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1 1 (CB1R) inhibitors, which are devoid of the neuropsychiatric adverse effects observed with brain-pen
4 s (NPS) that mimic the effects of controlled neuropsychiatric and illicit drugs have been forensicall
5 that appear to be selectively vulnerable to neuropsychiatric and neurodegenerative diseases, althoug
7 dence suggests that MECP2 may underlie other neuropsychiatric and neurological conditions, and perhap
8 may be a cross-diagnostic feature of several neuropsychiatric and neurological disorders in which dop
10 had a more complex phenotype with additional neuropsychiatric and/or developmental comorbidities.
11 vidence base for the treatment of cognitive, neuropsychiatric, and motor symptoms in patients with Le
18 aco-resistant and 60% are affected by severe neuropsychiatric comorbid conditions, including impairme
20 disorders in Parkinson's disease are common neuropsychiatric complications associated with dopamine
24 eurological (conversion) disorder (FND) is a neuropsychiatric condition whereby individuals present w
25 20), and we observed novel correlations with neuropsychiatric conditions (P-values < 7.9 x 10-4).
26 effects of therapies for sleep disorders on neuropsychiatric conditions and also secondarily conside
27 connections between cognitive impairments in neuropsychiatric conditions and in the human population
29 From the clinical perspective, a number of neuropsychiatric conditions are defined by the presence
31 To the extent that sleep problems affect neuropsychiatric conditions, it may be possible to addre
32 implicated in both PTSD and highly comorbid neuropsychiatric conditions, such as anxiety and depress
33 a commonly disrupted intracellular target in neuropsychiatric conditions, whether it be via alteratio
41 otein; and maladaptive avoidance behavior in neuropsychiatric conditions.(2-5) Unlike fear, pathologi
42 ic factor (BDNF) have been linked to cancer, neuropsychiatric, diabetes, and gynecological disorders.
43 hypotheses derived from prior research into neuropsychiatric disease and cancer, gliomas may be expe
44 esults support the "dimensional" approach to neuropsychiatric disease classification and suggest pote
46 is population is exceptionally vulnerable to neuropsychiatric disease presentation during the hormona
48 n reside in open chromatin, we reasoned that neuropsychiatric disease risk variants may affect chroma
49 traits ranging from Parkinson's disease and neuropsychiatric disease to cardiovascular and metabolic
50 y to developing schizophrenia, a devastating neuropsychiatric disease with high heritability but few
51 tal pathway and how its dysfunction leads to neuropsychiatric disease, we developed a method to conve
52 neural substrates for the pathophysiology of neuropsychiatric disease-associated cognitive dysfunctio
53 gion-specific mutations in Neurexin1alpha, a neuropsychiatric disease-associated synaptic molecule, i
62 oup, with variable overlap between different neuropsychiatric diseases and heterogeneously expressed
63 erentiation, and its dysregulation can cause neuropsychiatric diseases and increase cancer severity.
64 understanding of the heterogeneous nature of neuropsychiatric diseases and overcome existing bottlene
65 orrelate with impulsive behaviour in several neuropsychiatric diseases and there is post-mortem evide
66 Motor stereotypies occurring in early-onset neuropsychiatric diseases are associated with dysregulat
67 in the SHANK3 human gene leads to different neuropsychiatric diseases including Autism Spectrum Diso
68 the contribution of genetic risk factors to neuropsychiatric diseases is limited to abnormal neurode
71 k "attractors" could be a defining aspect of neuropsychiatric diseases such as schizophrenia, represe
73 tion is characteristically impaired in major neuropsychiatric diseases, emphasizing its interest for
76 en recently linked to neurodevelopmental and neuropsychiatric diseases, suggesting a role for RNA reg
80 Tourette syndrome (TS) is a childhood-onset neuropsychiatric disorder characterized by repetitive mo
84 -compulsive disorder (OCD) is a debilitating neuropsychiatric disorder with a genetic risk component,
87 e and epigenome, with disruptions in several neuropsychiatric disorder-associated pathways and gene f
91 This work demonstrates increased rates of neuropsychiatric disorders [e.g., increased autism spect
93 ned aggression is characteristic of multiple neuropsychiatric disorders and can have various negative
95 has been implicated in a surprising range of neuropsychiatric disorders and cognitive and affective f
96 dings of human postmortem genomic studies of neuropsychiatric disorders and comparable animal models
98 based on large-scale GWAS data for different neuropsychiatric disorders and cortical brain measures,
99 fects in pathways previously associated with neuropsychiatric disorders and indications of interactio
100 ociations between T.gondii and various human neuropsychiatric disorders and outline how these may be
101 prenatal brain in susceptibility to various neuropsychiatric disorders and prioritize potential risk
102 creasingly associated with a wide variety of neuropsychiatric disorders and, more recently, causal fr
103 Neurodegenerative, neurodevelopmental and neuropsychiatric disorders are among the greatest public
106 Conditional analysis reveals that distinct neuropsychiatric disorders associate with distinct sets
108 ovide potential targets for the treatment of neuropsychiatric disorders characterized by cognitive in
109 alanin has been implicated in stress-related neuropsychiatric disorders in humans and rodent models.
