ライフサイエンスコーパス: leukoencephalopathy

1 hock and encephalopathy, 1 acute hemorrhagic leukoencephalopathy).

2 t arteriopathy with subcortical infarcts and leukoencephalopathy).

3 ected diagnosis of leukodystrophy or genetic leukoencephalopathy.

4 of the 190 evaluable participants had acute leukoencephalopathy.

5 iagnostic rates in patients with adult-onset leukoencephalopathy.

6 emyelinating disease, progressive multifocal leukoencephalopathy.

7 nces in patients with progressive multifocal leukoencephalopathy.

8 ntions, particularly those who develop acute leukoencephalopathy.

9 fection, resulting in progressive multifocal leukoencephalopathy.

10 ains of patients with progressive multifocal leukoencephalopathy.

11 ociation with risk of progressive multifocal leukoencephalopathy.

12 izumab treatment with progressive multifocal leukoencephalopathy.

13 immunodeficiency and progressive multifocal leukoencephalopathy.

14 sions consistent with progressive multifocal leukoencephalopathy.

15 cant clinical neurotoxicity and asymptomatic leukoencephalopathy.

16 ion within lesions of progressive multifocal leukoencephalopathy.

17 s and potentially for progressive multifocal leukoencephalopathy.

18 e diagnosed as having progressive multifocal leukoencephalopathy.

19 , inherited mutations in eIF2B cause a fatal leukoencephalopathy.

20 rain MRI demonstrated cerebellar atrophy and leukoencephalopathy.

21 ia, cutaneous vascular complications, and/or leukoencephalopathy.

22 a, JC nephropathy, or progressive multifocal leukoencephalopathy.

23 ed incidents of oral methotrexate-associated leukoencephalopathy.

24 stem, where it causes progressive multifocal leukoencephalopathy.

25 such as the risk for progressive multifocal leukoencephalopathy.

26 aging were consistent with a hypomyelinating leukoencephalopathy.

27 ting disease known as progressive multifocal leukoencephalopathy.

28 ted in three cases of progressive multifocal leukoencephalopathy.

29 e gastrointestinal dysmotility, cachexia and leukoencephalopathy.

30 rse events, including progressive multifocal leukoencephalopathy.

31 S) in humans known as progressive multifocal leukoencephalopathy.

32 l in the treatment of progressive multifocal leukoencephalopathy.

33 f immunotherapies for progressive multifocal leukoencephalopathy.

34 abnormalities can mimic the changes of toxic leukoencephalopathy.

35 One patient died of progressive multifocal leukoencephalopathy.

36 alcifications, can be associated with marked leukoencephalopathy.

37 ening adverse effect: progressive multifocal leukoencephalopathy.

38 (0.9%) had confirmed progressive multifocal leukoencephalopathy.

39 ting disease known as progressive multifocal leukoencephalopathy.

40 those susceptible to progressive multifocal leukoencephalopathy.

41 er therapies to avoid progressive multifocal leukoencephalopathy.

42 in patients with biochemically unclassified leukoencephalopathy.

43 inked to various unique leukodystrophies and leukoencephalopathies.

44 mprove the diagnostic process of adult-onset leukoencephalopathies.

45 exome sequencing in the diagnosis of genetic leukoencephalopathies.

46 ndicate the diagnosis of adult-onset genetic leukoencephalopathies.

47 .9%, respectively; P = .03), and subcortical leukoencephalopathy (20.5% vs 12.1%, respectively; P = .

48 omal dominant, with subcortical infarcts and leukoencephalopathy), a cerebral small-vessel arteriopat

49 Moreover, in treated mutants, leukoencephalopathy, a hallmark of the disease, was enha

50 he causative agent of progressive multifocal leukoencephalopathy, a rare demyelinating disease that o

51 the reader with the various causes of toxic leukoencephalopathy along with its differential diagnose

52 Survivors with acute leukoencephalopathy also had reduced white matter integr

53 Adult-onset genetic leukoencephalopathies and leukodystrophies are increasin

54 Both patients exhibited a reversible leukoencephalopathy and a urinary excretion of alpha-ket

55 Reversible posterior leukoencephalopathy and autoimmune hemolytic anemia are

56 ents from three unrelated families who had a leukoencephalopathy and complex III deficiency.

