コーパス検索結果 (１語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 arkinsonian patients (53 synucleinopathy, 24 tauopathy).
2 he P301L tau mutation linked to an inherited tauopathy.
3 the phenotypic and pathological evolution of tauopathy.
4 t abrogates some of the cardinal features of tauopathy.
5 100%) in distinguishing synucleinopathy from tauopathy.
6 revent disease progression in the setting of tauopathy.
7 DNP), with intact ADNP protecting against AD-tauopathy.
8 phenotype of a relevant mouse model of human tauopathy.
9 ive value when used as in vivo biomarkers of tauopathy.
10 es, often including amyloid-beta plaques and tauopathy.
11 ial tau variant leading to a robust model of tauopathy.
12 elevated in Braak IV or primary age-related tauopathy.
13 nst neurodegeneration in the setting of pure tauopathy.
14 including a Caenorhabditis elegans model of tauopathy.
15 opsychological burden in primary age-related tauopathy.
16 odegeneration in a transgenic mouse model of tauopathy.
17 tex, which is the common site of age-related tauopathy.
18 Alzheimer's disease and primary age-related tauopathy.
19 S-tg) mouse model of frontotemporal dementia/tauopathy.
20 ity to distinguish TDP-43 proteinopathy from tauopathy.
21 eatures of tau present in the brain in human tauopathy.
22 derstand the role of TREM2 in the context of tauopathy.
23 entorhinal cortex (MEC) in a mouse model of tauopathy.
24 brain regions, a typical localization of CTE tauopathy.
25 Alzheimer's disease and primary age-related tauopathy.
26 ed neuropathology in the PS19 mouse model of tauopathy.
27 acilitate the development of agents to treat tauopathy.
28 iotin as a potential therapeutic approach in tauopathy.
29 mediated neurodegeneration in the setting of tauopathy.
30 ptomatic than those with primary age-related tauopathy.
31 onic traumatic encephalopathy, a progressive tauopathy.
32 Alzheimer's disease and primary age-related tauopathy.
33 diated neurodegeneration in a mouse model of tauopathy.
34 r role in Alzheimer's disease (AD) and other tauopathies.
35 ct against the progression of AD and related tauopathies.
36 isease-modifying therapy for PSP and related tauopathies.
37 eneration in Alzheimer's disease and related tauopathies.
38 gy, two subcellular niches affected early in tauopathies.
39 cores of patient-derived fibrils from AD and tauopathies.
40 mproves cognitive function in AD and related tauopathies.
41 otentially be effective in the management of tauopathies.
42 ubset of frontotemporal dementias, and other tauopathies.
43 ture of Alzheimer's disease (AD) and primary tauopathies.
44 disease, frontotemporal dementias, and other tauopathies.
45 essive accumulation of tau pathology, namely tauopathies.
46 ark feature of Alzheimer's disease and other tauopathies.
47 tive diseases that are collectively known as tauopathies.
48 umber of neurodegenerative disorders, called tauopathies.
49 utoffs distinguishing synucleinopathies from tauopathies.
50 ditional neurodegenerative diseases known as tauopathies.
51 hallmarks of neurological disorders known as tauopathies.
52 logy, and a new therapeutic target for human tauopathies.
53 n several neurodegenerative disorders called tauopathies.
54 lsy and Picks' disease, two distinct primary tauopathies.
55 gies of Alzheimer's disease (AD) and primary tauopathies.
56 a class of neurodegenerative diseases called tauopathies.
57 olymorphs of tau are associated with certain tauopathies.
58 s seeding offer a possible route to managing tauopathies.
59 of neurodegenerative diseases, also known as tauopathies.
60 olecular pathways and processes perturbed in tauopathies.
61 degenerative disorders collectively known as tauopathies.
62 ansmission contributes to the progression of tauopathies.
63 PTM) in Alzheimer's disease (AD) and related tauopathies.
64 h are characteristic of human AD and related tauopathies.
65 subsequent neuropathology in AD and related tauopathies.
66 ion of tau aggregates in these non-Alzheimer tauopathies.
67 ing the diversity of neuropathology in human tauopathies.
68 ly structured amyloid fibril underlies human Tauopathies.
69 hallmark of Alzheimer disease (AD) and other tauopathies.
70 chronic traumatic encephalopathy, and other tauopathies.
71 disease-modifying treatment of AD and other tauopathies.
72 presents a common pathological event in many tauopathies.
73 roup of neurodegenerative disorders known as tauopathies.
74 pies may be a strategy for the treatment for tauopathies.
75 levated in frontotemporal lobar degeneration tauopathies.
