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1 eukin-1 receptor (TIR) domain exerts its pro-neurodegenerative action through NADase activity(9,10).
3 ch's ataxia (FRDA) is an autosomal-recessive neurodegenerative and cardiac disorder which occurs when
6 s are dysregulated during the progression of neurodegenerative and muscle degeneration disorders, the
7 nd imaged aluminium in human brain tissue in neurodegenerative and neurodevelopmental disease there a
9 l stimuli can be potentially useful to study neurodegenerative and neurological disorder therapy appl
11 zed research on human diseases, particularly neurodegenerative and psychiatric disorders, making it p
14 n many common diseases, including cancer and neurodegenerative, autoimmune, and metabolic diseases.
17 mechanism, elesclomol prevented detrimental neurodegenerative changes and improved the survival of t
24 diovascular, metabolic, musculoskeletal, and neurodegenerative conditions and various malignancies.
25 icipates in postinjury CNS recovery, chronic neurodegenerative conditions, and even higher brain func
26 sociated with a range of highly debilitating neurodegenerative conditions, including Parkinson's dise
32 yotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease affecting motoneurons (MNs) in
33 arkinson's disease is the second most common neurodegenerative disease after Alzheimer's disease and
34 its implication in the familial form of the neurodegenerative disease amyotrophic lateral sclerosis.
35 on four individuals from three families with neurodegenerative disease and homozygous frameshift muta
36 traits, hindbrain development, vascular and neurodegenerative disease and psychiatric conditions.
37 highlight 4E-BP1 as a therapeutic target in neurodegenerative disease and underscore the importance
39 Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with exposure to co
40 hared with progressive supranuclear palsy, a neurodegenerative disease associated with misfolding of
43 axia type 3 (SCA3) is a dominantly inherited neurodegenerative disease caused by CAG (encoding glutam
45 le in amyotrophic lateral sclerosis (ALS), a neurodegenerative disease characterized by extensive mot
47 t common movement disorder, is a progressive neurodegenerative disease characterized by substantia ni
48 Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the preferent
50 velopment of novel therapies for adult-onset neurodegenerative disease has been impeded by the limita
51 e, we investigate the molecular basis of the neurodegenerative disease hereditary ferritinopathy (HF)
53 nd gender, the OR comparing the odds of each neurodegenerative disease in OAG patients with the odds
56 action and effects in wild-type or in other neurodegenerative disease models may have an altered imp
57 professional soccer players with known high neurodegenerative disease mortality, hospital admissions
58 asmic transport (NCT) has been implicated in neurodegenerative disease pathogenesis; however, the mec
60 nhanced, which could lead to improvements in neurodegenerative disease research and engineering of in
65 a syndrome (CANVAS) is a recently recognized neurodegenerative disease with onset in mid- to late adu
66 STATEMENT Spinal muscular atrophy (SMA) is a neurodegenerative disease, characterized by synaptic los
67 o provide beneficial effects for age- and/or neurodegenerative disease-related changes in arousal and
80 d OR, 2.00; 95% CI, 1.79-2.22; and for other neurodegenerative disease: adjusted OR, 1.79; 95% CI, 1.
81 n cohort 2 for clinical AD dementia vs other neurodegenerative diseases (AUC, 0.96 [95% CI, 0.93-0.98
82 (n = 178), AD dementia (n = 121), and other neurodegenerative diseases (n = 99) (April 2017-Septembe
84 cfmtDNA (vCSF-cfmtDNA) in a diverse group of neurodegenerative diseases (NDDs) to determine if the in
85 resemble the cellular pathology of sporadic neurodegenerative diseases (NDs) and how this can be exp
88 tex microcircuit with the pathophysiology of neurodegenerative diseases affecting motor functions.