57 fter the diagnoses of progressive multifocal leukoencephalopathy and idiopathic CD4+ T-cell lymphocyt

58 Diffuse leukoencephalopathy and juxtacortical and/or callosal mi

59 tudy examines the associations between acute leukoencephalopathy and neurobehavioural, neurocognitive

60 he causative agent of progressive multifocal leukoencephalopathy and of JCV granule cell neuronopathy

61 patients (18 of 41; 44%; 95% CI: 28, 60) had leukoencephalopathy and one patient had a cytotoxic lesi

62 the most common being progressive multifocal leukoencephalopathy and pneumonia).

63 At MRI follow-up, regression of leukoencephalopathy and progressive leptomeningeal enhan

64 n to the diagnosis of progressive multifocal leukoencephalopathy and to review the literature on the

65 t arteriopathy with subcortical infarcts and leukoencephalopathy) and Alagille syndrome.

66 mentation, alopecia, apparently asymptomatic leukoencephalopathy, and facial, ocular, dental and acra

67 2hgdh mutation leads to L-2-HG accumulation, leukoencephalopathy, and neurodegeneration in mice, ther

68 n the pathogenesis of progressive multifocal leukoencephalopathy, and on its possible role in cerebel

69 our understanding of progressive multifocal leukoencephalopathy, and the mechanisms that may account

70 Leukoencephalopathies are a group of white matter disord

71 Leukodystrophies and genetic leukoencephalopathies are a rare group of disorders lead

72 Vascular genetic leukoencephalopathies are an important cause of leukoenc

73 d in Autosomal Recessive Spastic Ataxia with Leukoencephalopathy (ARSAL) patients.

74 The identification of progressive multifocal leukoencephalopathy as a risk of therapy is relatively s

75 molecular characterization of patients with leukoencephalopathy associated with a specific biochemic

76 natalizumab died from progressive multifocal leukoencephalopathy, associated with the JC virus, a hum

77 d except 1 death from progressive multifocal leukoencephalopathy at month 4.

78 gnitive impairment, psychosis, seizures, and leukoencephalopathy, beginning between the ages of 29 an

79 e risk stratified for progressive multifocal leukoencephalopathy by testing for John Cunningham virus

80 t arteriopathy with subcortical infarcts and leukoencephalopathy CADASIL is caused by more than a hun

81 t arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) and cerebral amyloid angio

82 t arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) are susceptible to smooth

83 t arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) arises from mutations in t

84 t arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a neurological syndrome

85 t arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is thought to be a pure ge

86 l arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), and mitochondrial and met

87 t arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), caused by dominant mutati

88 t arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), the most common inherited

89 t arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), which is associated with

90 e arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL), an inherited form of cere

91 disease analogous to progressive multifocal leukoencephalopathy caused by John Cunningham (JC) virus

92 gmented glia (ALSP) is an autosomal dominant leukoencephalopathy caused by mutations in colony stimul

93 Adult-onset leukodystrophies and genetic leukoencephalopathies comprise a diverse group of neurod

94 psin A-related arteriopathy with strokes and leukoencephalopathy correlate with an increased number o

95 Survivors with leukoencephalopathy demonstrated reduced cognitive fluen

96 Neuroimaging in this patient revealed severe leukoencephalopathy; diffusion-weighted imaging hyperint

97 Common genetic leukoencephalopathies discussed in detail include CSF1R,

98 Acute leukoencephalopathy during chemotherapy treatment, witho

99 , 1 patient developed progressive multifocal leukoencephalopathy during the observation period, with

100 sia and scarring, acral mutilation, cerebral leukoencephalopathy, failure to thrive, and recurrent me

101 Succinate dehydrogenase deficiency is a rare leukoencephalopathy, for which improved recognition by m

102 ients presenting with unexplained reversible leukoencephalopathy, for which SLC13A3 deficiency is a n

103 Survivors with a history of acute leukoencephalopathy had more neurobehavioural problems t

104 of identified causes of adult-onset genetic leukoencephalopathies has recently increased.

105 on has been extensively studied, that of the leukoencephalopathy has not been elucidated.

106 Cases of progressive multifocal leukoencephalopathy have occurred following monoclonal a

107 ding cases resembling progressive multifocal leukoencephalopathy) have been reported that appear to b

108 known to cause leukodystrophies and genetic leukoencephalopathies-heritable disorders that result in

109 nd absence of classic progressive multifocal leukoencephalopathy histopathology in underlying white m

110 [CI], 2.98-8.87) and progressive multifocal leukoencephalopathy (HR, 4.22; 95% CI, 2.49-7.17).

