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1 0 controls (i.e. patients without structural neurological disease).
2 t are indeed integral to the pathogenesis of neurological disease.
3 as albinism, significant visual disorders or neurological disease.
4 to study astrocyte subtype vulnerability in neurological disease.
5 microtubules, have been discovered to cause neurological disease.
6 ave gained attention as important players in neurological disease.
7 virus strains have also been associated with neurological disease.
8 een patient metadata, brain morphometry, and neurological disease.
9 oted an outbreak of enterovirus A71 (EV-A71) neurological disease.
10 e the varied effects of TBC1D24 mutations in neurological disease.
11 l of aGPCRs as novel therapeutic targets for neurological disease.
12 aII spectrin loss-of-function variants cause neurological disease.
13 during the same epidemic, after the onset of neurological disease.
14 tative diagnosis and systematic treatment of neurological disease.
15 ta-gut-brain communication during health and neurological disease.
16 on of RNAs could be a contributing factor to neurological disease.
17 with an estimated 14% of cases resulting in neurological disease.
18 it is a frequent cause of seizures and other neurological disease.
19 suggest that the TF protein is critical for neurological disease.
20 anism through which many gene variants cause neurological disease.
21 g-AD-H and human AD cortices correlated with neurological disease.
22 investigation and surveillance of suspected neurological disease.
23 the central nervous system (CNS) and severe neurological disease.
24 trains of the CC can produce novel models of neurological disease.
25 ndrome (CANVAS) is a progressive late-onset, neurological disease.
26 pportunistic infection that can cause severe neurological disease.
27 tandem repeat expansions are known to cause neurological disease.
28 ebrile illness, which can progress to severe neurological disease.
29 l function and its disruption contributes to neurological disease.
30 increases in immune-mediated and infectious neurological disease.
31 hrough which altered mTOR signaling leads to neurological disease.
32 ve immune modulatory effects and more severe neurological disease.
33 on real-time PCR analysis despite concurrent neurological disease.
34 ategies for its inhibition in the context of neurological disease.
35 hanges associated with either respiratory or neurological disease.
36 with pathological states in psychiatric and neurological disease.
37 scular disease, cancer, diabetes and chronic neurological diseases.
38 ia dynamics may prevent hyperexcitability in neurological diseases.
39 brain may be a useful strategy for treating neurological diseases.
40 uld shed new light on the pathophysiology of neurological diseases.
41 d into the brain and is disrupted in several neurological diseases.
42 with dysregulation contributing to numerous neurological diseases.
43 ng by pharmacological means for treatment of neurological diseases.
44 day life and especially common in a range of neurological diseases.
45 further inflammation in the brain following neurological diseases.
46 smission and contribute to excitotoxicity in neurological diseases.
47 ausal variants of sQTLs and their associated neurological diseases.
48 ion and devising novel treatment methods for neurological diseases.
49 acted attention due to its promising role in neurological diseases.
50 alterations in Nup genes are linked to human neurological diseases.
51 rrant cell motility is a phenotype for these neurological diseases.
52 ingly recognized as critical determinants of neurological diseases.
53 a therapeutic platform for the treatment of neurological diseases.
54 tochondrial stress contributes to a range of neurological diseases.
55 euronal homeostasis and is perturbed in many neurological diseases.
56 uman pathologies, including inflammatory and neurological diseases.
57 eir therapeutic efficacy in animal models of neurological diseases.
58 cancer and haematological, immunological and neurological diseases.
59 central nervous system (CNS), causing severe neurological diseases.
60 is therapeutic for myriad cardiovascular and neurological diseases.
61 stem-cell-derived cells for the treatment of neurological diseases.
62 at is implicated in the etiology of numerous neurological diseases.
63 nd flow, providing a potential mechanism for neurological diseases.
64 uroprotective compounds for the treatment of neurological diseases.
65 an be used to study the role of microglia in neurological diseases.
66 ential therapeutic drugs to treat a range of neurological diseases.
67 compound associated with cardiovascular and neurological diseases.
68 causal relationships between biomarkers and neurological diseases.
69 pansions within genes is associated with >30 neurological diseases.
70 ging as attractive therapeutic strategies in neurological diseases.
71 sed as a core factor in the etiology of many neurological diseases.
72 or-mediated signalling is linked to numerous neurological diseases.
73 anipulations could lead to new treatments of neurological diseases.