76 at identifying tau pathologies in the non-AD tauopathies.
77 lmarks of Alzheimer's disease (AD) and other tauopathies.
78 eutic use of DBS and synaptic stimulation in tauopathies.
79 d ameliorate tau pathology in AD and related tauopathies.
80 r's disease (AD) and other neurodegenerative tauopathies.
81 e of MID1 in the pathology of AD and related tauopathies.
82 d mitigate the levels of tau prions in human tauopathies.
83 ngles (NFTs), which are associated in AD and tauopathies.
84 sease-modifying therapies for AD and related tauopathies.
85 terminus (ie, PAD exposure) occurs in non-AD tauopathies.
86 s may explain the diverse characteristics of tauopathies.
87 alleviate tau pathology in FTLD and related tauopathies.
88 common feature in several neurodegenerative tauopathies.
89 icated in Alzheimer's disease (AD) and other tauopathies.
90 nts is the defining pathological hallmark of tauopathies.
91 y contribute to development of therapies for tauopathies.
92 rative diseases, collectively referred to as tauopathies.
93 ecific structures associated with individual tauopathies.
94 the lack of disease-modifying therapies for tauopathies.
95 ations observed in the preclinical stages of tauopathies.
96 f patients of AD and other neurodegenerative tauopathies.
97 her promising compounds for the treatment of tauopathies.
98 ophysiology in Alzheimer's disease and other tauopathies.
99 a group of neurodegenerative diseases called tauopathies.
100 nset and progression of tau pathology across tauopathies.
101 ions and cell type specificities as in human tauopathies.
103 red in neurodegenerative disorders including tauopathies, a group of diseases pathologically defined
104 ward genetic screen in a Drosophila model of tauopathy, a class of neurodegenerative disorders charac
105 mpal atrophy in cases of primary age-related tauopathy, a pathological entity with features that stro
106 al degeneration (CBD) is a neurodegenerative tauopathy-a class of disorders in which the tau protein
107 ing Alzheimer's disease, primary age-related tauopathy, ageing-related tau astrogliopathy and multipl
109 cting against neurodegeneration in models of tauopathy, Alzheimer's disease, and Huntington's disease
110 o would help to develop biomarkers for these tauopathies and clinical trials of disease-modifying the
111 ay be part of the early pathology in various Tauopathies and could be exploited therapeutically.
112 cannot reliably differentiate non-Alzheimer tauopathies and may not detect early Braak stages of neu
114 as a therapeutic target for the treatment of tauopathies and other neurodegenerative proteinopathies
115 potential drug targets for the treatment of tauopathies and provide insight into how phosphorylated
116 flammasome activation in the pathogenesis of tauopathies and support the amyloid-cascade hypothesis i
117 then discuss their clinical implications for tauopathies and synucleinopathies and propose a working
118 on may occur in a localized fashion in human tauopathies and synucleinopathies, followed by seed-depe
120 inding to pathologically affected regions in tauopathies and TDP-43-related disease, and which is use
121 ical, pathological, and genetic diversity of tauopathies and the discoveries underlying the emerging
124 ological trajectories of primary age-related tauopathy and Alzheimer's disease has not been thoroughl
125 and memory reactivation in a mouse model of tauopathy and amyloidosis implanted with a recording arr
126 ogressive supranuclear palsy, globular glial tauopathy and argyrophilic grain disease(10), CBD is cha