111 ther complex phospholipid defects that cause leukoencephalopathies in humans, emphasizing the importa

112 MRI revealed leukoencephalopathy in 53% of survivors, and 37% had evi

113 clinical spectrum of progressive multifocal leukoencephalopathy in HIV-infected individuals; althoug

114 emyelinating disease, progressive multifocal leukoencephalopathy in immunocompromised individuals.

115 demyelinating disease progressive multifocal leukoencephalopathy in immunocompromised patients.

116 Homozygous mutants also experience leukoencephalopathy in multiple brain areas and male ste

117 osure) was associated with increased risk of leukoencephalopathy in multivariable analysis (P = .038)

118 An animal model of progressive multifocal leukoencephalopathy in non-human primates will facilitat

119 ment of demyelinating progressive multifocal leukoencephalopathy in patients with multiple sclerosis

120 Herein, we have identified a unique form of leukoencephalopathy in seven patients presenting at ages

121 to the development of progressive multifocal leukoencephalopathy in the natalizumab-associated cases

122 p and one patient (3%) with fatal multifocal leukoencephalopathy in the placebo group).

123 he risk of developing progressive multifocal leukoencephalopathy increases with the duration of treat

124 Inflammatory progressive multifocal leukoencephalopathy (iPML) with enhancing magnetic reson

125 Succinate dehydrogenase-deficient leukoencephalopathy is a complex II-related mitochondria

126 Progressive multifocal leukoencephalopathy is a currently untreatable infection

127 Progressive multifocal leukoencephalopathy is a deadly demyelinating disease of

128 Progressive multifocal leukoencephalopathy is a demyelinating disease of the ce

129 n and particularly imaging findings of toxic leukoencephalopathy is critical for early treatment and

130 d only if the risk of progressive multifocal leukoencephalopathy is high and outweighs the benefits o

131 Leukoencephalopathy is observed in some children undergo

132 Progressive multifocal leukoencephalopathy is the most common clinical presenta

133 he etiologic agent of progressive multifocal leukoencephalopathy, JCV granule cell neuronopathy, and

134 perfusion patterns of progressive multifocal leukoencephalopathy lesions by arterial spin labelling p

135 in and at the edge of progressive multifocal leukoencephalopathy lesions in a subset of subjects.

136 Perfusion within progressive multifocal leukoencephalopathy lesions was determined by arterial s

137 e ischemic lesions, 8 progressive multifocal leukoencephalopathy lesions, and 10 central nervous syst

138 f oligodendrocytes in progressive multifocal leukoencephalopathy; less common forms of central nervou

139 t arteriopathy with subcortical infarcts and leukoencephalopathy)-like patients, including two novel

140 cation algorithms and progressive multifocal leukoencephalopathy management strategies have been deve

141 causing nephropathy, progressive multifocal leukoencephalopathy, Merkel cell carcinoma, pruritic ras

142 yelin injury, namely, progressive multifocal leukoencephalopathy, metachromatic leukodystrophy and su

143 atalizumab-associated progressive multifocal leukoencephalopathy (NTZ-PML) patients may show imaging

144 Whereas progressive multifocal leukoencephalopathy of the brain is caused by rearranged

145 For these reasons, patients with genetic leukoencephalopathies often endure a long diagnostic ody

146 l problems than survivors with no history of leukoencephalopathy on organisation (adjusted T-score 56

147 Two cases of progressive multifocal leukoencephalopathy, one of which was fatal, were diagno

148 here were no cases of progressive multifocal leukoencephalopathy or deaths.

149 r hyperintensities, with delayed posthypoxic leukoencephalopathy or diffuse brain atrophy.

150 No cases of progressive multifocal leukoencephalopathy or evidence of reactivation of JC vi

151 emorrhage, intestinal perforation, posterior leukoencephalopathy or growth plate abnormalities were n

152 Med search (search terms: 'spinal cord' AND 'leukoencephalopathy' OR 'leukodystrophy'; 'spinal cord'

153 In addition to progressive multifocal leukoencephalopathy, other CNS opportunistic infections

154 atalizumab-associated progressive multifocal leukoencephalopathy, our understanding of progressive mu

155 polyomavirus-induced progressive multifocal leukoencephalopathy over three different epochs.

156 carbon monoxide [DL(co)(corr); P = .04), and leukoencephalopathy (P = .02).