74 d in healthy controls or patients with other neurological diseases.
75 ated for increasing drug or gene delivery in neurological diseases.
76 revious evidence of mtDNA variation in other neurological diseases.
77 amental properties of the nervous system and neurological diseases.
78 anding brain function and the development of neurological diseases.
79 athological conditions, including cancer and neurological diseases.
80 s microRNAs that may serve as biomarkers for neurological diseases.
81 brain have a close relationship with typical neurological diseases.
82 calable, in vivo studies of neurobiology and neurological diseases.
83 nervous system and potential aberrations in neurological diseases.
84 otransmission and are implicated in numerous neurological diseases.
85 lthy control subjects and other inflammatory neurological diseases.
86 and their malfunction that may underlie some neurological diseases.
87 entral to the etiology of a wide spectrum of neurological diseases.
88 isease mechanisms and therapeutic targets in neurological diseases.
89 inactivate the underlying genetic causes of neurological diseases.
90 function in the brain and may play a role in neurological diseases.
91 th and is emerging as a potential target for neurological diseases.
92 ing of aggregate formation by RBP in certain neurological diseases.
93 herefore would be prone to manganese-related neurological diseases.
94 holic fatty liver disease, and diabetes) and neurological diseases.
95 Diencephalic defects underlie an array of neurological diseases.
96 (hMGL) offers a novel approach for treating neurological diseases.
97 er PROs are associated with survival time in neurological diseases.
98 inct neuroanatomic regions during multifocal neurological diseases.
99 osphorylation has been implicated in several neurological diseases.
100 to study normal human brain development and neurological diseases.
101 ron-glial interaction and its alterations in neurological diseases.
102 ing potential treatment strategies for these neurological diseases.
103 reening drug candidates for the treatment of neurological diseases.
104 e pyroptosis in the pathogenesis of multiple neurological diseases.
105 function, and a possible underlying cause of neurological diseases.
106 rain and have roles in brain homeostasis and neurological diseases.
107 thophysiology of epilepsy and possibly other neurological diseases.
108 ions for understanding Parkinson's and other neurological diseases.
109 d can influence the onset and progression of neurological diseases.
110 ance of prenatal brain development to common neurological diseases.
111 t with the potential for clinical benefit in neurological diseases.
112 peutic strategies against CNS infections and neurological diseases.
113 eutical drugs developed for the treatment of neurological diseases.
114 particularly in the oral cavity, may lead to neurological diseases.
115 ith healthy controls and patients with other neurological diseases.
117 (9/50), post-operative paralysis 14% (7/50), neurological diseases 8% (4/50), trauma 2% (1/50) and ot
118 Examples of the application of GT in various neurological diseases alongside clinical development cha
120 tative tools to predict clinical severity of neurological disease and a clinical scale that advances
121 ertiary-level hospital, with suspected acute neurological disease and a history of suspected arbovira
122 % at distances greater than 26 km for severe neurological disease and at distances greater than 7 km
123 EV) is a New World Alphavirus that can cause neurological disease and death in humans and equines fol
124 normobaric 11% O2 from an early age prevents neurological disease and dramatically improves survival
126 suggest a role for astrocyte dysfunction in neurological disease and identify key regions of infecti
127 monstrate promising results as treatment for neurological disease and injury, owing to their innate a
128 -brain barrier breakdown in this complicated neurological disease and opens up alternative approaches
129 id derivatives as new therapeutic agents for neurological disease and, once scaled, enable robust and
130 using mTORC1 inhibitors to treat cancer and neurological disease and, potentially, to improve health
131 iting opportunities for in vitro modeling of neurological diseases and for advancing drug development
133 n finding in patients with complex inherited neurological diseases and may be subclinical or a major
135 In addition, several brain diseases, such as neurological diseases and mood disorders, have deleterio
136 current understanding of the role of EVs in neurological diseases and raise some of the limitations
137 he evidence implicating necroptosis in these neurological diseases and suggest that targeting RIPK1 m
139 T signal, how immune response contributes to neurological disease, and how it might be therapeuticall
140 60 years (range, 61-96 years) with no known neurological disease, and individuals older than 60 year
142 be prognostic for hard clinical outcomes in neurological disease, and supports PROs as a meaningful
144 fection of the nervous system causes various neurological diseases, and synaptic degeneration is like
145 nderpin dysregulated microglia activation in neurological diseases, and we reveal therapeutic targets
149 eporting the vulnerability of hub regions to neurological disease, as well as provide support for can
150 he clinical characteristics of children with neurological disease associated with EV-A71 were compare
151 71 were compared with those of children with neurological disease associated with other enteroviruses
153 g VRAC for the treatment of stroke and other neurological diseases associated with excitotoxicity.