91 rstanding of p75NTR in acute brain injuries, neurodegenerative diseases and general response to cellu
92 M106B locus have been implicated in multiple neurodegenerative diseases and in healthy brain ageing.
94 n of central nervous system drug candidates, neurodegenerative diseases and numerous oncology targets
97 ained considerable attention in AD and other neurodegenerative diseases because it has been linked to
98 glycosyltransferases in the pathogenesis of neurodegenerative diseases but differentiating cause fro
99 istinct arrhythmias as well as two different neurodegenerative diseases caused by variants in amyloid
100 ntribute to their enhanced susceptibility to neurodegenerative diseases characterized by aberrant pro
103 nnovative use of this technology in studying neurodegenerative diseases has emerged with the neurosen
106 eful for investigating early stage events in neurodegenerative diseases in both cellular and animal m
107 rs are available to support the diagnosis of neurodegenerative diseases in clinical and research sett
108 ociated with an elevated risk of age-related neurodegenerative diseases including Alzheimer's disease
109 a common feature of proteins associated with neurodegenerative diseases including prion protein (PrPC
110 rphic amyloid fibrils is a common feature in neurodegenerative diseases involving protein aggregation
111 he role of abnormal brain iron metabolism in neurodegenerative diseases is still insufficiently under
112 that is alternatively spliced and linked to neurodegenerative diseases is tau (microtubule-associate
113 fic role of immune and inflammatory cells in neurodegenerative diseases remain poorly understood.
114 injury is associated with elevated rates of neurodegenerative diseases such as Alzheimer's disease a
116 ndicate that reduced cfmtDNA is a feature of neurodegenerative diseases such as Parkinson's disease,
117 s a risk factor for the later development of neurodegenerative diseases that may have various underly
118 rontotemporal dementia (FTD) are two related neurodegenerative diseases that present with similar TDP
119 tamine (polyQ) disorders are a group of nine neurodegenerative diseases that share a common genetic c
121 ltiple studies have utilized hiPSC models of neurodegenerative diseases to study autophagy and evalua
122 au181 differentiated AD dementia from non-AD neurodegenerative diseases with an accuracy similar to t
124 f the protein Tau is involved in a number of neurodegenerative diseases, also known as tauopathies.
125 applied the framework to two representative neurodegenerative diseases, Alzheimer's disease (AD) and
127 anticoagulation, the interaction of ICH with neurodegenerative diseases, and our approach to prognost
128 of diseases including heart disease, cancer, neurodegenerative diseases, and the general aging proces
129 human Msp1 homologue has been implicated in neurodegenerative diseases, and we show that the lack of
130 misfolded proteins potentially underly many neurodegenerative diseases, but individual targets which
132 n Alzheimer's disease and many other related neurodegenerative diseases, collectively referred to as
133 uding infection, traumatic brain injury, and neurodegenerative diseases, has become increasingly evid
134 creasingly implicated in the pathogenesis of neurodegenerative diseases, including ALS caused by a C9
135 nic amino acid that has been associated with neurodegenerative diseases, including amyotrophic latera
136 gregation contributes to the pathogeneses of neurodegenerative diseases, including amyotrophic latera
137 ated proteins have been reported in multiple neurodegenerative diseases, including C9orf72 Amyotrophi
140 deficits in these pathways are implicated in neurodegenerative diseases, including Parkinson's and am
141 ils coalescing into pathologic inclusions in neurodegenerative diseases, including Parkinson's diseas
144 innate immune system for the development of neurodegenerative diseases, review immune pathway genes
145 erous proteins that form toxic aggregates in neurodegenerative diseases, such as amyotrophic lateral
146 Mutations of proteins in the pathway cause neurodegenerative diseases, suggesting defective mitocho
147 the onset of retinal vascular and even some neurodegenerative diseases, the ability to visualize and
148 ransporter expression is reduced in numerous neurodegenerative diseases, the contributions of transpo
149 g mechanisms involved in the pathogenesis of neurodegenerative diseases, using both in vivo and in vi
203 se (HD) is an autosomal dominantly inherited neurodegenerative disorder caused by a CAG repeat expans
