ライフサイエンスコーパス: LSD

1 LSD also increased global integration by inflating the l

2 LSD altered sensorimotor gating in a human model of psyc

3 LSD dissociates exceptionally slow from both 5-HT2BR and

4 LSD has profound modulatory effects on consciousness and

5 LSD induces profound psychedelic effects, including chan

6 LSD may alter meaningfulness by increasing activity in c

7 LSD produced dose-related subjective effects across the

8 LSD significantly increased blood pressure, heart rate,

9 LSD therapies for systemic diseases have been developed,

10 LSD's marked effects on the visual cortex did not signif

11 LSDs mainly stem from deficiencies in lysosomal enzymes,

12 inding of 5-HT(1a) receptors as well as 125I-LSD-labeled binding of 5-HT(2a) receptors were evaluated

13 Autoradiographic analysis of 125I-LSD-labeled 5-HT(2a) receptor binding revealed no signif

14 raphy with 3H-lysergic acid diethylamide (3H-LSD), 3H-8-hydroxy-2-[di-N-propylamine] tetralin (3H-8-O

15 on in 5-HT receptor binding measured with 3H-LSD was observed between midgestation and infancy, and b

16 k order of affinity for displacement of [3H]-LSD from the cloned human 5-HT7 receptor was: methiothep

17 methyltransferase, 22 JmjC demethylase and 4 LSD demethylase genes in F. vesca.

18 the mobility of this lid greatly accelerates LSD's binding kinetics and selectively dampens LSD-media

19 conformational rearrangements to accommodate LSD, providing a structural explanation for the conforma

20 ealed marked changes in brain activity after LSD that correlated strongly with its characteristic psy

21 o the full agonist 5-HT, the partial agonist LSD, and the inverse agonist Ketanserin.

22 Moreover, all LSD cells studied show extraordinary sensitivity to bref

23 alidated the interaction between miR-137 and LSD-1.

24 Moreover, DOI and LSD showed similarities in the transcriptome fingerprint

25 to neurodegeneration and tissue injury, and LSD defects in immune cells may not preclude an appropri

26 hedelic substances: psilocybin, ketamine and LSD.

27 While lisuride and LSD both act at 2AR expressed by cortex neurons to regul

28 (range 50-90 days) in children with MSD and LSD and in their respective controls.

29 eight or nine eligible children with MSD and LSD at each site during each fortnight in three age stra

30 Participants with both MSD and LSD had significantly more linear growth faltering than

31 Since MSD and LSD have similar aetiologies, interventions targeting ro

32 owed that most attributable cases of MSD and LSD were due to rotavirus, Cryptosporidium spp, enteroto

33 y outcomes were to characterise, for MSD and LSD, the pathogen-specific attributable risk and populat

34 chondrial and lysosomal pathways in NBIA and LSD, respectively, and with Parkinson's disease represen

35 ial therapeutic properties of psilocybin and LSD, as well as their ability to modulate functional bra

36 By studying wild-type and LSD mice at diverse time-points after HCT, we showed the

37 In animals, LSD disrupts prepulse inhibition (PPI) of the acoustic s

38 t associated with the development of another LSD, Tay-Sachs disease, thus suggesting general applicab

39 The mucopolysaccharidoses (MPS) are LSDs defined by the storage of glycosaminoglycans.

40 s that use of psychedelic substances such as LSD or psilocybin may have positive effects on mood and

41 orders and alcohol dependence, drugs such as LSD showed initial therapeutic promise before prohibitiv

42 xicating properties of hallucinogens such as LSD.

43 Because the major attributable LSD-associated and MSD-associated pathogens are the same

44 Both LSD and efavirenz reduce ambulation in a novel open-fiel

45 netic memory, and that erasure of H3K4me2 by LSD/KDM1 in the germline prevents the inappropriate tran

46 thers, openness, and trust were increased by LSD.

47 The predominant effects induced by LSD included visual hallucinations, audiovisual synesthe

48 Adverse effects produced by LSD completely subsided within 72 hours.

49 cortex neurons to regulate phospholipase C, LSD responses also involve pertussis toxin-sensitive het

50 Augmenting cellular LSDs that affect PLIN2 associations with these proteins,

51 ent of Gaucher disease (GD), the most common LSD.

52 As a consequence, LSD chondrocytes fail to properly secrete collagens, the

53 e at the same health centres were considered LSD.

