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1 primed to provide specialized insights into neurological disease.
2 tropic flavivirus that can cause significant neurological disease.
3 , providing important new insight into human neurological disease.
4 romising target for treating psychiatric and neurological disease.
5 o endothelia and thrombocyte dysfunction and neurological disease.
6 on of RNAs could be a contributing factor to neurological disease.
7 ys an essential role in preventing a complex neurological disease.
8 herapy may offer a cure for this devastating neurological disease.
9 gands could lead to novel therapies to treat neurological disease.
10 l new model to understand corticogenesis and neurological disease.
11 es that have linked autophagy disruption and neurological disease.
12 en capable of causing lethal respiratory and neurological disease.
13 atory disease, abortion, and, in some cases, neurological disease.
14 7+/-9.7 years) and no history of dementia or neurological disease.
15 induced immune response in the generation of neurological disease.
16 with an estimated 14% of cases resulting in neurological disease.
17 een in the development of in vitro models of neurological disease.
18 understanding of aberrant gene expression in neurological disease.
19 g proteins were specifically associated with neurological disease.
20 tative diagnosis and systematic treatment of neurological disease.
21 ential of ASOs as a source of drugs to treat neurological disease.
22 entists, due to associated newborn and adult neurological disease.
23 opment and plasticity of neural circuits and neurological disease.
24 ion in mammalian brain and are implicated in neurological disease.
25 to treat disease, with specific attention to neurological disease.
26 itochondrial dynamics are emerging causes of neurological disease.
27 function in cells and cause or contribute to neurological disease.
28 ppressed the incidence of retrovirus-induced neurological disease.
29 it is a frequent cause of seizures and other neurological disease.
30 LMNB1-related ADLD is a slowly progressive neurological disease.
31 ed clinical DENV isolate without evidence of neurological disease.
32 the central nervous system (CNS) and severe neurological disease.
33 hanism for suppression of retrovirus-induced neurological disease.
34 potential clinical approach for treatment of neurological disease.
35 suggest that the TF protein is critical for neurological disease.
36 SC)-derived neural cells in animal models of neurological disease.
37 ypical imaging data and 165 controls without neurological disease.
38 patients with difficulty traveling owing to neurological disease.
39 f homeostatic signaling and genetic links to neurological disease.
40 applied to studies of neuronal function and neurological disease.
41 g to the brain and reduce retrovirus-induced neurological disease.
42 anism through which many gene variants cause neurological disease.
43 ta-gut-brain communication during health and neurological disease.
44 g-AD-H and human AD cortices correlated with neurological disease.
45 investigation and surveillance of suspected neurological disease.
46 the central nervous system (CNS) and severe neurological disease.
47 trains of the CC can produce novel models of neurological disease.
48 rstanding diverse astrocyte contributions to neurological disease.
49 connections to the causes and progression of neurological disease.
50 nd oxidative stress are hallmarks of various neurological diseases.
51 w drug design in cancer, cardiovascular, and neurological diseases.
52 or-mediated signalling is linked to numerous neurological diseases.
53 en leads to repeat expansion associated with neurological diseases.
54 for modulating neural function and treating neurological diseases.
55 t expansions cause at least twelve inherited neurological diseases.
56 infection may exacerbate MS as well as other neurological diseases.
57 ts in lipid regulation are linked to various neurological diseases.
58 n the human DYNC1H1 gene are associated with neurological diseases.
59 ystem could be useful to treat spasticity in neurological diseases.
60 signaling may contribute to a broad range of neurological diseases.
61 red, when using high doses in rat models for neurological diseases.
62 l generation have been found to cause severe neurological diseases.
63 erapeutic potential for neuroinflammation in neurological diseases.
64 sed as a core factor in the etiology of many neurological diseases.
65 brain function and the pathogenesis of many neurological diseases.
66 cal channelopathies can cause many different neurological diseases.
67 aberrant spine morphology is linked to many neurological diseases.
68 developing effective antibody therapies for neurological diseases.
69 oskeleton in neurons have been implicated in neurological diseases.
70 ticulum (ER) stress are associated with many neurological diseases.
71 the better we understand what goes wrong in neurological diseases.
72 anipulations could lead to new treatments of neurological diseases.
73 es to the cognitive deficits associated with neurological diseases.
74 rived neurons towards modeling complex human neurological diseases.
75 mplications for other RBP-associated genetic neurological diseases.
