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1 ton's disease (HD) is a dominantly inherited neurodegenerative disease.
2 bose from proteins have been associated with neurodegenerative disease.
3 mmon form of dementia and the most prevalent neurodegenerative disease.
4 e subject of intense research in relation to neurodegenerative disease.
5 enty brains from donors without recognisable neurodegenerative disease.
6 se is a rare, fatal, and exceptionally rapid neurodegenerative disease.
7 teraction mechanisms in prion-like models of neurodegenerative disease.
8 motherapy-induced peripheral neuropathy, and neurodegenerative disease.
9 enic protein spread is a ubiquitous theme in neurodegenerative disease.
10 er's disease (AD) is a debilitating, chronic neurodegenerative disease.
11 bition may be a safe therapeutic approach in neurodegenerative disease.
12 mone receptor coactivator likely involved in neurodegenerative disease.
13 on of Hp and select periodontal pathogens on neurodegenerative disease.
14 d could serve as a new animal model to study neurodegenerative disease.
15 neuroinflammation can stimulate axon loss in neurodegenerative disease.
16 ascular disease, obesity, mental health, and neurodegenerative disease.
17 d mitochondrial transport has been linked to neurodegenerative disease.
18 n multiple sclerosis (MS), an autoimmune and neurodegenerative disease.
19 in vivo, providing mechanistic insights into neurodegenerative disease.
20 way, has important implications for fighting neurodegenerative disease.
21 sition to a microglial state associated with neurodegenerative disease.
22 lymorphic fibrils, including their PTMs, and neurodegenerative disease.
23 he autophagy pathway itself can also lead to neurodegenerative disease.
24 metabolism as a contributor to this retinal neurodegenerative disease.
25 concern, even in the absence of recognizable neurodegenerative disease.
26 , has shown promise for multiple cancers and neurodegenerative disease.
27 ophic lateral sclerosis (ALS), a devastating neurodegenerative disease.
28 entia and ALS in many individuals with these neurodegenerative diseases.
29 e selectively cellular processes involved in neurodegenerative diseases.
30 ine pathways for therapeutic intervention in neurodegenerative diseases.
31 its, such as those associated with aging and neurodegenerative diseases.
32 well-controlled manner for the treatment of neurodegenerative diseases.
33 he degradation of mutant proteins that cause neurodegenerative diseases.
34 ay have increased odds of SD, MCI, and other neurodegenerative diseases.
35 xidative events surfacing at early stages of neurodegenerative diseases.
36 in a subset of patients diagnosed with other neurodegenerative diseases.
37 logical structures that are formed by tau in neurodegenerative diseases.
38 associated with several diseases, including neurodegenerative diseases.
39 system represents a new target in combating neurodegenerative diseases.
40 less successful in clinical trials for other neurodegenerative diseases.
41 hological hallmark shared across adult-onset neurodegenerative diseases.
42 been correlated with its toxicity in various neurodegenerative diseases.
43 early events in the pathogenesis of several neurodegenerative diseases.
44 ciated with neurodevelopmental disorders and neurodegenerative diseases.
45 clerosis, frontotemporal dementia, and other neurodegenerative diseases.
46 arly stages of Alzheimer's disease and other neurodegenerative diseases.
47 etection of DA levels for early diagnosis of neurodegenerative diseases.
48 es, including cardiovascular, metabolic, and neurodegenerative diseases.
49 ive impairment (MCI), AD dementia and non-AD neurodegenerative diseases.
50 translate these findings into therapies for neurodegenerative diseases.
51 s to the pathogenesis of a growing number of neurodegenerative diseases.
52 amyloid-like fibrils reminiscent of those in neurodegenerative diseases.
53 are emerging as a critical component in most neurodegenerative diseases.
54 n of toxic oligomers associated with several neurodegenerative diseases.
55 ble links between repetitive head injury and neurodegenerative diseases.
56 ochondrial dysfunction or loss is evident in neurodegenerative diseases.
57 ological heterogeneity are well described in neurodegenerative diseases.
58 ery promising strategy to treat a variety of neurodegenerative diseases.