54 D's binding kinetics and selectively dampens LSD-mediated beta-arrestin2 recruitment.

55 d that the mRNA level of H3K4me2 demethylase LSD/KDM1, spr-5, was significantly reduced in the F0 exp

56 ry of a lysine-specific histone demethylase (LSD 1).

57 T (CoREST), and lysine-specific demethylase (LSD) 1.

58 ibition of the lysine-specific demethylases (LSDs or KDM1s) and JmjC families of N-methyl-lysine deme

59 and morphological changes during developing LSDs that are extremely critical for many metabolic proc

60 dren with episodes of less-severe diarrhoea (LSD) seeking care at health centres serving six GEMS sit

61 ing MSD and the other less-severe diarrhoea (LSD).

62 ared (FTIR) spectrometer: low-sulfur diesel (LSD), ultralow-sulfur diesel (ULSD), and a blend of 20%

63 an-biodiesel process, and low-sulfur diesel (LSD).

64 ce subjected to 7 days of a low sodium diet (LSD) containing 0.01% Na(+) , a normal sodium diet (NSD)

65 hedelics such as lysergic acid diethylamide (LSD) and dissociative drugs such as phencyclidine (PCP)

66 se of ayahuasca, lysergic acid diethylamide (LSD) and magic mushrooms; demographics, current well-bei

67 f (3)H-labeled d-lysergic acid diethylamide (LSD) binding to recombinant human 5-hydroxytryptamine 6

68 nterest in using lysergic acid diethylamide (LSD) in clinical psychiatric research and practice.

69 Lysergic acid diethylamide (LSD) is a non-selective serotonin-receptor agonist that

70 Lysergic acid diethylamide (LSD) is the prototypical psychedelic drug, but its effec

71 e the effects of lysergic acid diethylamide (LSD) on the human brain but the underlying dynamics are

72 the efficacy of lysergic acid diethylamide (LSD), 3,4-methylenedioxymethamphetamine (MDMA), psilocyb

73 ing the ergoline lysergic acid diethylamide (LSD), and a series of substituted tryptamine and pheneth

74 dministration of lysergic acid diethylamide (LSD), and after pretreatment with Ketanserin (a selectiv

75 ery low doses of lysergic acid diethylamide (LSD), known as microdosing, improves mood and cognitive

76 psilocybin, and lysergic acid diethylamide (LSD), profoundly affect perception, cognition, and mood.

77 llucinogens like lysergic acid diethylamide (LSD), psilocybin, and substituted N-benzyl phenylalkylam

78 The hallucinogen lysergic acid diethylamide (LSD; 0.1 mg/kg, i.p.) caused a time-dependent increase i

79 "psilocybin," "lysergic acid diethylamide," "LSD," "ayahuasca," "3,4-methylenedioxymethamphetamine,"

80 ite of action of lysergic acid diethylamine (LSD), appears to dominate efavirenz's behavioral profile

81 hat toxic lipids relevant to three different LSDs disrupt multiple lysosomal and other cellular funct

82 otent to LSD in rats trained to discriminate LSD from saline.

83 drug-lever responding in rats discriminating LSD from saline, and this effect is abolished by selecti

84 (SP), goat pox (GP), and lumpy skin disease (LSD), caused by capripoxviruses (CaPVs), are economicall

85 ) deficits due to lysosomal storage disease (LSD mice).

86 manifestations of lysosomal storage disease (LSD) are a significant health problem for affected patie

87 bbe disease) is a lysosomal storage disease (LSD) caused by a deficiency in galactocerebrosidase (GAL

88 neurodegenerative lysosomal storage disease (LSD) caused by a deficiency in palmitoyl protein thioest

89 ) is an inherited lysosomal storage disease (LSD) caused by pathogenic variants in the Npc1 or Npc2 g

90 GD was the first lysosomal storage disease (LSD) for which enzyme therapy became available, and alth

91 neurodegenerative lysosomal storage disease (LSD) that has no effective treatment.