157 tine autosomal dominant microangiopathy with leukoencephalopathy (PADMAL) family.

158 More progressive multifocal leukoencephalopathy patients are now negative for JC vir

159 oductive infection in progressive multifocal leukoencephalopathy patients, little is known regarding

160 prolonged survival in progressive multifocal leukoencephalopathy patients.

161 ipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL).

162 e sclerosis died from progressive multifocal leukoencephalopathy (PML) after having received 37 doses

163 thritis who developed progressive multifocal leukoencephalopathy (PML) after rituximab treatment.

164 come in patients with progressive multifocal leukoencephalopathy (PML) and cross-recognize the polyom

165 h natalizumab-related progressive multifocal leukoencephalopathy (PML) and full-blown immune reconsti

166 inating brain disease progressive multifocal leukoencephalopathy (PML) carry single amino acid substi

167 NfL are biomarkers of progressive multifocal leukoencephalopathy (PML) during natalizumab treatment.

168 sclerosis who develop progressive multifocal leukoencephalopathy (PML) following treatment with natal

169 Progressive multifocal leukoencephalopathy (PML) has recently been described in

170 demyelinating disease progressive multifocal leukoencephalopathy (PML) in immunosuppressed individual

171 demyelinating disease progressive multifocal leukoencephalopathy (PML) in individuals with depressed

172 th the development of progressive multifocal leukoencephalopathy (PML) in multiple sclerosis (MS) pat

173 d with a few cases of progressive multifocal leukoencephalopathy (PML) in multiple sclerosis and Croh

174 Progressive multifocal leukoencephalopathy (PML) in natalizumab-treated MS pati

175 is a risk factor for progressive multifocal leukoencephalopathy (PML) in patients on natalizumab.

176 irmatory diagnosis of progressive multifocal leukoencephalopathy (PML) in patients whose clinical sym

177 estimates of risk of progressive multifocal leukoencephalopathy (PML) in patients with multiple scle

178 demyelinating disease progressive multifocal leukoencephalopathy (PML) in the brains of immunosuppres

179 Progressive multifocal leukoencephalopathy (PML) is a debilitating disease resu

180 Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease of

181 Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease of

182 Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease tri

183 Progressive multifocal leukoencephalopathy (PML) is a devastating CNS infection

184 Progressive multifocal leukoencephalopathy (PML) is a fatal demyelinating disea

185 Progressive multifocal leukoencephalopathy (PML) is a fatal demyelinating disea

186 Progressive multifocal leukoencephalopathy (PML) is a fatal demyelinating disea

187 Progressive multifocal leukoencephalopathy (PML) is a fatal disease caused by r

188 Progressive multifocal leukoencephalopathy (PML) is a fatal disease with limite

189 Progressive multifocal leukoencephalopathy (PML) is a lethal CNS demyelinating

190 Progressive multifocal leukoencephalopathy (PML) is a rare brain disease caused

191 Progressive multifocal leukoencephalopathy (PML) is a rare but often fatal brai

192 Progressive multifocal leukoencephalopathy (PML) is a rare opportunistic infect

193 Progressive multifocal leukoencephalopathy (PML) is a rare, potentially devasta

194 Progressive multifocal leukoencephalopathy (PML) is a rare, severe, otherwise f

195 Progressive multifocal leukoencephalopathy (PML) is a rare, typically fatal, ce

196 Progressive multifocal leukoencephalopathy (PML) is a serious side effect assoc

197 Progressive multifocal leukoencephalopathy (PML) is a severe demyelinating dise

198 Progressive multifocal leukoencephalopathy (PML) is a usually fatal cerebral wh

199 Progressive Multifocal Leukoencephalopathy (PML) is an often fatal disease caus

200 Progressive multifocal leukoencephalopathy (PML) is an often-fatal demyelinatin

201 Progressive multifocal leukoencephalopathy (PML) is an opportunistic brain infe

202 Progressive multifocal leukoencephalopathy (PML) is associated with natalizumab

203 MPORTANCE The disease progressive multifocal leukoencephalopathy (PML) is caused by the infection of

204 atalizumab-associated progressive multifocal leukoencephalopathy (PML) is of crucial clinical relevan

205 Progressive multifocal leukoencephalopathy (PML) occurs in a fraction of patien

206 omise and manifest as progressive multifocal leukoencephalopathy (PML) or granule cell neuronopathy (

207 fluid [CSF]) from 19 progressive multifocal leukoencephalopathy (PML) patients, we attempted to reve

208 s (JCV) infection and progressive multifocal leukoencephalopathy (PML) remains unclear.