59 ociated proteins have been linked to various neurodegenerative diseases.
60 health outcomes, such as cardiometabolic and neurodegenerative diseases.
61 rodents, leading to clinical trials in human neurodegenerative diseases.
62 iscuss its role in identifying biomarkers of neurodegenerative diseases.
63 , mild cognitive impairment (MCI), and other neurodegenerative diseases.
64 sociated with human autoimmune disorders and neurodegenerative diseases.
65 quent antecedent to the onset of dementia in neurodegenerative diseases.
66 ting regeneration in development, aging, and neurodegenerative diseases.
67 ead to cellular dysfunctions associated with neurodegenerative diseases.
68 of clinical importance in neural injury and neurodegenerative diseases.
69 Alzheimer disease (AD) and two dozen related neurodegenerative diseases.
70 may be a general pathomechanistic driver of neurodegenerative diseases.
71 s/peptides associated with many systemic and neurodegenerative diseases.
72 c variants are risk factors for AD and other neurodegenerative diseases.
73 ophagy to the development and progression of neurodegenerative diseases.
74 xic amyloid aggregates are a feature of many neurodegenerative diseases.
75 e development of chronic diseases, including neurodegenerative diseases.
76 regulated changes in response to injury and neurodegenerative diseases.
77 has been associated with various cancers and neurodegenerative diseases.
78 of ADEVs are likely beneficial for treating neurodegenerative diseases.
79 form of PrP(C) responsible for prion-induced neurodegenerative diseases.
80 ess and its effects are nor clearly known in neurodegenerative diseases.
81 e to tackle protein aggregation toxicity and neurodegenerative diseases.
82 GS transport that may have implications for neurodegenerative diseases.
83 ontribution of mitophagy to pathologies like neurodegenerative diseases.
84 xcess and deficiency cause hematological and neurodegenerative diseases.
85 elopmental vascular disorders to age-related neurodegenerative diseases.
86 cal conditions, including cancer, aging, and neurodegenerative diseases.
87 lized as important pathogenic mechanisms for neurodegenerative diseases.
88 rogression is a common theme underlying many neurodegenerative diseases.
89 g congenital diseases as well as cancers and neurodegenerative diseases.
90 jor role in the etiology and pathogenesis of neurodegenerative diseases.
91 influence an individual's predisposition to neurodegenerative diseases.
92 antagonists for patients with TRPV4-related neurodegenerative diseases.
93 g contrasts the gender differences in common neurodegenerative diseases.
94 onal circuits is an important determinant of neurodegenerative diseases.
95 tau protein are associated with a variety of neurodegenerative diseases.
96 ear or cytoplasmic aggregates in age-related neurodegenerative diseases.
97 effects of senolytics on glaucoma and other neurodegenerative diseases.
98 f patients that present across a spectrum of neurodegenerative diseases.
99 huge unmet need for effective treatments for neurodegenerative diseases.
100 ropagate the pathology seen across different neurodegenerative diseases.
101 gical disorders and could even contribute to neurodegenerative diseases.
102 ent in patients with AD and, possibly, other neurodegenerative diseases.
103 ribed processes in psychiatric disorders and neurodegenerative diseases.
104 implicated in the proteotoxicity-associated neurodegenerative diseases.
105 chanism based stratification in the field of neurodegenerative diseases.
106 an brain are implicated in typical aging and neurodegenerative diseases.
107 understanding of aging-related disorders and neurodegenerative diseases.
108 urgently necessitate new approaches to treat neurodegenerative diseases.
109 rewire their communication to modify chronic neurodegenerative diseases.
110 lved in the onset and progression of various neurodegenerative diseases.
111 ged mitochondria has been implicated in many neurodegenerative diseases.
112 hophysiology of behavioural, psychiatric and neurodegenerative diseases.
113 by explain horses' susceptibility to certain neurodegenerative diseases.
114 ning and regenerating photoreceptor cells in neurodegenerative diseases.
115 es, as observed in psychiatric disorders and neurodegenerative diseases.