92 ease, a prevalent lysosomal storage disease (LSD), is caused by insufficient activity of acid beta-gl

93 Lysosomal storage diseases (LSD) are metabolic disorders characterized by accumulati

94 For most lysosomal storage diseases (LSDs) affecting the CNS, there is currently no cure.

95 common for other lysosomal storage diseases (LSDs) and whether BK channel agonists rescue abnormal ly

96 Lysosomal storage diseases (LSDs) are a class of metabolic disorders caused by mutat

97 Lysosomal storage diseases (LSDs) are a family of disorders that result from inherit

98 Lysosomal storage diseases (LSDs) are a group of 70 monogenic disorders characterize

99 Lysosomal storage diseases (LSDs) are a group of heterogeneous disorders caused by d

100 Lysosomal storage diseases (LSDs) are monogenic disorders of metabolism caused by de

101 Lysosomal storage diseases (LSDs) are typically caused by a deficiency in a soluble

102 presence of four lysosomal storage diseases (LSDs) at increased frequency in the Ashkenazi Jewish pop

103 Lysosomal storage diseases (LSDs) represent a group of monogenic inherited metabolic

104 Lysosomal storage diseases (LSDs) represent a significant portion of inborn metaboli

105 Lysosomal storage diseases (LSDs), as a group, are among the most common inherited d

106 dysfunction and lysosomal storage diseases (LSDs), but the mechanisms by which lysosomes acquire and

107 s of neuropathic lysosomal storage diseases (LSDs), Gaucher's and Krabbe's diseases.

108 eutic agents for lysosomal storage diseases (LSDs), inherited metabolic disorders caused by defects i

109 d in a number of lysosomal storage diseases (LSDs).

110 dysfunction and lysosomal storage diseases (LSDs).

111 large family of lysosomal storage diseases (LSDs).

112 o five different lysosomal storage diseases (LSDs): MPSI, MPSIIIB, MPSVII, Niemann-Pick type A/B, and

113 osomal recessive lysosomal storage disorder (LSD) caused by deficiency of the lysosomal enzyme acid a

114 ations cause the lysosomal storage disorder (LSD) mucolipidosis type IV (MLIV), contributes to upregu

115 inflammation in the lipid storage disorder (LSD) Niemann-Pick C (NPC), we deleted the macrophage inf

116 n's disease and lysosomal storage disorders (LSD) with the common theme being a combined lysosomal-mi

117 ases, including lysosomal storage disorders (LSD).

118 o virtually all lysosomal storage disorders (LSDs) and to common neurodegenerative diseases like Alzh

119 n 50 hereditary lysosomal storage disorders (LSDs) are currently described.

120 urodegenerative lysosomal storage disorders (LSDs) are severe and untreatable, and mechanisms underly

121 lable for other lysosomal storage disorders (LSDs) but none of these highly expensive treatments has

122 ment option for lysosomal storage disorders (LSDs) caused by deficiencies of soluble lysosomal enzyme

123 an 40 different lysosomal storage disorders (LSDs) cumulatively affect one in 5000 live births, and i

124 Lysosomal storage disorders (LSDs) occur at a frequency of 1 in every 5,000 live birt

125 Neuropathic lysosomal storage disorders (LSDs) present with activated pro-inflammatory microglia.

126 In lysosomal storage disorders (LSDs), a number of highly prevalent alleles have missens

127 ases, including lysosomal storage disorders (LSDs), for which hematopoietic cell transplantation (HCT

128 majority of >50 lysosomal storage disorders (LSDs).

129 bone growth in lysosomal storage disorders (LSDs).

130 ent epitopes were identified in two distinct LSD disease models, implying a unique vascular signature

131 usly described large T stabilization domain (LSD) loop that binds E3 ligases, such as Fbw7.

132 resence of the large T stabilization domain (LSD), which is known to be responsible for cell transfor

133 d by sT through its LT-stabilization domain (LSD).

134 R Ca(2+) or blocking IP3Rs caused a dramatic LSD-like lysosome storage phenotype.

135 LIN2 associates with lipid storage droplets (LSDs), but other functions of PLIN2 remain unclear.

136 n addition to marked hallucinogenic effects, LSD exerts methylenedioxymethamphetamine-like empathogen

137 As expected, LSD did not alter measured GFR and increased the abundan

138 eased following MSD and, to a lesser extent, LSD.

139 ation in moisture (LSD<1.33), dietary fibre (LSD<0.15) and total sugar (LSD<0.09) were found to be in

140 ng; and provides a molecular explanation for LSD's actions at human serotonin receptors.

