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1 paminergic neuronal system exacerbates motor deficit.
2 ody, suggesting a more generalized attention deficit.
3 object recognition task as a model of memory deficit.
4  a downstream mechanism following peripheral deficit.
5 ues their hippocampal long-term potentiation deficit.
6 atterns associated with autistic-like social deficits.
7 h variations typically associated with brain deficits.
8 w repetitive grooming and social interaction deficits.
9 s toward reducing children's physical growth deficits.
10  important factor underlying these cognitive deficits.
11 ed evidence that obesity can cause cognitive deficits.
12 ments in populations with progressing memory deficits.
13 ted in moderate improvements of sensorimotor deficits.
14 using a frailty index comprised of 47 health deficits.
15 sing new drug target for different cognitive deficits.
16 ron loss, dendritic degeneration, and memory deficits.
17 connectivity that may underlie these hearing deficits.
18  in turn leading to depression and cognitive deficits.
19 aptic F-actin contributes directly to memory deficits.
20 mproved lipopolysaccharide-induced cognitive deficits.
21 av1.3 channels resulted in social behavioral deficits.
22 visual phenotype and the presence of hearing deficits.
23  aged mice was accompanied by spatial memory deficits.
24  is thinking, may contribute to these social deficits.
25 eepiness, depression, anxiety, and cognitive deficits.
26 revent the development of central processing deficits.
27 cognitive assessment resulted in significant deficits.
28 levels of inflammatory cytokines, and memory deficits.
29 combat head trauma-induced chronic cognitive deficits.
30 sing therapeutic approach to treat cognitive deficits.
31  activation, which is associated with memory deficits.
32 lipids, and smoking associate with cognitive deficits.
33 cessive fission and associated mitochondrial deficits.
34 (ID), and frequently presents with attention deficits.
35 tes accounting for these common neurological deficits.
36 ganese levels and parkinsonian-like movement deficits.
37 tivity may mitigate or reverse some of these deficits.
38 ficits (42%) compared with those without any deficits (26%) had worse 6MWD = -109 m (95% confidence i
39            LTx candidates with 2 or 3 muscle deficits (42%) compared with those without any deficits
40 d dibenzoylmethane treatment restored memory deficits, abrogated development of neurological signs, p
41 16)A(+/-) mice showed a significant learning deficit accompanied by reduced spatial map stability and
42      However, diffuse cross-sectional volume deficits across all subfields were found in the more chr
43  priori contrast-based analysis, significant deficits across patient groups (vs controls) were observ
44  durably improves resistant visual attention deficits after brain injury.
45  loss of dendritic spines and rescues memory deficits after TBI.
46 tential therapeutic target to restore memory deficits after TBI.SIGNIFICANCE STATEMENT Traumatic brai
47 p loss produces well-characterized cognitive deficits, although there are large individual difference
48 ncies of chi on temperature, vapour pressure deficit and elevation; and that these same dependencies
49 ical cyclone intensity, the central pressure deficit and the peak near-surface wind speed, is a long-
50  cocaine-exposed sires have memory formation deficits and associated reductions in NMDA receptor-medi
51 isease with patients developing neurological deficits and cardiomyopathy in the long-term, among othe
52               Investigation of neuromuscular deficits and diseases such as SMA, as well as for next g
53 sorder and may lead to their decision-making deficits and excessive worry about everyday problems by
54 mitochondrial fragmentation and distribution deficits and improve mitochondrial function in the CRND8
55 teraction, partly accounted for by cognitive deficits and medication.
56 tes the ischemia-induced brain damage, motor deficits and mortality.
57 pecific cognitive and higher visual function deficits and patients who develop such symptoms early in
58 regulation of a miRNA target and SCZ-related deficits and provide key insights into beneficial LoF mu
59 h drugs were neuroprotective, rescued memory deficits and reduced hippocampal atrophy.
60 omic Ts65Dn mouse model of DS shows synaptic deficits and reproduces the essential cognitive disabili
61 SD) is characterized by social communication deficits and restricted, repetitive patterns of behavior
62 hroughout the brain, leading to intellectual deficits and sensory dysfunction in the fragile X syndro
63  of classic dyslexia, specific comprehension deficit, and language learning disability.