110 s its relationship to novel therapeutics for neuropsychiatric disorders in humans, and conclude by re
112 l affiliation are central features of severe neuropsychiatric disorders including autism spectrum dis
113 n being considered as a therapeutic for many neuropsychiatric disorders including depression, anxiety
114 le promise as a therapeutic intervention for neuropsychiatric disorders including depression, anxiety
115 s also associated with an increased risk for neuropsychiatric disorders including schizophrenia and a
116 could lead to novel treatment strategies for neuropsychiatric disorders involving OFC dysfunction.
117 ment and sex to impart risk for multifaceted neuropsychiatric disorders is also unlikely to be unders
118 nical studies indicate it is dysregulated in neuropsychiatric disorders like autism and addiction, ma
119 ns and have also been implicated in multiple neuropsychiatric disorders like fragile X syndrome, auti
120 des could explain the neurodevelopmental and neuropsychiatric disorders observed in mice and humans w
122 ric history, medication or family history of neuropsychiatric disorders predicted cognitive and/or be
123 jority of common risk alleles identified for neuropsychiatric disorders reside in noncoding regions o
124 relationships, and test whether dystonia and neuropsychiatric disorders share a genetic relationship.
125 ompared with subcortical findings from other neuropsychiatric disorders studied by the ENIGMA consort
126 mber of the GPCR family and is implicated in neuropsychiatric disorders such as anxiety and depressio
127 rant genetic risk variants for developmental neuropsychiatric disorders such as schizophrenia (SCZ) a
128 is an important target for the treatment of neuropsychiatric disorders such as schizophrenia and Par
130 considerable progress has been made linking neuropsychiatric disorders to genetic underpinnings.
132 es, from the synaptic to the behavioural, in neuropsychiatric disorders where decision-making biases
133 dical challenges in cancer, neurological and neuropsychiatric disorders, and infectious, chronic infl
134 ades the broad role of opioids in addiction, neuropsychiatric disorders, and pain states has been som
135 ship between ciliary protein dysfunction and neuropsychiatric disorders, for e.g. interconnections of
136 ns are implicated in the pathology of severe neuropsychiatric disorders, for which effective treatmen
137 3.3 microdeletion is associated with several neuropsychiatric disorders, including autism and schizop
139 sregulation is a hallmark symptom of several neuropsychiatric disorders, including generalized anxiet
140 exposure towards increased vulnerability to neuropsychiatric disorders, including posttraumatic stre
141 (MIA) is a proposed risk factor for multiple neuropsychiatric disorders, including schizophrenia.
142 alience network (SN) is dysregulated in many neuropsychiatric disorders, including substance use diso
143 (MFC) centrally implicated in several major neuropsychiatric disorders, it is critical to understand
144 lap between MND, frontotemporal dementia and neuropsychiatric disorders, particularly mood disorders.
145 has been associated with a broad spectrum of neuropsychiatric disorders, prompting investigations int
146 ted in multiple human neurodevelopmental and neuropsychiatric disorders, such as autism, schizophreni
147 ation of the human brain serotonin system in neuropsychiatric disorders, such as major depression and
149 cated across multiple neurodevelopmental and neuropsychiatric disorders, there has been considerable
150 m of severity in striatal dysfunction across neuropsychiatric disorders, where dysfunction was most s
151 rms an important framework for understanding neuropsychiatric disorders, which are proposed to be the
152 e results have implications for treatment of neuropsychiatric disorders, which may be characterized b
153 Dysregulation of inhibition can lead to neuropsychiatric disorders, yet little is known about th
154 this approach to GWAS data from two related neuropsychiatric disorders-autism spectrum disorder and
206 es across patients diagnosed with four major neuropsychiatric disorders: autism spectrum condition (A
207 idered as a promising therapeutic target for neuropsychiatric disorders; its pharmacology, however, r
209 well as stress-related and stress-inducible neuropsychiatric endophenotypes in both man and mouse.