116 ns are a common neuropathological feature of neurodegenerative diseases.
117 cluding ischemic stroke, trauma, and chronic neurodegenerative diseases.
118 ing therapeutic target for retinal and other neurodegenerative diseases.
119 ve dramatically changed our understanding of neurodegenerative diseases.
120 mplication of these pathways across multiple neurodegenerative diseases.
123 d OR, 2.00; 95% CI, 1.79-2.22; and for other neurodegenerative disease: adjusted OR, 1.79; 95% CI, 1.
124 yotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease affecting motoneurons (MNs) in
125 tex microcircuit with the pathophysiology of neurodegenerative diseases affecting motor functions.
126 arkinson's disease is the second most common neurodegenerative disease after Alzheimer's disease and
128 f the protein Tau is involved in a number of neurodegenerative diseases, also known as tauopathies.
129 lectively vulnerable to neuropsychiatric and neurodegenerative diseases, although little is known abo
130 applied the framework to two representative neurodegenerative diseases, Alzheimer's disease (AD) and
131 induction as a potential therapy in several neurodegenerative diseases-Alzheimer's disease, Parkinso
132 its implication in the familial form of the neurodegenerative disease amyotrophic lateral sclerosis.
133 on four individuals from three families with neurodegenerative disease and homozygous frameshift muta
134 traits, hindbrain development, vascular and neurodegenerative disease and psychiatric conditions.
135 y pathways can be targeted simultaneously in neurodegenerative disease and supports consideration of
136 highlight 4E-BP1 as a therapeutic target in neurodegenerative disease and underscore the importance
138 rstanding of p75NTR in acute brain injuries, neurodegenerative diseases and general response to cellu
139 M106B locus have been implicated in multiple neurodegenerative diseases and in healthy brain ageing.
141 n of central nervous system drug candidates, neurodegenerative diseases and numerous oncology targets
142 on and necroptosis are major contributors to neurodegenerative disease, and axon dysfunction and dege
143 vealed extensive links between autophagy and neurodegenerative disease, and disruptions to autophagy
144 ially leading to increased susceptibility to neurodegenerative disease, and we highlight the need to
147 anticoagulation, the interaction of ICH with neurodegenerative diseases, and our approach to prognost
148 tions in p97 have been linked to a number of neurodegenerative diseases, and overexpression of wild t
149 of diseases including heart disease, cancer, neurodegenerative diseases, and the general aging proces
150 human Msp1 homologue has been implicated in neurodegenerative diseases, and we show that the lack of
153 , using human pathologies such as cancer and neurodegenerative diseases as examples, we explore the n
154 Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with exposure to co
155 hared with progressive supranuclear palsy, a neurodegenerative disease associated with misfolding of
157 , while considering an expanding spectrum of neurodegenerative diseases associated with pathogenic TD
159 n cohort 2 for clinical AD dementia vs other neurodegenerative diseases (AUC, 0.96 [95% CI, 0.93-0.98
160 over 1000 natural products with relevance to neurodegenerative disease, bacterial and parasitic infec
161 ndolysosomal system is often associated with neurodegenerative disease because postmitotic neurons ar
162 ained considerable attention in AD and other neurodegenerative diseases because it has been linked to
164 glycosyltransferases in the pathogenesis of neurodegenerative diseases but differentiating cause fro
165 glycosyltransferase is sufficient to cause a neurodegenerative disease, but connection between neurod
166 misfolded proteins potentially underly many neurodegenerative diseases, but individual targets which
167 ells is the defining pathological feature of neurodegenerative diseases called synucleinopathies.