127 Ser-324-positive tau both in mouse models of tauopathy and in patients with Alzheimer's disease.
128 associations between post-mortem measures of tauopathy and intrinsic connectivity dysfunction reached
130 insA ADNP mutation frequency to Braak stage (tauopathy) and showed more ADNP mutations in AD specimen
131 tial as an early-stage diagnostic for AD and tauopathies, and also could guide the development of pro
132 previously been evaluated in the context of tauopathy, and here we observed increased deposition of
133 el combining markers for amyloid deposition, tauopathy, and neurodegeneration (ATN), in accordance wi
135 ted with chromosome 17, three unclassifiable tauopathy, and one argyrophilic grain disease); FTLD-TDP
136 rhinal cortex, which exhibits early signs of tauopathy, and the inferior temporal region, which is mo
144 uropathological attributes of AD and primary tauopathies are similar, the etiology and behavioral out
146 viduals with symptomatic primary age-related tauopathy are commonly of more advanced ages with milder
148 irect relevance to phenotypic variability of tauopathies, as the ratios of fast and slowly aggregatin
150 of amyloidosis and later by tauopathy, with tauopathy being the proteinopathy associated with clinic
152 Intracerebral injections of distinct human tauopathy brain-derived tau strains into 6hTau mice reca
153 al injection of tau aggregates isolated from tauopathy brains causes similar pathology in the recipie
156 on propensity and cause dominantly inherited tauopathies, but their biophysical mechanism driving amy
157 related to the common age-related entorhinal tauopathy, but this dysfunction was independent of amylo
158 f the UPR(ER) participate in amelioration of tauopathy by constitutively active XBP-1, possibly throu
159 mpact of LC degeneration in a mouse model of tauopathy by lesioning the LC of male and female P301S t
161 MAPT P301L mutation carrier had an atypical tauopathy characterized by grain-like tau-containing neu
165 ver, in a relevant transgenic mouse model of tauopathy, down-regulation of VPS35 results in an exacer
166 rms in brains of Pick's disease and familial tauopathy due to G272V tau mutation were sensitively det
167 alsy, corticobasal degeneration and familial tauopathy due to N279K tau mutation and 3-repeat isoform
168 ltiple fronto-temporal lobar pathologies and tauopathies, e2 was not significantly associated with pa
172 e [IQR] = 6.0, 12.3; n = 26) compared to the tauopathy group (median = 12.5pg/ml; IQR = 10.7, 15.0; n
176 port the hypothesis that primary age-related tauopathy has distinct neuropathological and clinical fe
177 ous studies showing that primary age-related tauopathy has slower cognitive decline than Alzheimer's
178 been associated with different phenotypes of tauopathies, has led to controversial assumptions about
179 n brain, the pathological tau from different tauopathies have distinct isoform compositions and cell
180 nd drug development and the broader field of tauopathies in general, potentially paving the way to fu
181 autopsy-proven ageing-associated and primary tauopathies in which there was no known history of expos
184 of D2-family dopamine receptors ameliorated tauopathy in multiple models including a Caenorhabditis
185 tic reduction in RanBP9 not only ameliorates tauopathy in Tau-P301S mice but also rescues the deficit
186 Our findings suggest an epilepsy-related tauopathy in temporal lobe epilepsy, which contributes t
188 ct of human APP (hAPP)/Abeta accumulation on tauopathy in the entorhinal cortex-hippocampal (EC-HIPP)
189 cline is indicative of accumulation of early tauopathy in the medial temporal lobe, specifically in t
190 acellular aggregates of tau proteins, termed tauopathies, include Alzheimer's disease (AD), frontotem
193 class of neurodegenerative diseases known as tauopathies, including Alzheimer's disease and related d
194 Os, isolated from brain tissues of different tauopathies, including Alzheimer's disease, progressive
196 ylase biotin levels are reduced in mammalian tauopathies, including brains of human Alzheimer's disea
197 l excitability underlies the pathogenesis of tauopathies, including frontotemporal dementia (FTD) wit
198 enesis of several forms of dementia known as tauopathies-including Alzheimer's disease, frontotempora
200 tmortem-derived tau filaments from different tauopathies injected in rodents have led to striking fin
201 neurodegeneration in Alzheimer's disease and tauopathies is generally assumed to start in a normally
202 eature of Alzheimer's disease (AD) and other tauopathies is the misfolding, aggregation and cerebral
206 n the temporal lobe, but primary age-related tauopathy lacks the requisite amyloid plaques central to
207 rphosphorylated tau protein is a hallmark of tauopathies like Alzheimer and many other neurodegenerat
210 eviously demonstrated that human CBD and PSP tauopathy lysates (CBD-tau and PSP-tau) contain distinct
211 dogenous genes in transgenic mouse models of tauopathy make it difficult to draw definitive conclusio
212 t the unique features of clinically distinct tauopathies may be a reflection of the strain of misfold
213 y for treating Alzheimer disease and related tauopathies may be inhibition of O-GlcNAcase (OGA), whic
215 at overexpressing LSD1 in the hippocampus of tauopathy mice, even after pathology has formed, is suff
217 Next, we optimized a SH-SY5Y cell based tauopathy model by introducing a novel 5-fold Tau mutati
218 nds healthy lifespan ( 25%) in wild type and tauopathy model C. elegans at least as effectively as ot
219 avior and electrophysiological properties in tauopathy model mice despite a paradoxical evolution of
221 We now report the development of a sporadic tauopathy model to study human tau strains by intracereb
227 Interestingly, chronic SYK inhibition in a tauopathy mouse model profoundly reduced Tau accumulatio
230 Patients had autopsy-confirmed FTLD with tauopathy (n = 31), TDP-43 proteinopathy (n = 49), or AD
231 reactive astrocytes causes glial activation, tauopathy, neuronal death, brain atrophy, cognitive impa
232 of CTE neuropathology from other mixed 3R/4R tauopathies of Alzheimer's disease and ageing may rest s
233 ease (AD) the impact of amyloid and regional tauopathy on cerebral glucose metabolism and subsequent
235 eloped, specific markers identifying primary tauopathies or TDP-43 proteinopathies are still lacking.
