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1 erlies neurodegenerative diseases, including Alzheimer's.
3 s with neurodegenerative diseases, including Alzheimer's and Parkinson's disease, are thought to spre
7 differentiating between clinically diagnosed Alzheimer's and subcortical vascular cognitive impairmen
8 according to US National Institute on Aging-Alzheimer's Association neuropathological criteria, and
9 microglial proliferation in a mouse model of Alzheimer's beta-amyloidosis was increased threefold.
11 h their associations with amyloid plaques in Alzheimer's brains: RTN3, but not RTN1, is abundantly en
12 tudy eligibility criteria, from the National Alzheimer's Coordinating Center (NACC) (n = 5,073, 158 A
16 d be categorised as stage 2 or 3 preclinical Alzheimer's disease (A+T+N-, A+T-N+, and A+T+N+; 86% at
17 STATEMENT Understanding how risk factors for Alzheimer's disease (AD) affect brain function and cogni
20 nosis of neurodegenerative disorders such as Alzheimer's disease (AD) and related Dementias has been
22 l destruction methods.SIGNIFICANCE STATEMENT Alzheimer's disease (AD) and similar dementias are commo
23 ingulate cortex (PCC) predicts conversion to Alzheimer's disease (AD) and tracks disease progression,
27 splant (KT) may develop post-KT dementia and Alzheimer's disease (AD) associated with their long-stan
28 laques, a potential biomarker present in the Alzheimer's disease (AD) brain is crucial for both clini
29 a-amyloid (Abeta) plaques are key lesions in Alzheimer's disease (AD) but both pathologies also occur
30 pse degeneration and cognitive impairment in Alzheimer's disease (AD) by reactivating expression of t
31 A genome-wide survival analysis of 14,406 Alzheimer's disease (AD) cases and 25,849 controls ident
34 lot study on differentiating early stages of Alzheimer's disease (AD) from Dementia with Lewy Bodies
48 ein E-epsilon4 carriers, is a major risk for Alzheimer's disease (AD) is increasing steadily, with ov
51 current frontline symptomatic treatment for Alzheimer's disease (AD) is whole-body upregulation of c
52 y-Camacho et al. (2017) generate a humanized Alzheimer's disease (AD) model that reveals species-spec
53 FASS-LTP analysis in two well-characterized Alzheimer's disease (AD) mouse models (3xTg and Tg2576)
54 oinflammation is an important contributor to Alzheimer's disease (AD) pathogenesis, as underscored by
60 protein (oAbeta) isolated from the brains of Alzheimer's disease (AD) patients have been shown experi
63 al, and symptomatic heterogeneity underlying Alzheimer's disease (AD) requires a deep understanding o
66 myloid-beta pathology early in the course of Alzheimer's disease (AD) with high sensitivity and speci
67 with frontotemporal dementia (FTD-ALS), and Alzheimer's disease (AD), and found profound apical dend
68 s upregulated in the brains of patients with Alzheimer's disease (AD), and its expression levels infl
69 ques are a key histopathological hallmark of Alzheimer's disease (AD), and soluble Abeta species are
70 s the most important genetic risk factor for Alzheimer's disease (AD), ApoE3 is neutral, and ApoE2 is
71 gate the effect of a genetic risk factor for Alzheimer's disease (AD), ApolipoproteinE epsilon4 (APOE
73 at the intermediate and late Braak stages of Alzheimer's disease (AD), as well as in other neurodegen
74 eta) plays a key role in the pathogenesis of Alzheimer's disease (AD), but little is known about the
75 ne loss is recognized as an early feature of Alzheimer's disease (AD), but the underlying mechanisms
76 gomers is one of the earliest impairments in Alzheimer's Disease (AD), driving initial cognitive defi
77 of tau proteins, termed tauopathies, include Alzheimer's disease (AD), frontotemporal lobar degenerat
79 been the central dogma in drug discovery for Alzheimer's disease (AD), leading to many small-molecule
80 rophy in seven neurodegenerative conditions (Alzheimer's disease (AD), Parkinson's disease (PD) and H
82 Age is, by far, the greatest risk factor for Alzheimer's disease (AD), yet few AD drug candidates hav
117 d the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) battery (Word List Learning,
121 Cog]) and self-reported QoL (Quality of Life Alzheimer's Disease [QoL-AD]) for the person with dement
122 ociated with type 2 diabetes (T2D), with the Alzheimer's disease amyloid-beta (Abeta) peptide modulat
123 onstitute the histopathological hallmarks of Alzheimer's disease and are prominent targets for novel
124 ed the relationship between genetic risk for Alzheimer's disease and cortical thickness, such that in
125 e more clearly detected by PBB3 in brains of Alzheimer's disease and diffuse neurofibrillary tangles
126 ementia with Lewy bodies, five patients with Alzheimer's disease and five healthy control subjects to
127 to investigate pathological states including Alzheimer's disease and HIV-associated neurocognitive di
128 participants, but not those of patients with Alzheimer's disease and MCI, possess effective phagocyto
129 The innate immune system of patients with Alzheimer's disease and mild cognitive impairment (MCI)
131 unction ranging from severe loss, as seen in Alzheimer's disease and Parkinson's disease, to relative
133 eases associated with hippocampal pathology (Alzheimer's disease and schizophrenia) are more enriched
135 Alzheimer's Disease trial, 180 patients with Alzheimer's disease and symptoms of agitation or psychos
138 e decline (greater impairment on the 11-item Alzheimer's Disease Assessment Scale cognitive subscale
140 ipants who received IVIG performed better on Alzheimer's Disease Assessment Scale-cognitive subscale
143 relevance not only to the pathophysiology of Alzheimer's disease but also diet-associated obesity.