209 Progressive multifocal leukoencephalopathy (PML) typically affects the CNS whit

210 ing of the brain, and progressive multifocal leukoencephalopathy (PML) was ultimately confirmed by br

211 The increased risk of progressive multifocal leukoencephalopathy (PML) with natalizumab treatment is

212 JC virus (JCV) causes progressive multifocal leukoencephalopathy (PML), a demyelinating disease in hu

213 st described in 1958, progressive multifocal leukoencephalopathy (PML), a demyelinating disease of th

214 Progressive multifocal leukoencephalopathy (PML), a fatal demyelinating disease

215 infection can lead to progressive multifocal leukoencephalopathy (PML), a fatal demyelinating disease

216 ystem (CNS) and cause progressive multifocal leukoencephalopathy (PML), a fatal demyelinating disease

217 at risk of developing progressive multifocal leukoencephalopathy (PML), a rare demyelinating disorder

218 ised, JCPyV can cause progressive multifocal leukoencephalopathy (PML), a rare, fatal, demyelinating

219 he etiologic agent of progressive multifocal leukoencephalopathy (PML), an acquired immunodeficiency

220 human virome, causes progressive multifocal leukoencephalopathy (PML), an oft-fatal demyelinating br

221 ple sclerosis in whom progressive multifocal leukoencephalopathy (PML), an opportunistic viral infect

222 he risk of developing progressive multifocal leukoencephalopathy (PML), and the occurrence of rebound

223 Progressive multifocal leukoencephalopathy (PML), caused by JC virus (JCV), can

224 ed with CD treatment (progressive multifocal leukoencephalopathy (PML), serious infections, and lymph

225 ains of patients with progressive multifocal leukoencephalopathy (PML), whereas the archetype RR is p

226 demyelinating disease progressive multifocal leukoencephalopathy (PML), which is commonly seen in AID

227 Progressive multifocal leukoencephalopathy (PML)-derived noncoding control regi

228 by the occurrence of progressive multifocal leukoencephalopathy (PML).

229 demyelinating disease progressive multifocal leukoencephalopathy (PML).

230 demyelinating disease progressive multifocal leukoencephalopathy (PML).

231 ciated with a risk of progressive multifocal leukoencephalopathy (PML).

232 n of the brain called progressive multifocal leukoencephalopathy (PML).

233 cation) of developing progressive multifocal leukoencephalopathy (PML).

234 demyelinating disease progressive multifocal leukoencephalopathy (PML).

235 o predict the risk of progressive multifocal leukoencephalopathy (PML).

236 ppression may lead to progressive multifocal leukoencephalopathy (PML).

237 by rare occurrence of progressive multifocal leukoencephalopathy (PML).

238 of JCV, the agent of progressive multifocal leukoencephalopathy (PML).

239 he causative agent of progressive multifocal leukoencephalopathy (PML).

240 ay be associated with progressive multifocal leukoencephalopathy (PML).

241 demyelinating disease progressive multifocal leukoencephalopathy (PML).

242 rare, fatal disease, progressive multifocal leukoencephalopathy (PML).

243 reactivate and cause progressive multifocal leukoencephalopathy (PML).

244 lbeit associated with progressive multifocal leukoencephalopathy (PML).

245 l dominant retinal vasculopathy and cerebral leukoencephalopathy (previously known as hereditary endo

246 nificantly greater in progressive multifocal leukoencephalopathy progressors than in survivors (12.8%

247 port the diagnosis of progressive multifocal leukoencephalopathy, regardless of the type of immunosup

248 Toxic leukoencephalopathy results from damage to the white mat

249 Progressive multifocal leukoencephalopathy results from lytic infection of the

250 ce degradation of the progressive multifocal leukoencephalopathy/retinoic acid receptor alpha oncopro

251 nalyze three cases of progressive multifocal leukoencephalopathy seen at our center in three patients

252 osed adult patients referred to a specialist leukoencephalopathy service.