204 Huntington's disease (HD) is an inherited neurodegenerative disorder caused by an expanded CAG rep
207 Niemann-Pick type C (NPC) disease is a fatal neurodegenerative disorder caused by mutations in NPC1 a
208 In particular, vps13A mutants result in the neurodegenerative disorder Chorea-Acanthocytosis (ChAc).
210 Parkinson's disease (PD) is a progressive neurodegenerative disorder involving dopaminergic neuron
213 dysfunction has long been implicated in the neurodegenerative disorder Parkinson's disease (PD); how
215 .g. developmental pruning, toxic insult from neurodegenerative disorder), Wallerian degeneration asso
216 ifactorial malady and the second most common neurodegenerative disorder, characterized by loss of dop
217 Alzheimer's disease (AD) is the most common neurodegenerative disorder, resulting in the progressive
218 genesis, and is also mutated in a hereditary neurodegenerative disorder, spinocerebellar ataxia type
220 gestation and in excitatory neurons, whereas neurodegenerative-disorder risk genes showed increasing
223 Lysosome pH (pHlys) is often increased in neurodegenerative disorders and predicted to be decrease
224 ic potential for many neurodevelopmental and neurodegenerative disorders as a consequence of its modu
225 tion in the basal ganglia is associated with neurodegenerative disorders in aging and cognitive defic
227 he frontotemporal dementia (FTD) spectrum of neurodegenerative disorders includes a heterogeneous gro
228 f different microRNAs (miRNAs) is altered in neurodegenerative disorders including tauopathies, a gro
229 ifiers of dosage-sensitive genes involved in neurodegenerative disorders is imperative to discover no
230 D, suggest that the key proteins involved in neurodegenerative disorders such as alpha-synuclein and
232 (ALS) and frontotemporal dementia (FTD) are neurodegenerative disorders that overlap in their clinic
233 MAGMA to five psychiatric disorders and four neurodegenerative disorders to interrogate biological pa
236 differentiate Alzheimer's disease from other neurodegenerative disorders, and identify Alzheimer's di
237 CNS and altered in patients that suffer from neurodegenerative disorders, are orphans from a structur
238 hondrial bioenergetics, as observed in other neurodegenerative disorders, are significantly altered i
239 athophysiology at the earliest stage of some neurodegenerative disorders, but do not have the scalabi
240 a ubiquitous feature associated with several neurodegenerative disorders, especially Alzheimer's dise
241 ters in the differential diagnosis of common neurodegenerative disorders, including Alzheimer disease
242 .21-98.24% across cohorts), as well as other neurodegenerative disorders, including frontotemporal de
243 t is genetically implicated in a spectrum of neurodegenerative disorders, including Kufor-Rakeb syndr
244 vely targeting CB2 hold promise for treating neurodegenerative disorders, inflammation, and pain whil
245 condition has similar heritability to other neurodegenerative disorders, no other genetic risk loci
246 ubunits, as well as CLP1, are known to cause neurodegenerative disorders, yet the mechanisms underlyi
274 ta-Gal) deficiency and clinical onset of the neurodegenerative lysosomal storage disease, GM1 ganglio
275 rates and onset of the progressive and fatal neurodegenerative lysosomal storage disease, GM1 ganglio
276 N3 Batten disease is an autosomal recessive, neurodegenerative, lysosomal storage disease caused by m
277 onal soccer players (n=7676) with known high neurodegenerative mortality and their matched general po
278 rrently underway, across neurodevelopmental, neurodegenerative, muscular dystrophy, epilepsy, chronic
279 ain remained a challenge in the treatment of neurodegenerative (ND) disorders, for these different ap
280 orting the recently suggested dichotomy of a neurodegenerative NPH and a true idiopathic NPH, with th
281 (TDP-43) has emerged as a key player in many neurodegenerative pathologies, including frontotemporal
282 as the source of both neurodevelopmental and neurodegenerative pathology in PNKP-mutated disease, and
283 rent research into how these changes reflect neurodegenerative pathology, and recommendations for fur
285 ns between predicted DNA methylation age and neurodegenerative phenotypes might represent false posit
286 ein 1 (SARM1) is a central regulator of this neurodegenerative process(5-8), and its Toll/interleukin
287 ly for hTET3CD, significantly attenuates the neurodegenerative process, including reduced Abeta accum
294 recognition of individuals who are not in a neurodegenerative prodrome, while greater use of this di
298 SPECT quantitative methods in patients with neurodegenerative syndromes as referenced to neuropathol