76 e function, and their association with other neurological diseases.
77 f mutations in aminoacyl-tRNA synthetases in neurological diseases.
78 precede or hasten the progression of several neurological diseases.
79 d in healthy controls or patients with other neurological diseases.
80 n development and regenerative approaches to neurological diseases.
81 e age-like effects of brain injury and other neurological diseases.
82 ated for increasing drug or gene delivery in neurological diseases.
83 h patients who have both hypopituitarism and neurological diseases.
84 and underlie the subtype specificity of many neurological diseases.
85 of neurodegeneration implicated in numerous neurological diseases.
86 ent to the brain is associated with multiple neurological diseases.
87 vated in macrophages that respond to various neurological diseases.
88 unds that have been associated with numerous neurological diseases.
89 revious evidence of mtDNA variation in other neurological diseases.
90 for the screening of BBB-targeting drugs in neurological diseases.
91 amental properties of the nervous system and neurological diseases.
92 displays therapeutic efficacy toward various neurological diseases.
93 vels could underlie cognitive dysfunction in neurological diseases.
94 g the importance of fatty-acid metabolism in neurological diseases.
95 anding brain function and the development of neurological diseases.
96 athological conditions, including cancer and neurological diseases.
97 s microRNAs that may serve as biomarkers for neurological diseases.
98 brain have a close relationship with typical neurological diseases.
99 calable, in vivo studies of neurobiology and neurological diseases.
100 nervous system and potential aberrations in neurological diseases.
101 otransmission and are implicated in numerous neurological diseases.
102 lthy control subjects and other inflammatory neurological diseases.
103 ging as attractive therapeutic strategies in neurological diseases.
104 and their malfunction that may underlie some neurological diseases.
105 entral to the etiology of a wide spectrum of neurological diseases.
106 inactivate the underlying genetic causes of neurological diseases.
107 function in the brain and may play a role in neurological diseases.
108 sed as a core factor in the etiology of many neurological diseases.
109 th and is emerging as a potential target for neurological diseases.
110 ing of aggregate formation by RBP in certain neurological diseases.
111 herefore would be prone to manganese-related neurological diseases.
112 holic fatty liver disease, and diabetes) and neurological diseases.
113 Diencephalic defects underlie an array of neurological diseases.
114 er PROs are associated with survival time in neurological diseases.
115 inct neuroanatomic regions during multifocal neurological diseases.
116 herapeutic or diagnostic agents against many neurological diseases.
117 ypothesis underlying the development of many neurological diseases.
118 for humans but also are common therapies for neurological diseases.
120 niae infection, but also in patients without neurological disease (8% vs 9%; p = 0.87), whereas anti-
123 % at distances greater than 26 km for severe neurological disease and at distances greater than 7 km
124 with a wide variety of conditions, of which neurological disease and brain lesions represent a subst
126 normobaric 11% O2 from an early age prevents neurological disease and dramatically improves survival
128 suggest a role for astrocyte dysfunction in neurological disease and identify key regions of infecti
129 cargo-motor assemblies contributes to human neurological disease and provide insight into the influe
130 HL1 were found to play critical roles in the neurological disease and PSMA1, PSMA3, PSMC2, PSMD11, an
131 interferon receptor (Ifnar1(-/-)) developed neurological disease and succumbed to ZIKV infection, wh
132 using mTORC1 inhibitors to treat cancer and neurological disease and, potentially, to improve health
135 loidogenic protein is implicated in multiple neurological diseases and capable of generating a number
136 on and are associated with a large number of neurological diseases and disorders, as well as parasiti
138 nson's disease (PD) is among the most common neurological diseases and is best known for its adverse
139 the critical role of autophagy in preventing neurological diseases and maintaining neuronal health.