64 nto question the view that motion processing deficits are due to poor reading experience.
65                           Although cognitive deficits are one of the factors most strongly associated
66  may not reflect a global sensory-processing deficit, as has often been reported, but rather a tempor
67 evelopment of CAA, negated short-term memory deficits, as assessed by object-recognition tests, and w
68 e in DBN levels is correlated with cognitive deficits associated with ageing and dementia, it was hyp
69  of this process could contribute to various deficits associated with alcohol dependence.
70 logical, neurophysiological, and behavioural deficits associated with Friedreich's ataxia.
71  design of new treatments for the behavioral deficits associated with nutritional n-3 PUFAs' imbalanc
72 ome die or acquire irreversible neurological deficits before they can respond, and relapses can occur
73 was mostly accounted for by processing speed deficit, but this deficit remained when accounting for w
74 eatment of contour irregularities and volume deficits, but the proposed US Food and Drug Administrati
75 ne remodeling that contributes to behavioral deficits by altering synaptic connections, and RhoA-ROCK
76 ibutes to synaptic dysfunction and cognitive deficits by triggering Abeta and Tau accumulation throug
77                            CF-related growth deficits can be improved via inhibition of HDAC6, furthe
78 ing and protected mice against the metabolic deficits caused by the consumption of a high-fat diet.
79 R potentiators reduce spatial working memory deficits caused by the nonselective NMDAR antagonist ket
80 e relative change in trait value under water-deficit compared with control conditions.
81     Transgenic mice showed less neurological deficit compared with wild-type mice (n=6).
82 eny in primary roots under control and water deficit conditions simulated by polyethylene glycol trea
83                          Significantly, this deficit contributes to the pathophysiology of FXS as the
84 ate [i.e. 35-year mean annual climatic water deficit (CWD)] and competition (i.e. tree basal area) on
85 his treatment prevented pre-synaptic protein deficit, decreased glycogen synthase kinase-3beta (GSK3b
86  may help explain some of the neurocognitive deficits described in these children.
87 compromised during the early stages of motor deficit development.
88 under abiotic constraints such as soil water deficit (drought [D]) and high temperature (heat [H]).
89 , the mass of the surface layer and the mass deficit due to point defects such as impurities and vaca
90                 Importantly, neurobehavioral deficits, E/I imbalance, and histological damage are all
91 nsis exhibits exceptional tolerance to water-deficit environments and is therefore an excellent choic
92 er behavioral and nigrostriatal dopaminergic deficits had developed, rats underwent STN-DBS electrode
93     Protein aggregation and axonal transport deficits have been implicated in the disease.
94 ts circuit reorganizations and gap detection deficits, highlighting the potential for using sound the
95 th autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD) and schizophrenia
96  psychiatric conditions, including attention deficit hyperactivity disorder (ADHD) and substance use
97  mixed on the relationship between attention-deficit hyperactivity disorder (ADHD) and younger relati
98  to the adult outcome of childhood attention deficit hyperactivity disorder (ADHD) could guide novel
99 ive-compulsive disorder (OCD), and attention deficit hyperactivity disorder (ADHD).
100 cluding schizophrenia, depression, attention-deficit hyperactivity disorder and substance abuse disor
101 f monozygotic twins discordant for attention deficit hyperactivity disorder can elucidate mechanisms
102 tes under clinical development for attention deficit hyperactivity disorder, binge eating disorder, c
103  mg/kg, IP) dose-dependently ameliorated PPI deficits, hyperactivity, and risk-taking behaviors, in a
104  disorder (94.2 [1.69]; P = .004), attention-deficit/hyperactivity disorder (96.3 [0.91]; P = .002),
105                                    Attention-deficit/hyperactivity disorder (ADHD) affects 39 million
106                                    Attention-deficit/hyperactivity disorder (ADHD) and bipolar disord
107 as long been effective in treating attention-deficit/hyperactivity disorder (ADHD) and is currently t
108 demonstrated that individuals with attention-deficit/hyperactivity disorder (ADHD) are more likely to
109                                    Attention-deficit/hyperactivity disorder (ADHD) diagnosis is based
110 utism spectrum disorders (ASD) and attention-deficit/hyperactivity disorder (ADHD) frequently co-occu
111            Neuroimaging studies of attention-deficit/hyperactivity disorder (ADHD) have most commonly
112 c differences were associated with attention-deficit/hyperactivity disorder (ADHD) in a recent multi-
113                                    Attention-deficit/hyperactivity disorder (ADHD) is associated with
114                                    Attention-deficit/hyperactivity disorder (ADHD) often persists int
115 er understand the underpinnings of attention-deficit/hyperactivity disorder (ADHD), we targeted the r
116 between atopic dermatitis (AD) and attention-deficit/hyperactivity disorder (ADHD).
