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1 ars, 123 participants developed dementia (97 Alzheimer disease).
2 l tremor), probable DLB, and non-DLB (mainly Alzheimer disease).
3 with risk of dementia (all-cause dementia or Alzheimer disease).
4 strongest genetic risk factor for late-onset Alzheimer disease.
5 ll be beneficial in arresting progression of Alzheimer disease.
6 strongest genetic risk factor for late-onset Alzheimer disease.
7 licated in neurodegenerative disorders, like Alzheimer disease.
8 robable dementia with Lewy bodies (DLB) from Alzheimer disease.
9 etection of amyloid plaques, one hallmark of Alzheimer disease.
10 cated as central players in the pathology of Alzheimer disease.
11 notype and cortical atrophy in patients with Alzheimer disease.
12 one of the major pathological mechanisms for Alzheimer disease.
13 on of amyloid peptides playing a key role in Alzheimer disease.
14 wa mutant, associated with an early onset of Alzheimer disease.
15 .5%) participants, including 194 (9.5%) with Alzheimer disease.
16 hosphorylation in the 3xTg-AD mouse model of Alzheimer disease.
17 PP) gene have been implicated in early onset Alzheimer disease.
18 pposite direction in previous studies in the Alzheimer disease.
19 brain, is associated with a strong risk for Alzheimer disease.
20 mulates in the brain of subjects affected by Alzheimer disease.
21 uced neurotoxicity in experimental models of Alzheimer disease.
22 the design of gamma-secretase modulators for Alzheimer disease.
23 pportunities for therapeutic intervention in Alzheimer disease.
24 o been associated with an increased risk for Alzheimer disease.
25 l CSF amyloid levels do not exclude incident Alzheimer disease.
26 hared with amyotrophic lateral sclerosis and Alzheimer disease.
27 impairments, and neurotoxicity that underlie Alzheimer disease.
28 e preclinical or early symptomatic stages of Alzheimer disease.
29 ominent and early role in the progression of Alzheimer disease.
30 ion) may represent a potential treatment for Alzheimer disease.
31 ate of functional decline among persons with Alzheimer disease.
32 rative diseases, including prion disease and Alzheimer disease.
33 ases such as frontotemporal degeneration and Alzheimer disease.
34 slowly in neurodegenerative diseases such as Alzheimer disease.
35 rotein and a key molecule in the etiology of Alzheimer disease.
36 transmissible spongiform encephalopathy and Alzheimer disease.
37 , and the volumes of brain areas affected by Alzheimer disease.
38 ns of future secondary prevention trials for Alzheimer disease.
39 y (ADT) and cognitive dysfunction, including Alzheimer disease.
40 to define neurodegeneration associated with Alzheimer disease.
41 eptors may contribute to the pathobiology of Alzheimer disease.
42 le of vascular disease in the development of Alzheimer disease.
43 ate of functional decline among persons with Alzheimer disease.
44 e dementia in the MI cohort was 9% (2.8% for Alzheimer disease, 1.6% for vascular dementia, and 4.5%
45 edian: 12 y) of follow-up, 116 men developed Alzheimer disease, 64 men developed vascular dementia, a
46 ve decline and lower rates of progression to Alzheimer disease (Abeta-N+, 6.5% vs Abeta+N+, 32.6%) we
48 plaques are key histopathologic features in Alzheimer disease (AD) and are considered targets for th
49 mage-based classifier to distinguish between Alzheimer disease (AD) and behavioral variant frontotemp
50 Cerebral amyloidosis is a key abnormality in Alzheimer disease (AD) and can be detected in vivo with
51 nsive review of knowledge of the genomics of Alzheimer disease (AD) and DNA amyloid beta 42 (Abeta42)
52 accumulation is essential for understanding Alzheimer disease (AD) and for design of antiamyloid dru
53 eral prefrontal cortex (DLPFC) plasticity in Alzheimer disease (AD) and its association with working
54 d single-subject prediction of patients with Alzheimer disease (AD) and mild cognitive impairment (MC
56 ulation contributes to the pathology of both Alzheimer disease (AD) and progressive supranuclear pals
57 u imaging may become a diagnostic marker for Alzheimer disease (AD) and provides insights into the pa
60 nts with mild cognitive impairment (MCI) and Alzheimer disease (AD) are defective in phagocytosis and
65 tides play a central role in the etiology of Alzheimer disease (AD) by exerting cellular toxicity cor
68 ormal or MCI status to death, derived from 4 Alzheimer Disease (AD) Centers in the United States.