140 n finding in patients with complex inherited neurological diseases and may be subclinical or a major
141 ocesses, and neuronal death are hallmarks of neurological diseases and retinal degenerations, we test
142 lar distribution are associated with several neurological diseases and we demonstrate that AQP4 clust
143 oping serious comorbidities, such as cancer, neurological disease, and atherosclerosis, suggesting th
144 provide insights into brain development and neurological disease, and enable discovery and developme
146 break of febrile illness, is associated with neurological disease, and has spread across the Pacific
147 60 years (range, 61-96 years) with no known neurological disease, and individuals older than 60 year
148 be prognostic for hard clinical outcomes in neurological disease, and supports PROs as a meaningful
149 ued drug targets, with relevance for several neurological diseases, and a number of allosteric modula
150 n barrier is a pathological hallmark of many neurological diseases, and the resulting multiple drug r
153 nction, inflammatory diseases/processes, and neurological diseases are enhanced in the substantia nig
154 ng and the few applications in patients with neurological diseases are limited to case reports and qu
158 d respiratory disease and increased terminal neurological disease associated with altered in vitro in
159 sed by TMEV and identify new models of human neurological diseases associated with antecedent infecti
160 approach for the prevention and treatment of neurological diseases associated with DHA deficiency, su
161 y, several KICSTOR components are mutated in neurological diseases associated with mutations that lea
162 , we find that Mdm1 truncations analogous to neurological disease-associated SNX14 alleles fail to te
163 nt in the brain tissue of individuals before neurological disease becomes overt or serious.IMPORTANCE
164 cells are critical tools for studying human neurological diseases by allowing one to study the effec
165 as been associated with an increased risk of neurological disease, cancer and cognitive dysfunction.
166 ospholipase D (PLD) superfamily is linked to neurological disease, cancer, and fertility, and a recen
167 argely representative of all cases; however, neurological disease cases aged <5 y or from the lowest
168 ance detected 26% (95% CI 18%-33%) of severe neurological disease cases and 18% (95% CI 16%-21%) of f
170 The cultural impact of rabies, the fatal neurological disease caused by infection with rabies vir
171 onia type 1 (DYT1) is a dominantly inherited neurological disease caused by mutations in TOR1A, the g
172 eral sclerosis (ALS) is a fatal, adult-onset neurological disease characterized by a progressive dege
173 ary familial brain calcification (PFBC) is a neurological disease characterized by calcium phosphate
174 ilial Danish dementia (FDD) are degenerative neurological diseases characterized by amyloid pathology
175 might explain a breakdown of the DMN in many neurological diseases characterized by declined cognitiv
176 cinations were more common in the group with neurological disease compared to the psychiatric, struct
177 erence compound for H3R in rodent models for neurological diseases connected with neurotransmitter dy
178 (51 male, 33 female, and 7 not recorded), 34 neurological disease control individuals (19 male and 15
179 postulated in relation to symptomatology and neurological disease course, but lacks experimental conf
181 interferon receptor knockout mice, including neurological disease development and high mortality.
183 ross the central nervous system (CNS) during neurological diseases do not address the heterogeneity o
185 te the urgent need for better treatments for neurological diseases, drug development for these devast
186 tudy of 61 children with enterovirus-related neurological disease during a 2013 outbreak of EV71 in S
188 ge encephalopathy reverses their established neurological disease, evidenced by improved behavior, ci
189 nding of the characteristics of EV71-related neurological disease, factors related to outcome, and po
192 cute flaccid myelitis (AFM) is a devastating neurological disease for which there are no treatments o
193 models enable cross-mammalian comparison of neurological disease from core cellular pathophysiology
194 nal studies of seasonal influenza-associated neurological disease (IAND) and none from the Southern H
195 nal studies of seasonal influenza associated neurological disease (IAND) and none from the Southern h
200 e brain could explain the absence of primary neurological disease in Hutchinson-Gilford progeria synd
201 mportant human pathogen that causes a severe neurological disease in immunocompromised individuals.
203 ed by the ZIKV epidemic, but the spectrum of neurological disease in the adults appears broader as ca
204 absence of STAT1, STAT2, or IRF9 exacerbates neurological disease in transgenic mice with CNS product
208 nd, foot, and mouth disease (HFMD) and fatal neurological diseases in infants and young children due
210 conducted at a tertiary referral center for neurological diseases in Rio de Janeiro, Brazil, between
211 ided by contrasting these changes with other neurological diseases in which there is also BBB malfunc
213 eostasis, and is critically involved in many neurological diseases including brain trauma, epilepsies
214 West Nile virus (WNV) can cause severe human neurological diseases including encephalitis and meningi
216 in the brain accompanies several high-impact neurological diseases including multiple sclerosis (MS),
217 links perturbations in the gut microbiota to neurological disease, including disease risk, activity,
218 l biological functions and are implicated in neurological diseases, including ataxias, amyotrophic la
219 r injury that is a precursor for a number of neurological diseases, including cerebral palsy (CP) and
220 ction contributes to various psychiatric and neurological diseases, including drug addiction and Park
221 these molecules are associated with various neurological diseases, including genetic diseases leadin
224 ies aimed at addressing the role of CXCR3 in neurological diseases indicate potent, but diverse, func
225 cause hereditary spastic paraplegia (HSP), a neurological disease involving dying-back degeneration o
226 ic targets for acute stroke injury and other neurological diseases involving capillary flow impairmen
227 brain tissue of HIV patients without serious neurological disease is consistent with their emergence
229 werful means to study neuronal diversity and neurological disease is to establish methods to produce
230 lid mouse models of slowly progressing human neurological diseases is challenging, not least because
231 rticular its cellular regulation and role in neurological disease, is an area of expanding interest.