117 isting attention problems, such as attention deficit/hyperactivity disorder (ADHD).
118 isk genes have been identified for attention-deficit/hyperactivity disorder (ADHD).
119 ysfunction of which is a factor in attention-deficit/hyperactivity disorder (ADHD).
120 (HR, 0.83 [95% CI, 0.62-1.13]), or attention-deficit/hyperactivity disorder (HR, 0.99 [95% CI, 0.79-1
121           Some conditions, such as attention-deficit/hyperactivity disorder and inpatient well-newbor
122 reatment of insomnia [sleep aids], attention-deficit/hyperactivity disorder drugs, antidepressant dru
123 io [HR], 2.02 [95% CI, 1.80-2.26]; attention-deficit/hyperactivity disorder HR, 2.21 [95% CI, 2.04-2.
124 e and inpatient well-newborn care, attention-deficit/hyperactivity disorder, and asthma among all con
125  disorders in offspring, including attention deficit/hyperactivity disorder, autism, and schizophreni
126 hem and schizophrenia, depression, attention-deficit/hyperactivity disorder, eating disorders, autism
127 or after the exclusion of comorbid attention-deficit/hyperactivity disorder.
128 w for Prodromal Syndromes, and for attention-deficit/hyperactivity, substance-related, and mood disor
129 several studies failed to induce performance deficit implementing this approach.
130                              There was a 30% deficit in (18)F-FDG concentration, which was restored b
131 ation aims to precisely quantify the process deficit in anxious individuals and determine the degree
132 y, it is important to estimate any resulting deficit in biodiversity and functions.
133 eeks of intensified training and mild energy deficit in elite race walkers increases peak aerobic cap
134 emoval of auditory cortex PNNs resulted in a deficit in fear learning and consolidation.
135            The identification of a molecular deficit in HSP in Mecp2 KO neurons provides potentially
136                                         This deficit in HSP is bidirectional because Mecp2 KO neurons
137 ) in the NAc core, TLR4.KO animals exhibit a deficit in low-frequency stimulation-induced NMDAR-depen
138 mster prion strain 263K suffer from a severe deficit in mitochondrial oxygen consumption in response
139 riminate and evaluate the severity of myelin deficit in mouse and rhesus monkey brains.
140          Notably, we identified a pronounced deficit in neuronal adaptation to repetitive whisker sti
141 ool for identification and evaluation myelin deficit in preclinical animals and potentially in para-c
142              Unexpectedly, DeltaXX showed no deficit in replication in vivo in a variety of tissues a
143 ic protein alterations are associated with a deficit in the ability of cerebellar neurons to form syn
144  causes a stimulus-specific and long-lasting deficit in the ability of the conditioned stimulus to be
145 f extracellular d9-choline uptake revealed a deficit in the amount of d9-choline found inside NECL4-d
146 tonomic neuropathy is an early and prominent deficit in the db/db model and have implications for the
147 th the extent of the peripheral visual field deficit in this cohort.
148 SF1 prevents neurodegeneration and locomotor deficits in a Drosophila model of C9ORF72-related diseas
149  However, the mechanism underlying lysosomal deficits in AD remains poorly understood.
150 lating Abeta levels and attenuating synaptic deficits in AD.SIGNIFICANCE STATEMENT beta-Site amyloid
151 risomy 21 contribute significantly to memory deficits in adult life in DS.
152 of such reorganization events during sensory deficits in adulthood.