253 classic demyelinating progressive multifocal leukoencephalopathy, some of the 21 monkeys exhibited me

254 t arteriopathy with subcortical infarcts and leukoencephalopathy syndrome (CADASIL), a disorder cause

255 sive encephalopathy and reversible posterior leukoencephalopathy syndrome (RPLS), is a neurotoxic syn

256 ular myasthenia gravis, posterior reversible leukoencephalopathy syndrome, pseudotumor cerebri, distu

257 ved early, with the exception of posthypoxic leukoencephalopathy that can manifest itself 1-2 weeks a

258 nd one in five asymptomatic patients develop leukoencephalopathy that can persist until the end of th

259 ients with retinal vasculopathy and cerebral leukoencephalopathy that harboured periventricular white

260 f the basal ganglia and cerebellum is a rare leukoencephalopathy that was identified using magnetic r

261 stinct magnetic resonance imaging pattern of leukoencephalopathy to detect biallelic mutations in LYR

262 The cases of progressive multifocal leukoencephalopathy, two fatal and one disabling, result

263 l of 22 patients with progressive multifocal leukoencephalopathy underwent a clinical evaluation and

264 active therapy were systematically coded for leukoencephalopathy using Common Terminology Criteria fo

265 Leukoencephalopathy was found in 73 (20.6%) of 355 asymp

266 The leukoencephalopathy was present in all Nrf2-null mice mo

267 The genetic origin of 2 patient's leukoencephalopathy was resolved before randomization.

268 s rare side effect of progressive multifocal leukoencephalopathy, we conducted cross-sectional and lo

269 h succinate dehydrogenase deficiency-related leukoencephalopathy were reviewed for neuroradiological,

270 ic encephalopathy and progressive multifocal leukoencephalopathy were seen more than once.

271 nal patients from a database of unclassified leukoencephalopathies who were scanned for mutations in

272 onocytes in patients with hereditary diffuse leukoencephalopathy with axonal spheroids (HDLS), which

273 The term "adult-onset leukoencephalopathy with axonal spheroids and pigmented

274 lt-onset neurological condition (adult-onset leukoencephalopathy with axonal spheroids and pigmented

275 Importance: Adult-onset leukoencephalopathy with axonal spheroids and pigmented

276 sm, may confer benefit in hereditary diffuse leukoencephalopathy with axonal spheroids and suggest th

277 Adult-onset leukoencephalopathy with axonal spheroids, a probably un

278 members of a family with hereditary diffuse leukoencephalopathy with axonal spheroids.

279 discovered as causal for hereditary diffuse leukoencephalopathy with axonal spheroids.

280 ophy of the basal ganglia and cerebellum and leukoencephalopathy with brain-stem and spinal cord invo

281 phy of the basal ganglia and cerebellum, and leukoencephalopathy with brain-stem and spinal cord invo

282 ng U8 snoRNA cause the neurological disorder leukoencephalopathy with calcifications and cysts (LCC)

283 noRNA U8, cause the cerebral microangiopathy leukoencephalopathy with calcifications and cysts (LCC),

284 koencephalopathies are an important cause of leukoencephalopathy with calcifications.

285 agnetic resonance imaging (MRI) shows patchy leukoencephalopathy with cavities, and vascular permeabi

286 Megalencephalic leukoencephalopathy with cysts (MLC) is a genetic diseas

287 C13A3 deficiency causes acute and reversible leukoencephalopathy with marked accumulation of alphaKG.

288 Hereditary diffuse leukoencephalopathy with neuroaxonal spheroids (HDLS) is

289 Mutations in at least 60 genes can lead to leukoencephalopathy with often overlapping clinical and

290 ing in all patients demonstrated a symmetric leukoencephalopathy with punctate regions of restricted

291 Hereditary diffuse leukoencephalopathy with spheroids (HDLS) in humans is a

292 Hereditary diffuse leukoencephalopathy with spheroids (HDLS) is an autosoma

293 CSF1R are known to cause hereditary diffuse leukoencephalopathy with spheroids (HDLS), an adult-onse

294 SF1R gene as the cause of hereditary diffuse leukoencephalopathy with spheroids (HDLS), offering the

295 Adult-onset leukoencephalopathy with spheroids and pigmented glia (A

296 have analyzed functions for megalencephalic leukoencephalopathy with subcortical cysts 1 (Mlc1), an

297 adhesion molecule mutated in megalencephalic leukoencephalopathy with subcortical cysts, targets the

298 options are known for progressive multifocal leukoencephalopathy with underlying immunodeficiency.

299 Certain mutations in the EIF2B genes cause leukoencephalopathy with vanishing white matter (VWM), a

300 f2 gene in mice caused vacuolar (spongiform) leukoencephalopathy with widespread astrogliosis.