141 The new analogue substituted fully for LSD in drug discrimination studies and was 5-fold more p

142 of geographic distribution was observed for LSD versus NLSD mutations-with some being more common in

143 tributable incidence per 100 child-years for LSD versus MSD, by age stratum, for rotavirus was 22.3 v

144 present a potential therapeutic approach for LSDs.

145 lls as a potentially universal biomarker for LSDs.

146 d are in the development of gene therapy for LSDs.

147 As a group, LSDs affect ~1 in 5000 live births; however, each indivi

148 The prototypical hallucinogen LSD acts via serotonin receptors, and here we describe t

149 tives of different classes of hallucinogens (LSD, 5-MeO-DALT, mescaline) and of a selected group of 2

150 M3 expression) failed to alter adiposity in LSD animals.

151 nner for treating the global CNS deficits in LSD patients.

152 leads to a blockage of the autophagy flux in LSD chondrocytes.

153 ified AAVs expressing the enzymes lacking in LSD mice reconstituted enzyme activity throughout the br

154 the systemic nature of lipid perturbation in LSD.

155 ife" of lysosomes in the normal state and in LSDs.

156 characteristic feature of affected cells in LSDs.

157 and peripheral nervous system dysfunction in LSDs.

158 eutic target to rescue enzyme homeostasis in LSDs.

159 ation and function of proteins implicated in LSDs.

160 show a protective function for microglia in LSDs and how this is corrupted by lipid lysosomal overlo

161 ulation to rescue destabilizing mutations in LSDs.

162 despread cellular perturbations occurring in LSDs, how they might be linked and interventions that ma

163 ion, in modulating lysosomal proteostasis in LSDs.

164 disease processes and treatment response in LSDs.

165 oop to correct abnormal lysosomal storage in LSDs.

166 gonists rescue abnormal lysosomal storage in LSDs.

167 the diverse pathogenic mechanisms at work in LSDs.

168 s that will be most effective for individual LSDs.

169 otype in that some 5-HT(2A)R agonists induce LSD-like hallucinations, while others lack this psychoac

170 2A complexed with the arrestin-biased ligand LSD or the inverse agonist methiothepin.

171 f the zinc-finger transcription factor LOL1 (LSD ONE LIKE1; CcLOL1) as the gene underlying pc1.

172 ip or with refinery fractions of ULSD, low- (LSD), and high sulfur diesel (HSD) and monitored for sul

173 channels underlies the pathogenesis of many LSDs and possibly that of metabolic and common neurodege

174 king with Bayesian and non-Bayesian methods (LSD, TreeTime, and treedater), we found that no method p

175 (LSD<0.05), while the variation in moisture (LSD<1.33), dietary fibre (LSD<0.15) and total sugar (LSD

176 eins (VCAM1 and MCP1) were found in multiple LSDs.

177 titute the transforming activity of a mutant LSD sT protein.

178 PPT1, cause a devastating neurodegenerative LSD, INCL.

179 L) is the most devastating neurodegenerative LSD, which is caused by inactivating mutations in the pa

180 rophy (MLD), a progressive neurodegenerative LSD.

181 mon (one in 12,500 births) neurodegenerative LSDs.

182 the most common childhood neurodegenerative LSDs.

183 neurodegenerative and non-neurodegenerative LSDs and suggest that the beneficial effects of chemical

184 neurodegenerative and non-neurodegenerative LSDs.

185 neurodegenerative and non-neurodegenerative LSDs.

186 ed for the correction of severe neurological LSDs where GluSph or GalSph play a significant role in d

187 We identify three members of the Neurospora LSD complex (LSDC): LSD1, PHF1, and BDP-1.

188 re consistent both with the known actions of LSD on serotonin receptors and with limited evidence tha

189 Administration of LSD to healthy subjects produced pronounced alterations

190 Common aspects of LSD pathogenesis and the major current therapeutic appro

191 tures for millennia [1]; however, because of LSD's unique potency and the timing of its discovery (co

192 In the case of LSD, the NH3 emissions were elevated, and in the case of

193 are approximately three times more cases of LSD than MSD in the population, more deaths are expected

194 ined the effects of single very low doses of LSD (0-26 mug) on mood and behavior in healthy volunteer

195 d with limited evidence that higher doses of LSD (100-200 mug) positively bias emotion processing.

196 t, the effects of such subthreshold doses of LSD have not been tested in a controlled laboratory sett

197 The subjective effects of LSD are fully blocked by a 5-HT2A receptor antagonist.

198 Here we studied the effects of LSD on intrinsic functional connectivity within the huma

199 ver, no data are available on the effects of LSD on PPI in humans.