170 rk of aging and many human diseases, such as neurodegenerative diseases, cardiovascular diseases, and
172 nocerebellar ataxia type 1 (SCA1) is a fatal neurodegenerative disease caused by abnormal expansion o
173 axia type 3 (SCA3) is a dominantly inherited neurodegenerative disease caused by CAG (encoding glutam
174 Krabbe disease) is a progressive, incurable neurodegenerative disease caused by deficient activity o
176 istinct arrhythmias as well as two different neurodegenerative diseases caused by variants in amyloid
177 le in amyotrophic lateral sclerosis (ALS), a neurodegenerative disease characterized by extensive mot
179 t common movement disorder, is a progressive neurodegenerative disease characterized by substantia ni
180 Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the preferent
182 ntribute to their enhanced susceptibility to neurodegenerative diseases characterized by aberrant pro
183 STATEMENT Spinal muscular atrophy (SMA) is a neurodegenerative disease, characterized by synaptic los
184 n Alzheimer's disease and many other related neurodegenerative diseases, collectively referred to as
187 he basal ganglia and cerebellum (H-ABC) is a neurodegenerative disease due to mutations in TUBB4A.
189 of optical-based biosensors in the field of neurodegenerative disease enable us to accelerate the ad
190 imer disease (AD) is the most common form of neurodegenerative disease, estimated to contribute 60-70
192 ight on the pathogenesis of a broad range of neurodegenerative diseases, for which glymphatic failure
193 ing-a pathway that is widely dysregulated in neurodegenerative diseases-generates a distinct reactivi
194 velopment of novel therapies for adult-onset neurodegenerative disease has been impeded by the limita
195 nnovative use of this technology in studying neurodegenerative diseases has emerged with the neurosen
196 uding infection, traumatic brain injury, and neurodegenerative diseases, has become increasingly evid
199 ulinism/hyperammonemia (HI/HA) syndrome, and neurodegenerative diseases have reinvigorated interest o
200 e, we investigate the molecular basis of the neurodegenerative disease hereditary ferritinopathy (HF)
201 thies and heterogeneous clinical symptoms in neurodegenerative diseases hinders the identification of
203 nd gender, the OR comparing the odds of each neurodegenerative disease in OAG patients with the odds
204 eful for investigating early stage events in neurodegenerative diseases in both cellular and animal m
205 rs are available to support the diagnosis of neurodegenerative diseases in clinical and research sett
206 infectious agents which cause rapidly lethal neurodegenerative diseases in humans and animals followi
207 on proteostasis of proteins associated with neurodegenerative diseases in Lund human mesencephalic d
208 presents an important pathologic hallmark of neurodegenerative diseases including Alzheimer's disease
209 ociated with an elevated risk of age-related neurodegenerative diseases including Alzheimer's disease
210 a common feature of proteins associated with neurodegenerative diseases including prion protein (PrPC
211 t sports participation and increased risk of neurodegenerative disease, including Alzheimer's disease
212 atic brain injury (TBI) is a risk factor for neurodegenerative disease, including chronic traumatic e
213 have been implicated in the pathogenesis of neurodegenerative diseases, including a non-cell autonom
214 creasingly implicated in the pathogenesis of neurodegenerative diseases, including ALS caused by a C9
216 nic amino acid that has been associated with neurodegenerative diseases, including amyotrophic latera
217 gregation contributes to the pathogeneses of neurodegenerative diseases, including amyotrophic latera
218 ated proteins have been reported in multiple neurodegenerative diseases, including C9orf72 Amyotrophi
221 deficits in these pathways are implicated in neurodegenerative diseases, including Parkinson's and am
222 ils coalescing into pathologic inclusions in neurodegenerative diseases, including Parkinson's diseas
223 buting to sustained microglial activation in neurodegenerative diseases, including Parkinson's diseas
224 emerging target for the treatment of cancer, neurodegenerative diseases, inflammation, and other dise
225 rphic amyloid fibrils is a common feature in neurodegenerative diseases involving protein aggregation
228 o the development of effective therapies for neurodegenerative disease is that available animal model
229 he role of abnormal brain iron metabolism in neurodegenerative diseases is still insufficiently under
230 that is alternatively spliced and linked to neurodegenerative diseases is tau (microtubule-associate
231 coma (FUS) can form pathogenic inclusions in neurodegenerative diseases like amyotrophic lateral scle
232 es, with immense impact on the perception of neurodegenerative diseases, mental dysfunction, and many
234 action and effects in wild-type or in other neurodegenerative disease models may have an altered imp
235 professional soccer players with known high neurodegenerative disease mortality, hospital admissions
236 (n = 178), AD dementia (n = 121), and other neurodegenerative diseases (n = 99) (April 2017-Septembe
238 cfmtDNA (vCSF-cfmtDNA) in a diverse group of neurodegenerative diseases (NDDs) to determine if the in
239 resemble the cellular pathology of sporadic neurodegenerative diseases (NDs) and how this can be exp
244 asmic transport (NCT) has been implicated in neurodegenerative disease pathogenesis; however, the mec
249 iologically-diverse diseases, including many neurodegenerative diseases, protein misfolding diseases,
250 o provide beneficial effects for age- and/or neurodegenerative disease-related changes in arousal and
251 fic role of immune and inflammatory cells in neurodegenerative diseases remain poorly understood.