153  to be responsible for a range of perceptual deficits in amblyopic humans, the neural basis for the e
154 asing brain p62 expression rescues cognitive deficits in APP/PS1 mice, a widely used animal model of
155  of Nrf2 significantly exacerbates cognitive deficits in APP/PS1, without altering gross motor functi
156 uction, which could contribute to behavioral deficits in AS, including motor dysfunction.
157 targeted therapies to help ameliorate social deficits in autism spectrum disorder.
158 e PFC, these alterations could contribute to deficits in behavioral control and decision-making in ad
159 s to and worsens the overall oxidative burst deficits in CF MDMs compared with non-CF MDMs.
160 gs effectively attenuate neural and vascular deficits in chronic and acute mouse models of CCM3 loss
161        Tobacco withdrawal is associated with deficits in cognitive function, including attention, wor
162 rmittent seizures drive persistent cognitive deficits in conditions accompanied by recurrent seizures
163      Diabetic patients experience functional deficits in dark adaptation, contrast sensitivity, and c
164 ns by determining the pathways through which deficits in EAP affect functioning would suggest when an
165  severe hyperglycemia along with significant deficits in echocardiographic measurements.
166 ) reduced in schizophrenia and 2) related to deficits in executive function.
167 om patients treated with bisphosphonates had deficits in fracture toughness, with lower crack-initiat
168 hough previous studies suggest glutamatergic deficits in fronto-striatal brain areas in both disorder
169 ld partially explain the auditory processing deficits in FXS.
170  underlying cause of the auditory processing deficits in FXS.SIGNIFICANCE STATEMENT Fragile X Syndrom
171  A recent hypothesis has suggested that core deficits in goal-directed behavior in obsessive-compulsi
172  prefrontal cortex reverses social dominance deficits in Grn+/- mice, an animal model of frontotempor
173  synapse, which may contribute to perceptual deficits in hearing.
174 ong-term potentiation (LTP), consistent with deficits in hippocampus-mediated behaviors.
175 ubstance use disorders, are characterized by deficits in impulse control, however the relationship be
176 rt inhibitor ALX5407 in the vmPFC alleviated deficits in impulse control.
177 sms of disease leading to neurodevelopmental deficits in infected infants remain undefined, but postu
178 ing barrel cortex neurons, and that eventual deficits in inhibition may have differential effects on
179                                   Behavioral deficits in integrating complex audiovisual stimuli in h
180  a constitutively active Rac3 can rescue the deficits in invadopodium function in Vav2-knockdown cell
181                              We propose that deficits in IP3-mediated Ca(2+) signaling represent a co
182  age < 10 years at diagnosis are at risk for deficits in IQ and PS in the absence of cranial radiatio
183 d with controls, monkeys with VS lesions had deficits in learning to select rewarding images but not
184 anfilippo syndrome, MPS IIIA-D, results from deficits in lysosomal enzymes that specifically degrade
185 been associated with cognitive and emotional deficits in mental illnesses.
186 e and rescues both neurogenic and behavioral deficits in mice lacking TrkB.
187  we were not able to identify any functional deficits in mutations I814T, D933N and N976S located bet
188                                              Deficits in neurite density appear fundamental to abnorm
189 f-function is a possible cause of motivation deficits in neurodegenerative diseases.
190                      Moreover, finding no RC deficits in offspring of BD patients suggest a different
191                     We also observed similar deficits in organoids derived from schizophrenia patient
192 ghly effective symptomatic therapy for motor deficits in Parkinson's disease (PD).
193  Indeed, depression often precedes cognitive deficits in patients with AD.
194 egration and organization and thus cognitive deficits in patients with PD.
195                              Model-predicted deficits in PEEP-dependent lung recruitment correlate wi
196                            Given significant deficits in quality of care, reforms encouraging first c
197 need to address manpower and infrastructural deficits in RI service delivery through the BPHS program
198 n of NMDAR hypofunction to predictive coding deficits in schizophrenia.
199                                   Functional deficits in sensory systems are commonly noted in neurod
200 ted to a transdiagnostic continuum of reward deficits in specific neural networks.
201 , partial hearing loss can produce prolonged deficits in speech perception and temporal processing.