200 s on the subjective and autonomic effects of LSD, and its endocrine effects are unknown.

201 many of the cardiovascular manifestations of LSD.

202 Single microdoses of LSD produced orderly dose-related subjective effects in

203 y thus reveals an unexpected binding mode of LSD; illuminates key features of its kinetics, stereoche

204 inster (spin) mutants, a Drosophila model of LSD-like neurodegeneration.

205 In mouse models of LSD, normalization of mTORC1 signaling or stimulation of

206 received 0 (placebo), 6.5, 13, or 26 mug of LSD in randomized order at 1-week intervals.

207 indicate that a threshold dose of 13 mug of LSD might be used safely in an investigation of repeated

208 n reduced expression of the worm ortholog of LSD-1 (T08D10.2), a histone demethylase; knockdown by RN

209 nation for the conformational selectivity of LSD's key diethylamide moiety.

210 acker et al. report the crystal structure of LSD in complex with one of its major targets in the brai

211 nd here we describe the crystal structure of LSD in complex with the human serotonin receptor 5-HT2B.

212 T(2A) receptors, which is also the target of LSD-like drugs.

213 ntal metrics studied are lower than those of LSD and comparable to soybean biodiesel.

214 The research to support the use of LSD and ayahuasca in the treatment of psychiatric disord

215 an model of psychosis, supporting the use of LSD in translational psychiatric research.

216 More than 60% of LSDs have CNS involvement.

217 mplex strategies for metabolic correction of LSDs.

218 There are many recognized forms of LSDs and, although individually rare, their combined pre

219 sses are also cytoprotective in all forms of LSDs studied.

220 K agonist, NS1619 and NS11021 in a number of LSDs including NPC1, mild cases of mucolipidosis type IV

221 f specific cell types in the pathogenesis of LSDs is a major challenge due to the secretion and subse

222 search pathways for therapeutic targeting of LSDs and other demyelinating diseases.

223 Over two-thirds of LSDs involve central nervous system (CNS) dysfunction (p

224 hyma and thus hinders effective treatment of LSDs with CNS involvement.

225 therapeutic approaches for the treatment of LSDs.

226 hat AP-5 deficiency represents a new type of LSDs.

227 r disease is one of the most common types of LSDs caused by mutations to the lysosomal beta-glucocere

228 vide a new approach to treat severe types of LSDs, including Gaucher disease with neurological compli

229 ts in vitro transforming activity depends on LSD interactions rather than PP2A targeting.

230 After the first English language report on LSD in 1950, psychedelics enjoyed a short-lived relation

231 The research on LSD and ayahuasca is observational, but available eviden

232 rrhoea matched to cases with MSD (n=3597) or LSD (n=4236).

233 For each included case of MSD or LSD, we enrolled one to three community control children

234 ins and in mouse models representing 6 other LSDs.

235 oach for the treatment of MPS IIIA and other LSDs with CNS involvement.

236 ikely improve therapeutic efficacy for other LSDs with complex pathological and clinical presentation

237 dysregulate lysosomal acidification in other LSDs and common neurodegenerative diseases.

238 The target tissues in other LSDs receive much lower doses of enzyme and intravenous

239 ed with ENT3 mutations and potentially other LSDs.

240 assay approach can be used for several other LSDs and genetic disorders, especially those that rely o

241 In particular, LSD increased effective connectivity from the thalamus t

242 Compared with placebo, LSD decreased PPI.

243 ctive serotonin 2A receptor antagonist) plus LSD in a double-blind, randomized, placebo-controlled, c

244 (MPSVII, Sly syndrome), develop progressive LSD unless provided with GUSB early in life.

245 pe IIIA (MPS IIIA) is an autosomic recessive LSD caused by a deficiency in sulfamidase, a sulfatase i

246 g ANOVA with a post hoc analysis of Fisher's LSD.

247 reported to delay neuronal loss in Sandhoff LSD mice by inhibiting macrophage infiltration.

248 In a controlled clinical setting, LSD can be used safely, but it produces significant symp

249 ution, in the Ashkenazi population, of seven LSD and seven NLSD mutations.