69 r prevent mild cognitive impairment (MCI) or Alzheimer disease (AD) dementia, markers of early detect
71 o identify older healthy persons at risk for Alzheimer disease (AD) for enrollment in AD prevention t
72 n tau pathology and the clinical symptoms of Alzheimer disease (AD) has been hypothesized, there is i
73 sociations between age, vascular health, and Alzheimer disease (AD) imaging biomarkers in an elderly
74 Importance: A reliable method of detecting Alzheimer disease (AD) in its prodromal state is needed
83 oid imaging by small-animal PET in models of Alzheimer disease (AD) offers the possibility to track a
84 l evidence strongly links Clusterin (CLU) to Alzheimer disease (AD) pathogenesis, the receptor for CL
89 nitive decline (SCD) and biomarkers of early Alzheimer disease (AD) pathophysiologic processes (accum
90 older people may be direct manifestations of Alzheimer disease (AD) pathophysiology at the preclinica
91 The role of amyloid in the progression of Alzheimer disease (AD) pathophysiology is of central int
93 rmalities and inflammation are found in many Alzheimer disease (AD) patients, but whether these chang
94 tion to plasma EPA and DHA concentrations in Alzheimer disease (AD) patients.In the present study, DN
95 Biomarkers do not determine conversion to Alzheimer disease (AD) perfectly, and criteria do not sp
98 1451 in cognitively healthy control (HC) and Alzheimer disease (AD) subjects, using reference region
103 on4 allele are at greater risk of developing Alzheimer disease (AD) than men, and the sex-dependent a
105 delusions or hallucinations, are frequent in Alzheimer disease (AD), affecting 40 to 60% of individu
106 ants, 50% had neuropathological diagnoses of Alzheimer disease (AD), and 35% of vascular dementia (Va
107 erol and egg intakes with incident dementia, Alzheimer disease (AD), and cognitive performance in mid
108 g substances in patients with early forms of Alzheimer disease (AD), and if so, to examine the extent
109 genic in neurodegenerative diseases, such as Alzheimer disease (AD), and in neurodevelopmental disord
110 regates form the two discrete pathologies of Alzheimer disease (AD), and oligomeric assemblies of eac
111 the brain is 1 of 2 pathologic hallmarks of Alzheimer disease (AD), and the spatial distribution of
112 ques, one of the two pathologic hallmarks of Alzheimer disease (AD), are associated with dystrophic n
113 Cognitive impairment and dementia, including Alzheimer disease (AD), are common within the aging popu
114 AD is an early marker of pathological tau in Alzheimer disease (AD), but its role in other tauopathie
115 the most significant genetic risk factor for Alzheimer disease (AD), may mask effects of other loci.
116 he impact of neurological disorders, such as Alzheimer disease (AD), on AMPK function and downstream
117 tous tau aggregates, the hallmark lesions of Alzheimer disease (AD), play key roles in neurodegenerat
119 uld greatly facilitate accurate diagnosis of Alzheimer disease (AD), staging and monitoring of diseas
120 In the amyloidogenic pathway associated with Alzheimer disease (AD), the amyloid precursor protein (A
122 s causally contribute to the pathogenesis of Alzheimer disease (AD), the most frequent neurodegenerat
123 beta) deposits in the brain is a hallmark of Alzheimer disease (AD), the soluble oligomers rather tha
124 BIN1 is a genetic risk factor of late-onset Alzheimer disease (AD), which was identified in multiple
125 e (Abeta) is a key player in the etiology of Alzheimer disease (AD), yet a systematic investigation o
147 einker syndrome (GSS)) n = 4), patients with Alzheimer disease (AD, n = 14) and age-matched controls
148 ith 13-y incident dementia and its subtypes (Alzheimer disease [AD] and mixed or vascular dementia) i
151 discuss such cross-interactions between the Alzheimer disease amyloid-beta (Abeta) peptide and other
152 diseases, included 6 3 with typical amnesic Alzheimer disease and 3 with atypical variants (posterio
153 developed dementia, of whom 935 (79.5%) had Alzheimer disease and 95 (8.1%) had vascular dementia.
155 association between microglia and late-onset Alzheimer disease and an association between schizophren
157 n vivo will lead to new diagnostic tools for Alzheimer disease and better understanding of its neurob
161 sted of 171 subjects including patients with Alzheimer disease and mild cognitive impairment and heal
163 traits assessed in the preclinical phase of Alzheimer disease and other dementias with the Revised N
164 pathology, the other major proteinopathy of Alzheimer disease and other tauopathies, or tau-mediated
169 d Communicative Disorders and Stroke and the Alzheimer Disease and Related Disorders Association crit
172 as they provide care for family members with Alzheimer disease and the difficulty in slowing function
174 implicated in neurologic disorders including Alzheimer disease and traumatic brain injury (TBI).