202                         Anxiety is linked to deficits in structural and functional connectivity betwe
203 with frequent exposure to loud music exhibit deficits in suprathreshold auditory performance consiste
204 pathy in Tau-P301S mice but also rescues the deficits in synaptic integrity and plasticity.
205                  Furthermore, stress-induced deficits in synaptic proteins and decreases in dendritic
206                       Findings indicate that deficits in thalamocortical, as well as corticocortical,
207 nses and elicits TS-like sensorimotor gating deficits in the D1CT-7 mouse, one of the best-validated
208 lacentation defects, which result from major deficits in the decidualisation response of the uterine
209 , these findings support the idea that spine deficits in the DLPFC may contribute to subcortical hype
210             These impairments likely reflect deficits in the maintenance of memory representations, n
211 imary cause of pathology, leading to further deficits in the mitochondrial axonal transport and onset
212 ese changes remain unclear, although genetic deficits in the molecular clock regularly render mice wi
213                           Mutant mice showed deficits in the novel object recognition task, suggestin
214 rosopagnosia (DP) is characterised by severe deficits in the recognition of faces, which the many-to-
215                                              Deficits in the salience network suggest an impaired abi
216                         Prefrontal-dependent deficits in the spatiotemporal coordination of NREM slee
217 d impaired sparse coding of information, and deficits in the temporal tuning of neural activity and i
218 plays a crucial role in development and that deficits in this ability may be the reason why preterm i
219 ociations of childhood blood lead level with deficits in verbal comprehension and processing speed we
220              However, the observed cognitive deficits in victimized individuals were largely explaine
221 ese analyses further revealed a continuum of deficits in which BPD showed intermediate levels of CC r
222              Experiment 3 revealed selective deficits in WM contributions and preserved RL value lear
223 ionately reduced in AS mice, indicating that deficits in WM development are a major factor underlying
224 al mechanism through which hypoxia may cause deficits in working memory.
225  in novel object recognition and less severe deficits in Y-maze behaviors.
226                              To address this deficit, in the present study, we established an in vitr
227 A1/A2 AMPARs in the NAc core mediated social deficits, independent of S831-GluA1 phosphorylation.
228 hancing properties and it ameliorated memory deficits induced by scopolamine.
229                                          The deficit irrigation treatment significantly increased pol
230 relationship between the effect of regulated deficit irrigation, cluster, developmental stages and tw
231                                          The deficit is rescued by selectively elevating levels of 2-
232 specific adverse outcomes such as behavioral deficits is a possibility that merits further investigat
233  in cognitive function from cannabis-induced deficits is challenging.
234                                Neurovascular deficits lead over time to impaired neuronal excitabilit
235        The data support a model in which EAP deficits lead to poor functional outcome via impaired co
236 A-tdTHz, we evaluated the severity of myelin deficit lesions in rhesus monkey brain induced by experi
237         Comparisons between number of muscle deficits (low muscle mass, quadriceps strength and physi
238  effects of BAY against Abeta-induced memory deficits might involve the regulation of neuroinflammati
239 ndom drift; predicted effects include energy deficit, muscle weakness, anomalies in cranial and skele
240     To examine whether the general cognitive deficit observed across psychotic disorders is similarly
241 actor contributing to the neurodevelopmental deficits observed in ASD.
242 s much effort with little benefit, through a deficit of ACC dopamine release triggered by high-effort
243     Disorders of water balance, an excess or deficit of total body water relative to body electrolyte
244  this study, we characterized the functional deficits of AIPL1 variations, some of which induce aberr
245 ently and robustly associated with cognitive deficits of ASD and ID in humans, and overexpression of
246 ivities and corrects the synaptotoxicity and deficits of axonal transport induced by Abeta.
247                        In addition, acquired deficits of multiple Ca(2+)-handling proteins can contri
248           Early detection of the behavioural deficits of neurodegenerative diseases may help to descr
249 ion in human cells, and it causes cell-cycle deficits of radial glial cells in the embryonic mouse co
250  DDC gene, bas-1, ameliorated the behavioral deficits of tau transgenic worms, reduced phosphorylated
251 SZ offspring were found to show connectivity deficits of the brain's central rich club (RC) system re
252                                       Volume deficits of the hippocampus in schizophrenia have been c
253 category score of 1 (mild or no neurological deficit) or 2 (moderate cerebral disability) was conside
254 potential, soil moisture, and vapor pressure deficit over 2 yr in the Northern Rocky Mountains, USA.