252 nhanced, which could lead to improvements in neurodegenerative disease research and engineering of in
254 innate immune system for the development of neurodegenerative diseases, review immune pathway genes
255 N1), a dosage-sensitive gene involved in the neurodegenerative disease spinocerebellar ataxia type 1
256 athogenic protein aggregates associated with neurodegenerative diseases spread from cell to cell thro
258 injury is associated with elevated rates of neurodegenerative diseases such as Alzheimer's disease a
259 nd epilepsy, and has also been implicated in neurodegenerative diseases such as Alzheimer's disease.
261 tory response, derived from tissue trauma or neurodegenerative diseases such as Alzheimer's, causes t
262 rapeutics to people suffering or at risk for neurodegenerative diseases such as Alzheimer's, Parkinso
263 ns in the human PANK2 gene are implicated in neurodegenerative diseases such as pantothenate kinase-a
264 differentiation; however, its involvement in neurodegenerative diseases such as Parkinson's disease (
265 lpha-syn) pathology plays a critical role in neurodegenerative diseases such as Parkinson's disease,
266 ndicate that reduced cfmtDNA is a feature of neurodegenerative diseases such as Parkinson's disease,
267 ider the emerging role of complement in some neurodegenerative diseases, such as Alzheimer disease, a
268 erous proteins that form toxic aggregates in neurodegenerative diseases, such as amyotrophic lateral
269 increase in the prevalence of age-associated neurodegenerative diseases, such as amyotrophic lateral
270 Mutations of proteins in the pathway cause neurodegenerative diseases, suggesting defective mitocho
271 ia overlapped with those identified in other neurodegenerative diseases, suggesting that similar even
274 ers, for early and differential diagnosis of neurodegenerative diseases that can lead to dementia.
275 s a risk factor for the later development of neurodegenerative diseases that may have various underly
276 rontotemporal dementia (FTD) are two related neurodegenerative diseases that present with similar TDP
277 tamine (polyQ) disorders are a group of nine neurodegenerative diseases that share a common genetic c
278 the onset of retinal vascular and even some neurodegenerative diseases, the ability to visualize and
279 ransporter expression is reduced in numerous neurodegenerative diseases, the contributions of transpo
282 ltiple studies have utilized hiPSC models of neurodegenerative diseases to study autophagy and evalua
284 g mechanisms involved in the pathogenesis of neurodegenerative diseases, using both in vivo and in vi
285 open-angle glaucoma (POAG) is a progressive neurodegenerative disease which leads to irreversible bl
286 Huntington's disease (HD) is a monogenetic neurodegenerative disease, which serves as a model of ne
288 report three unrelated children with severe neurodegenerative disease, who carry the same de novo c.
292 a syndrome (CANVAS) is a recently recognized neurodegenerative disease with onset in mid- to late adu
295 au181 differentiated AD dementia from non-AD neurodegenerative diseases with an accuracy similar to t
297 plasma P-tau217 discriminated AD from other neurodegenerative diseases, with significantly higher ac
298 are common among proteins that aggregate in neurodegenerative disease, yet how PTMs impact the aggre
299 bolic dysfunction occurs in many age-related neurodegenerative diseases, yet its role in disease etio
300 xisomal function has been implicated in many neurodegenerative diseases, yet the underlying molecular