178 e loss in neurodegenerative diseases such as Alzheimer disease, and may also find use as general cogn
179 knowledge, no effective treatments exist for Alzheimer disease, and new molecules are years away.
180 mate hazard ratios for dementia of any type, Alzheimer disease, and Parkinson disease in patients rec
181 sm leading to the neuronal damage present in Alzheimer disease, and soluble Abeta oligomers are thoug
183 cal diseases, such as Huntington disease and Alzheimer disease, are well-characterized proteinopathie
184 Parkinson disease (PD) is second only to Alzheimer disease as the most common human neurodegenera
185 ores (beta = -1.077, P < .001) and increased Alzheimer Disease Assessment Scale cognitive subscale sc
186 A major constituent of drusen deposits are Alzheimer disease-associated amyloid beta (Abeta) peptid
187 ragments including the proposed initiator of Alzheimer disease-associated dysfunctions, amyloid-beta.
188 cretase at the gamma-site similar to certain Alzheimer disease-associated mutations within the amyloi
189 beta) positron emission tomography and their Alzheimer disease-associated neurodegeneration status (t
190 " The main outcome was incident diagnosis of Alzheimer disease based on the International Classificat
191 This P450 is also a potential target for Alzheimer disease because it can be activated pharmacolo
192 .02]), and lower neuropathologically defined Alzheimer disease (beta = -0.53 score units [95% CI, -0.
194 F-T807) binds to neurofibrillary tangles in Alzheimer disease, but tissue studies assessing binding
195 ques and neurofibrillary tangles co-occur in Alzheimer disease, but with different topological and te
196 gnaling events, which have a central role in Alzheimer disease, cancer progression, and immune survei
198 the NIA-LOAD study were recruited from 23 US Alzheimer disease centers with ongoing data collection s
200 italopram in the Citalopram for Agitation in Alzheimer Disease (CitAD) study to identify individuals
201 ted tau proteins are closely associated with Alzheimer disease clinical phenotype and neurodegenerati
202 s enriched in the brains of individuals with Alzheimer disease compared with healthy aged controls.
203 r results suggest that ERK2 dysregulation in Alzheimer disease could lead to abnormal phosphorylation
204 beta) may contribute to cognitive decline of Alzheimer disease, defining the most critical forms has
205 orks during progression from normal aging to Alzheimer disease dementia (AD) has also been observed.
206 shorter disease duration than patients with Alzheimer disease dementia, little is known about which
209 ries from 2006 to 2013 and compared rates of Alzheimer disease diagnosis for 399 979 statin users 65
210 the association between statin exposure and Alzheimer disease diagnosis for different sexes, races a
211 s associated with a reduced risk of incident Alzheimer disease diagnosis for white women (HR, 0.84, 9
212 statins was associated with a lower risk of Alzheimer disease diagnosis for women (hazard ratio [HR]
213 in APP, PSEN1, and PSEN2 lead to early-onset Alzheimer disease (EOAD) but account for only approximat
214 zheimer Disease/National Cell Repository for Alzheimer Disease family study (hereinafter referred to
215 affect the natural history of progression in Alzheimer disease for the purpose of improving both clin
216 ly different between the nonimpaired and the Alzheimer disease groups (eg, neuroticism: beta = 0.00;
218 ic risk score analysis for the prediction of Alzheimer disease have given area under the curve (AUC)
219 ts were similar when excluding patients with Alzheimer disease (hazard ratio, 2.32; 95% CI, 1.73-3.12
220 such as chronic traumatic encephalopathy and Alzheimer disease; however, neither the severity nor fre
221 ptica spectrum disorders, Parkinson disease, Alzheimer disease, Huntington disease, and amyotrophic l
222 the association between statin exposure and Alzheimer disease incidence among Medicare beneficiaries
223 d in subjects with a low risk of preclinical Alzheimer disease indexed by the absence of MTA (n = 85)
224 peptide (Abeta), a key pathogenic factor in Alzheimer disease, induces profound alterations in neuro
227 hat accumulate in the brain of patients with Alzheimer disease, is abundant in platelets, but its phy
228 of clinical progression among patients with Alzheimer disease leads to difficulty in providing clini
229 Dementia-related pathologies assessed were Alzheimer disease, Lewy bodies, and the number of macroi
230 ives from an individually varying mixture of Alzheimer disease, Lewy body disease, and vascular brain
231 ls develop high levels of Abeta peptides and Alzheimer disease-like brain amyloidosis early in life.