250 In several LSDs, cells of the reticuloendothelial (RE) system are t

251 ly, autophagy, which is increased in several LSDs, is responsive to dietary intervention and is reduc

252 Macrophage numbers are expanded in several LSDs, leading to histiocytosis of unknown pathophysiolog

253 reveal shared principles relevant to several LSDs, in which diverse cellular and biochemical disrupti

254 peutic benefits in a mouse model of a severe LSD.

255 and Fe; most of which varied significantly (LSD<0.05) among the genotypes.

256 ontents were found to be vary significantly (LSD<0.05), while the variation in moisture (LSD<1.33), d

257 ed as small-molecule chaperones for specific LSDs.

258 lly distinguished by mutagenesis from MCV sT LSD-dependent 4E-BP1 hyperphosphorylation and viral DNA

259 Mutating the sT LSD decreases LT protein levels and eliminates synergism

260 mg to 37.77 mg per 100g edible strawberries (LSD<0.060).

261 omized, placebo-controlled, crossover study, LSD (200 mug) and placebo were administered to 16 health

262 ), dietary fibre (LSD<0.15) and total sugar (LSD<0.09) were found to be insignificant among the genot

263 c treatment was evaluated in 1 of the tested LSD mouse models.

264 in the CSTC model and provide evidence that LSD alters effective connectivity within CSTC pathways t

265 sent results provide the first evidence that LSD selectively expands global connectivity in the brain

266 We found that LSD alters the energy and the power of individual harmon

267 ntly published by and in Nature, reveal that LSD 1's specificity and activity is in fact regulated by

268 They showed that LSD 1, a nuclear amine oxidase homolog, is a bona fide h

269 cular dynamics (MD) simulations suggest that LSD's slow binding kinetics may be due to a "lid" formed

270 SH immunoreactivity was more than double the LSD value.

271 In the case of the LSD and ULSD fuels, the SCR system also significantly re

272 alidated this metric in a mouse model of the LSD Niemann-Pick type C1 disease (NPC1) and in a prospec

273 is uniquely comprehensive examination of the LSD state represents an important advance in scientific

274 iated MMP-9 activation is driven through the LSD, a known E3 ligase-targeting domain, in MCC.

275 enerally marked nervous tissue damage in the LSDs here evaluated.

276 5000 live births, and in the majority of the LSDs, neurodegeneration is a prominent feature.

277 rrected the impaired Ca(2+) release in these LSDs and successfully rescued the abnormal lysosomal sto

278 ated Ca(2+) release was compromised in these LSDs.

279 Thus, LSDs can be characterized as diseases of deficiency as w

280 diction, as (R)-2 proved to be equipotent to LSD in rats trained to discriminate LSD from saline.

281 Similar to LSD, efavirenz induces head-twitch responses in wild-typ

282 In order to more successfully treat LSDs, a shift in focus towards a combination therapy may

283 e targeted for therapeutic purposes to treat LSDs and other autophagic disorders.

284 uction or methanogenesis rates between ULSD, LSD, and HSD.

285 crease in global connectivity observed under LSD correlated with subjective reports of "ego dissoluti

286 the active repertoire of brain states under LSD closely follows power-laws indicating a re-organizat

287 ice, HSD for 1 week did not alter MAP versus LSD mice, but plasma gamma-MSH immunoreactivity was more

288 When LSD (10 microM) was directly applied to the PFC by rever

289 recruited 2368 children with MSD, 3174 with LSD, and one to three randomly selected community contro

290 ly, we hypothesized that cells affected with LSD have increased energy expenditure for biosynthesis b

291 month GEMS-1A follow-on study, children with LSD and matched controls, in addition to children with M

292 12 (0.4%) of 2962 children with LSD and seven (0.2%) of 4074 matched controls died durin

293 more deaths are expected among children with LSD than in those with MSD.

294 5-0.87, p=0.032), and lower in children with LSD than in those with non-dysenteric MSD (HR 0.29, 0.14

295 avioral effect in rodents is consistent with LSD-like activity mediated via the 5-HT(2A) receptor.

296 Inclusion of participants with LSD markedly expands the population of children who expe

297 on the first modern brain imaging study with LSD and three separate clinical trials of psilocybin for

298 lactosialidosis and possibly for others with LSDs that primarily involve the RE system.

299 The relatively small number of patients with LSDs and lack of validated biomarkers are substantial ch

300 ic phenotype in nonneuropathic patients with LSDs.