214 e current clinical guidelines, together with neuropsychiatric features, such as hallucinations and de
216 n-based study, we aimed to determine whether neuropsychiatric history, medication or family history o
222 s for sleep disorders have direct effects on neuropsychiatric illnesses that may be unrelated to thei
226 findings identify a mechanistic substrate of neuropsychiatric impairment after STN-DBS and suggest th
227 a chronic syndrome of recurrent seizures and neuropsychiatric impairment as well as inflammation of l
228 splasia and other symptoms of MAS, including neuropsychiatric impairments, are associated with increa
231 red, fully structured, or Mini International Neuropsychiatric Interview (MINI) diagnostic interviews
232 ression assessed with the Mini International Neuropsychiatric Interview depression module, taking ant
233 ADNC/LATE-NC was associated with lower total Neuropsychiatric Inventory and agitation factor scores t
235 onal/behaviour symptoms as assessed with the Neuropsychiatric Inventory questionnaire or across neuro
239 nd likely measures of neurological sequelae: neuropsychiatric morbidities, educational landmarks, use
243 more important determinant of postoperative neuropsychiatric outcomes than preoperative brain struct
244 ise as a pure form of reactive inhibition in neuropsychiatric patients displaying inhibitory deficits
245 cal dataset acquired from the Consortium for Neuropsychiatric Phenomics, we further demonstrated that
248 cation syndrome, a disorder characterized by neuropsychiatric phenotypes including hyperactivity and
251 isidentification syndromes occur commonly in neuropsychiatric practice and can be explained through a
255 ahydrocannabinol (THC) is linked to elevated neuropsychiatric risk and induces neuronal, molecular an
257 ns in glutamatergic neurons are enriched for neuropsychiatric risk variants, particularly those assoc
258 ASoC as a functional mechanism of noncoding neuropsychiatric risk variants, providing a powerful fra
259 longitudinal study of adverse post-traumatic neuropsychiatric sequelae (APNS) among participants seek
261 tantial subset develop adverse posttraumatic neuropsychiatric sequelae (APNS) such as posttraumatic s
263 se targeted to the brain, which may underlie neuropsychiatric sequelae, a considerable cause of posts
265 y of life, but can be complicated by adverse neuropsychiatric side-effects, including impulsivity.
266 ntia present with a wide range of cognitive, neuropsychiatric, sleep, motor, and autonomic symptoms.
267 om the altered nodes revealed an overlapping neuropsychiatric spectrum extending from MDD on one end,
270 changes (LATE-NC) is associated with greater neuropsychiatric symptom burden, compared to either path
273 nestic MCI, suggesting that anxiety may be a neuropsychiatric symptom of Alzheimer's disease (AD) pat
274 shared and distinct mechanisms that mediate neuropsychiatric symptoms across disorders, e.g. 22q11.2
276 Preclinical mutation carriers exhibited neuropsychiatric symptoms compared with non-carriers tha
277 ork localization of clinical, cognitive, and neuropsychiatric symptoms in Alzheimer's disease', by Te
278 isk' patients be identified prior to DBS; do neuropsychiatric symptoms relate to the distribution of
279 ions as a promising approach to the study of neuropsychiatric symptoms such as anxiety in cognitively
280 method to localize clinical, cognitive, and neuropsychiatric symptoms to brain networks, providing i
282 ed which combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle (year
283 ogy with combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle.
290 king; patient function, quality of life, and neuropsychiatric symptoms; caregiver burden and well-bei
291 hrenia is a common, chronic and debilitating neuropsychiatric syndrome affecting tens of millions of
292 -mediated disease characterized by a complex neuropsychiatric syndrome in association with an antibod
294 eron alpha, two proposed causative agents in neuropsychiatric systemic lupus erythematosus (NPSLE).
298 tic correlations between left-handedness and neuropsychiatric traits, including schizophrenia and bip
300 iscuss the intersection of the findings from neuropsychiatric treatments and homeostatic plasticity s