desmoglein 2 (DSG2).
272 stributions of autoradiographic labelling of Alzheimer's disease slices with 11C-PBB3 and 18F-AV-1451
275 icroglial activation was increased by 36% in Alzheimer's disease subjects compared with controls.
278 Of particular interest, the ATP7B(K832R) Alzheimer's disease susceptibility allele was found, for
279 alterations in mild cognitive impairment and Alzheimer's disease that can complement existing dimensi
280 ent a previously unrecognized contributor to Alzheimer's disease that is independent of neuronal hypo
281 d beta precursor protein), a major player in Alzheimer's disease that is known to have immune and inf
283 m antipsychotic prescribing for psychosis in Alzheimer's disease, the mechanisms underpinning antipsy
284 eptic activity is frequently associated with Alzheimer's disease; this association has therapeutic im
285 he Abeta peptides, which are associated with Alzheimer's disease through their presence in amyloid pl
286 the brain increases with the progression of Alzheimer's disease, thus classifying BChE as a promisin
287 HOD: In the Antipsychotic Discontinuation in Alzheimer's Disease trial, 180 patients with Alzheimer's
288 existing dimensional approaches for staging Alzheimer's disease using a variety of biomarkers, which
289 ckness, suggesting that cortical thinning in Alzheimer's disease-vulnerable brain regions is a mechan
291 s toxicity of amyloid-beta species linked to Alzheimer's disease was initially treated with scepticis
293 polygenic risk scores for the development of Alzheimer's disease were calculated using summary statis
294 oteins related to amyloid-beta metabolism or Alzheimer's disease were quantified by enzyme-linked imm
295 ker of neurodegenerative diseases, including Alzheimer's disease, where olfactory deficits precede de
296 erm memory performance and is reminiscent of Alzheimer's disease, which is characterized by degenerat
297 g network hyperexcitability in patients with Alzheimer's disease will identify whether AEDs or relate
298 has an important role in the pathogenesis of Alzheimer's disease with its three isoforms having disti
299 atment of clinical seizures in patients with Alzheimer's disease with select antiepileptic drugs (AED
300 rformance in individuals at genetic risk for Alzheimer's disease, with the caveat that the order of c
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