232 nal ER dysfunction is implicated in numerous neurological diseases, its role at nerve terminals is po
233 spiratory disease; however, there was severe neurological disease leading to 60% mortality, and the s
234 tiated from iPSCs to study their function in neurological diseases, like Alzheimer's disease (AD).
236 teracts with biological membranes to promote neurological disease might lead to the identification of
237 ral cell types that can be generated and the neurological disease modeling studies that have been rep
241 biogenic amine signaling contribute to human neurological diseases of mood, appetite, and movement.
243 sorganization is a prominent feature of many neurological diseases of the CNS, including Parkinson's
245 d </=4 years; less than half had preexisting neurological disease or other risk factors for severe in
246 </=4 years; less than half had pre-existing neurological disease or other risk factors for severe in
248 ssociation with dermatological, systemic and neurological diseases, or be the side effect of certain
249 ough the burden of more prevalent and severe neurological disease poses public health and clinical ch
250 rove useful not only in MS but also in other neurological diseases presenting inflammatory components
252 iously associated with behavioral processes, neurological disease, psychological disorders, cancer, o
253 s of iron homeostasis in the brain linked to neurological diseases ranging from rare syndromes to mor
255 , this mechanism might also be important for neurological diseases related to episodic ataxia, such a
256 lop or identifying diagnostic indicators for neurological diseases require the in-depth analysis of n
257 tingtin with an expanded polyQ and develop a neurological disease resembling Huntington disease.
258 act (LUT) dysfunction is a common sequela of neurological disease, resulting in symptoms that have a
259 d spinal cord and play a pivotal role in the neurological disease state of chronic pain, which is cau
261 ues, metastatic cancer, and inflammatory and neurological diseases such as Alzheimer's and Parkinson'
265 ng ZIC2 and SHANK1 which have been linked to neurological diseases such as autism spectrum disorder.
266 Dysregulation of synaptic genes results in neurological diseases such as autism spectrum disorders
267 the treatment of sleep disruption and other neurological diseases such as epilepsy and depression, n
268 uggest that single gene mutations that cause neurological diseases such as epilepsy may affect a surp
272 ause of triplet repeat expansions that cause neurological diseases such as Huntington disease and myo
273 f pathomechanisms that is relevant to common neurological diseases such as migraine and epilepsy.
274 legitimate stem cell research for incurable neurological diseases such as multiple sclerosis and amy
275 potentially be interesting for treatment of neurological diseases such as schizophrenia, Parkinson's
277 interpret the sensory processing deficits in neurological diseases, such as focal dystonia and Parkin
278 ons, including microcephaly and other severe neurological diseases, such as Guillain-Barre syndrome.
280 xon degeneration contributes to a variety of neurological diseases, such as multiple sclerosis (MS).
282 or functional recovery in patients suffering neurological diseases that involve the subcortical white
283 cell-to-cell signaling and interaction" and "neurological disease." The functional enrichment tool DA
284 RNA processing is increasingly implicated in neurological diseases, these approaches will continue to
285 open the possibility for novel treatments of neurological diseases through the immune system modulati
286 ese discoveries link two clinically distinct neurological diseases to the same gene, however, ATP1A3
288 ties, from a US tertiary referral center for neurological diseases using multiple conventional molecu
290 e whether C9ORF72 haploinsufficiency induces neurological disease, we created a C9orf72-deficient mou
291 is (MS) as an example of a complex polygenic neurological disease, we sought to determine whether cer
294 s resulted in susceptibility to LACV-induced neurological disease, whereas postinfection treatment wi
295 incidence and kinetics of retrovirus-induced neurological disease, which correlated with a significan
296 in gene expression and the potential risk of neurological disease, which is beneficial in the prevent
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
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