145 polyneuropathy, and Abeta42 associated with Alzheimer's disease by stabilizing their respective prot
146 ocortical, limbic and subcortical areas from Alzheimer's disease cases (n = 19), neurologically norma
147 dividuals with mild cognitive impairment and Alzheimer's disease clinical diagnoses can display signi
148 We applied this tool to the analysis of Alzheimer's disease data from three datasets CHS, FHS an
149 re achieved at very low amisulpride doses in Alzheimer's disease due to higher than anticipated occup
150 o be actively involved in the development of Alzheimer's disease due to its ability to seed the aggre
152 8F-AV-1451) associated with well-established Alzheimer's disease factors in a cohort including cognit
153 duals (5,728 AD, 5,653 CN controls) from the Alzheimer's Disease Genetics Consortium (ADGC), a Nation
154 and 9,386 older controls from Phase 1 of the Alzheimer's Disease Genetics Consortium (ADGC), providin
156 ntified rare coding variants associated with Alzheimer's disease in a three-stage case-control study
157 tor for frontotemporal dementia spectrum and Alzheimer's disease in an initial case-control study.
158 on of induced neuron-based model of sporadic Alzheimer's disease in mice and humans, and used this sy
159 l features of neurodegeneration occurring in Alzheimer's disease including age-dependent cortical atr
161 tion of AbetaOs in AD.SIGNIFICANCE STATEMENT Alzheimer's disease is characterized by progressive cogn
164 One of the main research topics related to Alzheimer's disease is the aggregation of the amyloid-be
165 on as seen in neurological disorders such as Alzheimer's disease may contribute to neurovascular dysf
167 th mitochondrial dysfunction in the brain of Alzheimer's disease mouse model CRND8 as early as 3 mont
171 ease neuropathology, 56 (26%) with low-level Alzheimer's disease neuropathology, 45 (21%) with interm
172 thy, we identified 49 (23%) patients with no Alzheimer's disease neuropathology, 56 (26%) with low-le
173 opathology, 45 (21%) with intermediate-level Alzheimer's disease neuropathology, and 63 (30%) with hi
176 al in groups with varying levels of comorbid Alzheimer's disease pathology according to US National I
177 's component features.SIGNIFICANCE STATEMENT Alzheimer's disease pathology appears earliest in brain
178 ociated with dementia that is independent of Alzheimer's disease pathology or larger infarcts (ie, la
181 ure in vivo may correlate with variations in Alzheimer's disease phenotype, in analogy to distinct pr
183 genic mechanisms resulting from the sporadic Alzheimer's disease risk factor apolipoprotein E (APOE)
184 ction between APOE varepsilon3/4 and another Alzheimer's disease risk factor, desmoglein 2 (DSG2).
185 stributions of autoradiographic labelling of Alzheimer's disease slices with 11C-PBB3 and 18F-AV-1451
187 icroglial activation was increased by 36% in Alzheimer's disease subjects compared with controls.