154 PCR) involved in various pathologies such as neurological diseases, autoimmune diseases, and cancers.
155 nt in the brain tissue of individuals before neurological disease becomes overt or serious.IMPORTANCE
156 f low-level ISR activation that may manifest neurological disease but leaves the cytoprotective effec
157 etabolic dysfunction are often implicated in neurological disease, but effective mechanism-based ther
158 abies virus (RABV) causes a severe and fatal neurological disease, but morbidity is vaccine preventab
159 ortant process in both brain development and neurological diseases, but whether neurons express compl
160 negative, Phase II and III trial outcomes in neurological diseases by highlighting examples that illu
161 in terms of broadening the knowledge of many neurological diseases by inducing them on animal models
162 as been associated with an increased risk of neurological disease, cancer and cognitive dysfunction.
164 ance detected 26% (95% CI 18%-33%) of severe neurological disease cases and 18% (95% CI 16%-21%) of f
168 olyneuropathy (FAP) is an autosomal dominant neurological disease, caused most frequently by a Val30M
170 l temporal lobe epilepsy (mTLE) is a chronic neurological disease characterized by recurrent seizures
171 translational CRISPR-based approach to treat neurological diseases characterized by abnormal circuit
172 might explain a breakdown of the DMN in many neurological diseases characterized by declined cognitiv
173 erence compound for H3R in rodent models for neurological diseases connected with neurotransmitter dy
174 into astrocytes are of interest for specific neurological diseases, creating a need for approaches th
175 between March 1 and November 30, 2018, with neurological disease (defined by non-mutually exclusive
176 ross the central nervous system (CNS) during neurological diseases do not address the heterogeneity o
180 ital Colorado were found to have enterovirus neurological disease; EV-A71 was identified in 43 (58%)
181 ge encephalopathy reverses their established neurological disease, evidenced by improved behavior, ci
182 rious genes are the mechanism behind several neurological diseases, found also to act as modifiers fo
183 ny of the molecular fingerprints of a severe neurological disease, globoid cell leukodystrophy, bette
185 ospinal fluid motion; however, their role in neurological diseases has not yet been established.
187 deaths and people with disabilities owing to neurological diseases have risen substantially, particul
188 nal studies of seasonal influenza-associated neurological disease (IAND) and none from the Southern H
189 nal studies of seasonal influenza associated neurological disease (IAND) and none from the Southern h
192 ed by the ZIKV epidemic, but the spectrum of neurological disease in the adults appears broader as ca
194 absence of STAT1, STAT2, or IRF9 exacerbates neurological disease in transgenic mice with CNS product
195 ted in the etiology of an autosomal dominant neurological disease in which patients are heterozygous
199 ided by contrasting these changes with other neurological diseases in which there is also BBB malfunc
200 Dysfunction of this process underlies many neurological diseases including ataxia and the most comm
201 eostasis, and is critically involved in many neurological diseases including brain trauma, epilepsies
202 West Nile virus (WNV) can cause severe human neurological diseases including encephalitis and meningi
203 in the brain accompanies several high-impact neurological diseases including multiple sclerosis (MS),
204 e they are associated with severe hepatitis, neurological disease, including meningitis and encephali
205 implicated in the pathogenesis of almost all neurological diseases, including Alzheimer's disease (AD
206 for the prevention and treatment of several neurological diseases, including Alzheimer's disease.
207 l biological functions and are implicated in neurological diseases, including ataxias, amyotrophic la
208 , and high mortality rates for patients with neurological diseases, including brain cancers and neuro
209 ction contributes to various psychiatric and neurological diseases, including drug addiction and Park
210 from nusinersen that can be applied to other neurological diseases, including method of delivery, dos
212 cause hereditary spastic paraplegia (HSP), a neurological disease involving dying-back degeneration o
213 ic targets for acute stroke injury and other neurological diseases involving capillary flow impairmen
214 lecules and drug candidates for treatment of neurological diseases involving excessive activities of
216 brain tissue of HIV patients without serious neurological disease is consistent with their emergence
217 tic, prognostic and monitoring biomarkers in neurological diseases is progressively increasing, and N
218 nal ER dysfunction is implicated in numerous neurological diseases, its role at nerve terminals is po
221 tiated from iPSCs to study their function in neurological diseases, like Alzheimer's disease (AD).