233 strong genetic covariance between late-onset Alzheimer disease (LOAD) and amyotrophic lateral scleros
235 isks of congenital abnormalities, cancer, or Alzheimer disease.Meta-analysis results indicate an infl
238 ao as well as chronic expression of familial Alzheimer disease mutant transgenes in model mice preven
239 ations of age- and sex-matched patients with Alzheimer disease (n = 34) and healthy control volunteer
240 f DLB and 29 patients with non-DLB dementia (Alzheimer disease, n = 16; behavioral variant frontotemp
241 : The National Institute on Aging Late-Onset Alzheimer Disease/National Cell Repository for Alzheimer
242 and Participants: This cohort study from the Alzheimer Disease Neuroimaging Initiative (ADNI) enrolle
243 rker that links a specific type of molecular Alzheimer disease neuropathologic condition with clinica
246 deviation decrease, 1.07-1.61), similar for Alzheimer disease only, and unaltered by accounting for
249 r results indicate a central role of NPCT in Alzheimer disease pathogenesis and suggest NPCT as a pot
251 week) was significantly correlated with less Alzheimer disease pathology including lower density of n
252 ecursor protein/presenilin 1 mice along with Alzheimer disease pathology progression (3, 6, and 12 mo
254 and neurodegeneration are viewed together as Alzheimer disease pathophysiology (ADP), the factors tha
255 tide (Abeta)-negative (Abeta-) suspected non-Alzheimer disease pathophysiology (SNAP) than in Abeta-p
256 duals are classified as having suspected non-Alzheimer disease pathophysiology (SNAP), defined as bio
260 therapeutics to improve memory impairment in Alzheimer disease patients.Molecular Psychiatry advance
261 ecursor protein (APP), whose mutations cause Alzheimer disease, plays an important in vivo role and f
262 ls of FKBP51 are increased with aging and in Alzheimer disease, potentially contributing to disease p
264 mortem brain tissue from PD cases but not in Alzheimer disease, progressive supranuclear palsy, or mu
265 58; P < .001; and 3 patients with nonamnesic Alzheimer disease, r = -0.51; P < .001; r = -0.63; P < .
266 18F]AV-1451 binding (3 patients with amnesic Alzheimer disease, r = -0.82; P < .001; r = -0.70; P < .
267 trehalose also alters the metabolism of the Alzheimer disease-related amyloid precursor protein (APP
270 amily members were followed up at the Knight Alzheimer Disease Research Center (1985-2015) and 1115 i
271 se-control study was conducted at the Knight Alzheimer Disease Research Center at Washington Universi
273 completed in January 2016, including Knight Alzheimer Disease Research Center patient data collected
274 dementia at the Charles F. and Joanne Knight Alzheimer Disease Research Center, Washington University
275 hort study used data collected at the Knight Alzheimer Disease Research Center, Washington University
280 nd rosuvastatin were associated with reduced Alzheimer disease risk for white women only (HR, 0.82, 9
284 argue that the amyloid cascade hypothesis in Alzheimer disease should be expanded to include cross-in
285 est that research on preclinical markers for Alzheimer disease should take the continuum of CSF amylo
286 There are conflicting results claiming that Alzheimer disease signature neurodegeneration may be mor
289 cerebral microcirculation may play a role in Alzheimer disease, the leading cause of late-life dement
290 tion trials for individuals at high risk for Alzheimer disease, there is increasing need for accurate
291 cated in cancers, arrhythmia, and late-onset Alzheimer disease, these findings may trigger research d
292 nome sequence data from families affected by Alzheimer disease to illustrate the application of the R
293 nase II in wild-type brain slices but not in Alzheimer disease transgenic brain slices or wild-type s
294 h mild cognitive impairment due to suspected Alzheimer disease) underwent dynamic PET imaging for up
295 h mild cognitive impairment due to suspected Alzheimer disease) underwent dynamic PET imaging for up
297 sks of congenital abnormalities, cancer, and Alzheimer disease.We conducted a systematic review of th
298 in the prefrontal cortex of individuals with Alzheimer disease were significantly enriched with genes
299 vFTD, 15 with semantic dementia, and 15 with Alzheimer disease) were recruited, and their eating beha
300 for amyloid-beta pathology with symptomatic Alzheimer disease who usually have tau pathology, epsilo
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