190 Of particular interest, the ATP7B(K832R) Alzheimer's disease susceptibility allele was found, for
191 alterations in mild cognitive impairment and Alzheimer's disease that can complement existing dimensi
192 ent a previously unrecognized contributor to Alzheimer's disease that is independent of neuronal hypo
193 d beta precursor protein), a major player in Alzheimer's disease that is known to have immune and inf
195 he Abeta peptides, which are associated with Alzheimer's disease through their presence in amyloid pl
196 HOD: In the Antipsychotic Discontinuation in Alzheimer's Disease trial, 180 patients with Alzheimer's
197 existing dimensional approaches for staging Alzheimer's disease using a variety of biomarkers, which
198 s toxicity of amyloid-beta species linked to Alzheimer's disease was initially treated with scepticis
200 oteins related to amyloid-beta metabolism or Alzheimer's disease were quantified by enzyme-linked imm
201 has an important role in the pathogenesis of Alzheimer's disease with its three isoforms having disti
202 atment of clinical seizures in patients with Alzheimer's disease with select antiepileptic drugs (AED
203 N = 14), controls (N = 14) and "asymptomatic Alzheimer's disease" (ASYMAD), i.e., individuals with si
204 unity on neurodegenerative disorders such as Alzheimer's disease, amyotrophic lateral sclerosis, Park
206 (Abeta) plays a crucial synaptotoxic role in Alzheimer's disease, and hyperphosphorylated tau facilit
207 he second most common form of dementia after Alzheimer's disease, and there is increasing awareness t
208 oid precursor protein (APP), a key player in Alzheimer's disease, belongs to the family of synaptic a
209 ds have a greater role for AMD compared with Alzheimer's disease, but a lesser role than for CAD.
212 s, with known revised diagnosis in over 25% (Alzheimer's disease, dementia with Lewy bodies, and prog
214 k1A might be an ideal therapeutic target for Alzheimer's disease, especially for Down syndrome and EG
215 mation of amyloid beta fibrils implicated in Alzheimer's disease, gamma-secretase is an important tar
216 or protein, BACE1 is a therapeutic target in Alzheimer's disease, however, consistent with its role i
217 and PTEN dysregulation and suggest that, in Alzheimer's disease, impairment of brain insulin signali
218 ith an increased risk of dementia, including Alzheimer's disease, in patients with prostate cancer.
219 n are associated with the pathophysiology of Alzheimer's disease, it is clear that amyloid precursor
220 alogs for the management of type 2 diabetes, Alzheimer's disease, or other diseases related to IAPP d
221 hology in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington
222 such as anxiety, depression, schizophrenia, Alzheimer's disease, Parkinson's disease, and pain, prov
223 y of developing age-related diseases such as Alzheimer's disease, Parkinson's disease, multiple scler
224 litating protein deposition diseases such as Alzheimer's disease, prion diseases, and type II diabete
225 various neurodegenerative diseases including Alzheimer's disease, progressive supranuclear palsy and
226 ought to result in neurodegeneration causing Alzheimer's disease, progressive supranuclear palsy, chr
227 m antipsychotic prescribing for psychosis in Alzheimer's disease, the mechanisms underpinning antipsy
228 the brain increases with the progression of Alzheimer's disease, thus classifying BChE as a promisin
229 ker of neurodegenerative diseases, including Alzheimer's disease, where olfactory deficits precede de
230 erm memory performance and is reminiscent of Alzheimer's disease, which is characterized by degenerat
231 rformance in individuals at genetic risk for Alzheimer's disease, with the caveat that the order of c
234 d BACE1 is accumulated in the distal axon of Alzheimer's disease-related mutant human APP transgenic
236 pt of cognitive aging to include evidence of Alzheimer's disease-related protein aggregation as an un
237 ckness, suggesting that cortical thinning in Alzheimer's disease-vulnerable brain regions is a mechan
287 is a dominant feature in the pathogenesis of Alzheimer's disease; however, it is not clear how indivi
288 eptic activity is frequently associated with Alzheimer's disease; this association has therapeutic im
290 ritical to the neurodegenerative pathways of Alzheimer's, Huntington's, and Parkinson's diseases and
291 associated with degenerative diseases (i.e., Alzheimer's, Huntington's, and Parkinson's diseases), ca
293 Abeta) aggregation in vitro and suppress the Alzheimer's-like phenotypes in a transgenic mouse model
295 s, the peptides and proteins associated with Alzheimer's, Parkinson's, type 2 diabetes and prion dise
296 s in episodic memory and the accumulation of Alzheimer's pathology are common in cognitively normal o
297 d 51% at age 80 years) or with suspected non-Alzheimer's pathophysiology (A-T+N-, A-T-N+, and A-T+N+;
299 obtained from the International Genomics of Alzheimer's Project (17,008 AD cases and 37,154 controls
300 controls from the International Genomics of Alzheimer's Project (IGAP Stage 1), we identified AD-ass
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