223 The dog is an unrivalled comparator for neurological disease modeling, however canine brain morp
226 phase transitions is an important driver of neurological diseases, notably amyotrophic lateral scler
227 biogenic amine signaling contribute to human neurological diseases of mood, appetite, and movement.
228 </=4 years; less than half had pre-existing neurological disease or other risk factors for severe in
229 Zinc and ZIP12 may confer resilience against neurological diseases or premature aging of the brain.
234 Patient-derived iPSCs from individuals with neurological diseases predicted disease-specific lack of
236 rove useful not only in MS but also in other neurological diseases presenting inflammatory components
237 iously associated with behavioral processes, neurological disease, psychological disorders, cancer, o
238 s of iron homeostasis in the brain linked to neurological diseases ranging from rare syndromes to mor
239 ells as well as early diagnosis of different neurological diseases related to abnormal levels of dopa
242 ng effective disease-modifying therapies for neurological diseases remains an important challenge in
243 r EVs play a key role in the pathogenesis of neurological diseases remains to be firmly established b
245 tingtin with an expanded polyQ and develop a neurological disease resembling Huntington disease.
246 g in dogs, like humans, might better predict neurological disease risk than patient chronological age
247 ough plasma proteins may serve as markers of neurological disease risk, the molecular mechanisms resp
249 ssense mutations were associated with milder neurological disease severity, but with a higher risk of
251 s such as Alzheimer's disease, but also with neurological diseases sharing pathophysiological pathway
252 non-polio EVs increasingly linked to severe neurological disease such as acute flaccid myelitis (EV-
253 matoid arthritis, and ulcerative colitis and neurological diseases such as amyotrophic lateral sclero
254 ng ZIC2 and SHANK1 which have been linked to neurological diseases such as autism spectrum disorder.
255 uggest that single gene mutations that cause neurological diseases such as epilepsy may affect a surp
258 ide repeats that are responsible for causing neurological diseases such as myotonic dystrophy type 1,
259 ource for stem cell transplantation to treat neurological diseases such as stroke and peripheral nerv
260 ALS, and multiple sclerosis as well as acute neurological diseases such as stroke and traumatic brain
265 xon degeneration contributes to a variety of neurological diseases, such as multiple sclerosis (MS).
266 ibute to increased susceptibility to several neurological diseases, such as multiple sclerosis and Pa
267 n is a critical event in the pathogenesis of neurological diseases, such as Parkinson or Alzheimer.
268 layed AxD after transection and in models of neurological disease, suggesting that inhibiting SARM1 i
269 in the neural underpinnings of cognition and neurological disease susceptibility between species.
270 herapeutic implications for the treatment of neurological diseases that are associated with altered n
271 or functional recovery in patients suffering neurological diseases that involve the subcortical white
272 s a common feature of genetic and idiopathic neurological diseases that thus far have been intractabl
275 active candidates to treat a wide variety of neurological diseases, their survival in immunocompetent
277 ockayne syndrome group B protein (CSB) cause neurological diseases, this unique member of the SWI2/SN
278 open the possibility for novel treatments of neurological diseases through the immune system modulati
282 The median age of the children with EV-A71 neurological disease was 22.7 months (IQR 4.0-31.9), and
283 is (MS) as an example of a complex polygenic neurological disease, we sought to determine whether cer
287 This is relevant in aging and age-related neurological diseases, where neuroinflammation contribut
288 TNR) expansions cause nearly 20 severe human neurological diseases which are currently untreatable.
290 tablishes mutations in CLCN6 associated with neurological diseases, whose spectrum of clinical featur
293 We report an early-onset autosomal-recessive neurological disease with cerebellar atrophy and lysosom
295 phic lateral sclerosis (ALS) is an incurable neurological disease with progressive loss of motor neur
296 loping novel mouse models of virally induced neurological diseases with heterogenous presentation, an
298 mic adeno-associated virus delivery in human neurological diseases with widespread brain lesions.
299 e of two diagnosis categories, RRMS or other neurological disease, with 87% accuracy by leave-one-out
300 , brain-machine interfaces, and treatment of neurological diseases, yet they remain limited in severa