255 tical stroke often leads to persistent motor deficits, prompting the need for more effective interven
256 ve function was assessed using the Perceived Deficits Questionnaire (PDQ).
257 ) drove akinesia, whereas movement execution deficits reflected the ratio of AMPARs in D2 versus D1 c
258 respect to social communication and language deficits relative to those with ASD with no identified g
259 ed for by processing speed deficit, but this deficit remained when accounting for working memory (Coh
260 ons (i.e. hypervigilance and impulse control deficits, respectively).
261  these neurons can compensate for behavioral deficits resulting from midbrain dopamine dysfunction.
262                The behavioral and anatomical deficits seen in fragile X syndrome (FXS) are widely bel
263 y lentiviral RNA interference reproduced the deficits seen in P311(-/-) mice.
264 n-deficient lines developed social dominance deficits similar to those in global Grn+/- mice, showing
265 ol conditions, 106 were detected under water-deficit stress, and 76 were detected for trait plasticit
266  thought to give rise to auditory perception deficits such as temporal processing impairments, hypera
267 er from a larger open circuit voltage (VOC ) deficit than narrower bandgap ones.
268                     Patients with a clinical deficit that is disproportionately severe relative to th
269 eukemia (ALL) are at risk for neurocognitive deficits that are associated with treatment, individual,
270 ain and underlie the mPFC-specific cognitive deficits that are comorbid with neuropathic pain.SIGNIFI
271 he authors demonstrate that axonal transport deficits that are observed in these cells can be rescued
272  patients with kidney disease have olfactory deficits that may influence their nutritional status.
273 5 despite the profound vestibular functional deficits that persist with treatment at this later time.
274 ividuals were largely explained by cognitive deficits that predated childhood victimization and by co
275   Schizophrenia is associated with cognitive deficits that reflect impaired cortical information proc
276  and related agonists for treating cognitive deficits, these data suggest that daily dosing may be cr
277 ases in oxidative damage and cellular energy deficits; these, in turn, impair mitophagy.
278 - and high-yielding regions, the contributed deficit to national production caused by increasing temp
279 ion of alphaLNNd can overcome polymerization deficits to increase laminin, stabilize BM structure, an
280 y more stable to expression changes by water deficit treatment than other genotype-specific expressio
281                            We addressed this deficit using principles of receptor silent substitution
282                      The increased locomotor deficit was associated with specific reduction in striat
283 al gap detection thresholds (GDTs), but this deficit was fully reversed by three 1 h sessions of expo
284  mice compared to control db/+ mice and this deficit was greater compared to reductions in intraepide
285             In schizophrenia, working memory deficit was mostly accounted for by processing speed def
286 58F, hDAT-G327R, and hDAT-L368Q, the folding deficit was remedied with the pharmacochaperone noriboga
287                         Acclimation to water deficit (WD) enables plants to maintain growth under unf
288                                   The memory deficits we observed in mouse prion disease were complet
289 e to spatial and temporal variation in water deficit, we analyze data from three forest dynamics plot
290                              To address this deficit, we generated samples of a wild-type GPCR (A2AR)
291 NMN can impact developmentally-set metabolic deficits, we compared treadmill exercise and NMN injecti
292 d that annual rainfall and accumulated water deficit were the main drivers of the distribution of tre
293                                        These deficits were accompanied by pronounced hippocampal atro
294                                 Finally, PPI deficits were exacerbated by allopregnanolone (10 mg/kg,
295                    Life expectancy gains and deficits were further disaggregated by age and cause of
296                                              Deficits were largely restricted to visual decisions.
297 orsened by a mean (SD) 2.5 (1.9) points, and deficits were limited to a single NIHSS item in 62 episo
298  that RTT-derived neurons have many cellular deficits when compared to control, such as: less synapse
299    Lentiviral transfer of P311 corrected the deficits, whereas down-regulation of P311 levels by lent
300 ether these changes are related to cognitive deficits, which have been described in ET patients.

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