238 o neuritic plaques (i.e. primary age-related tauopathy) or moderate to frequent neuritic plaques (i.e
239 proteinopathy of Alzheimer disease and other tauopathies, or tau-mediated neurodegeneration, is not c
240 non-AD pathologies, both primary age-related tauopathy (p < 0.05) and brain arteriolosclerosis pathol
242 totemporal lobar degeneration (FTLD) and (2) tauopathy patients have higher phosphorylated-tau levels
243 has enabled visualization of tau lesions in tauopathy patients, but the modes of their binding to di
247 decade to suggest that the misfolded tau in tauopathies possesses prion-like features and that such
249 's disease pathology, nine had non-Alzheimer tauopathies (progressive supranuclear palsy, corticobasa
251 aggregation pattern of BDTOs from different tauopathies, resulting in the formation of less neurotox
253 of human tauopathies.SIGNIFICANCE STATEMENT Tauopathies show great clinical and neuropathological he
254 egation that underlie the diversity of human tauopathies.SIGNIFICANCE STATEMENT Tauopathies show grea
255 pe (i.e., hyperphosphorylation and increased tauopathy spreading) were unexpectedly increased in MAPT
257 otein tau is a defining feature of so-called tauopathies such as Alzheimer's disease, progressive sup
259 n emission tomography, especially in primary tauopathies such as progressive supranuclear palsy.
260 l could contribute to the pathophysiology of tauopathies such as PSP by promoting tau accumulation an
261 of tau is related to synaptic impairment in tauopathies, such as Alzheimer's disease and frontotempo
263 been found in several sporadic and inherited tauopathies, suggesting that dysregulation of tau exon 1
264 xtracts differed among donors with different tauopathies, suggesting that particular fibril polymorph
265 ge and AQP4 polarization in a mouse model of tauopathy, suggesting that this clearance pathway may ha
266 s a disease specific marker for 3R/4R and 3R tauopathies, supporting uniquely modified tau species in
267 that drive the development of AD, including tauopathy, synaptic dysfunction, and neurodegeneration.
268 to three categories: amyloid deposition (A), tauopathy (T), and neurodegeneration or neuronal injury
271 blocked seeding by extracts from all of the tauopathies tested could be used to broadly inhibit seed
272 like prion diseases, synucleinopathies, and tauopathies that are collectively termed protein misfold
273 ced in in vivo and in vitro murine models of tauopathy that are based on expression of mutant tau(P30
275 encephalopathy (CTE) is a neurodegenerative tauopathy that is associated with repetitive head impact
276 findings support the new hypothesis that in tauopathies the change in the expression level of specif
277 athogenesis in Alzheimer's disease and other Tauopathies, the mechanism that initiates the aggregatio
278 d amyloid deposits is a primary pathology in tauopathies, the most common of which is Alzheimer's dis
279 ggregates that promote cognitive deficits in tauopathies, the most common of which is Alzheimer's dis
280 n regions in a relevant mouse model of human tauopathy, the hTau mice, in relationship with the devel
286 manner distinct from classical aging-related tauopathy, underlining the importance of assaying the ef
287 e created somatic transgenesis CNS models of tauopathy utilizing neonatal delivery of adeno-associate
288 n tissue extracts from different donors with tauopathies varied among individuals, indicating the pos
291 involvement in Alzheimer's disease and other tauopathies, was found to undergo liquid-liquid phase se
292 Alzheimer's disease and primary age-related tauopathy, we compared rates of decline in the sum of bo
293 Here, to address the role of p25/Cdk5 in tauopathy, we generated double-transgenic mice by crossi
294 To further validate the role of p25/Cdk5 in tauopathy, we used frontotemporal dementia patient-deriv
295 es many neurodegenerative diseases including tauopathies, where the misfolded tau protein propagates
296 Alzheimer's disease and primary age-related tauopathy, whether either protein is also associated wit
297 au-induced toxicity in a C. elegans model of tauopathy, while loss of no other dopamine or serotonin
298 r's disease and to distinguish it from other tauopathies with distinct clinical and pathological char
300 y the appearance of amyloidosis and later by tauopathy, with tauopathy being the proteinopathy associ