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 t arteriopathy with subcortical infarcts and leukoencephalopathy).

4 abnormalities can mimic the changes of toxic leukoencephalopathy.

5 ociation with risk of progressive multifocal leukoencephalopathy.

6 izumab treatment with progressive multifocal leukoencephalopathy.

7 immunodeficiency and progressive multifocal leukoencephalopathy.

8 sions consistent with progressive multifocal leukoencephalopathy.

9 cant clinical neurotoxicity and asymptomatic leukoencephalopathy.

10 ion within lesions of progressive multifocal leukoencephalopathy.

11 alcifications, can be associated with marked leukoencephalopathy.

12 s and potentially for progressive multifocal leukoencephalopathy.

13 e diagnosed as having progressive multifocal leukoencephalopathy.

14 , inherited mutations in eIF2B cause a fatal leukoencephalopathy.

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

16 a, JC nephropathy, or progressive multifocal leukoencephalopathy.

17 ed incidents of oral methotrexate-associated leukoencephalopathy.

18 stem, where it causes progressive multifocal leukoencephalopathy.

19 such as the risk for progressive multifocal leukoencephalopathy.

20 aging were consistent with a hypomyelinating leukoencephalopathy.

21 ting disease known as progressive multifocal leukoencephalopathy.

22 ening adverse effect: progressive multifocal leukoencephalopathy.

23 ted in three cases of progressive multifocal leukoencephalopathy.

24 e gastrointestinal dysmotility, cachexia and leukoencephalopathy.

25 rse events, including progressive multifocal leukoencephalopathy.

26 S) in humans known as progressive multifocal leukoencephalopathy.

27 l in the treatment of progressive multifocal leukoencephalopathy.

28 f immunotherapies for progressive multifocal leukoencephalopathy.

29 demyelinating disease progressive multifocal leukoencephalopathy.

30 t arteriopathy with subcortical infarcts and leukoencephalopathy.

31 of white matter volume, encephalomalacia, or leukoencephalopathy.

32 One patient died of progressive multifocal leukoencephalopathy.

33 ting disease known as progressive multifocal leukoencephalopathy.

34 those susceptible to progressive multifocal leukoencephalopathy.

35 er therapies to avoid progressive multifocal leukoencephalopathy.

36 in patients with biochemically unclassified leukoencephalopathy.

37 ected diagnosis of leukodystrophy or genetic leukoencephalopathy.

38 of the 190 evaluable participants had acute leukoencephalopathy.

39 iagnostic rates in patients with adult-onset leukoencephalopathy.

40 emyelinating disease, progressive multifocal leukoencephalopathy.

41 ntions, particularly those who develop acute leukoencephalopathy.

42 fection, resulting in progressive multifocal leukoencephalopathy.

43 ains of patients with progressive multifocal leukoencephalopathy.

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 (181%, 11/60), immunosuppressive associated leukoencephalopathy (12%, 7/60), central pontine myelino

48 .9%, respectively; P = .03), and subcortical leukoencephalopathy (20.5% vs 12.1%, respectively; P = .

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

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

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

52 Progressive multifocal leukoencephalopathy affects about 4 percent of patients

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

54 Survivors with acute leukoencephalopathy also had reduced white matter integr

55 Adult-onset genetic leukoencephalopathies and leukodystrophies are increasin

56 Reversible posterior leukoencephalopathy and autoimmune hemolytic anemia are

57 ies have established a link between familial leukoencephalopathy and chromosome 19.

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

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

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

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

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

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

64 ical presentations of progressive multifocal leukoencephalopathy, and advances in the understanding o

65 2hgdh mutation leads to L-2-HG accumulation, leukoencephalopathy, and neurodegeneration in mice, ther

66 ed brother had progressive aphasic dementia, leukoencephalopathy, and occipital calcifications.

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

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

69 almoparesis, or both; peripheral neuropathy; leukoencephalopathy; and mitochondrial abnormalities.

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 (AIDS), and survival after the diagnosis of leukoencephalopathy averages only about three months.

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

80 croglia in stroke and progressive multifocal leukoencephalopathy, but not expressed on microglia in p

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

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

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

84 t arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a genetically linked ne

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

86 t arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a vascular dementia ari

87 nt artriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) syndrome of premature stro

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

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

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

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

92 the first 2 cases of progressive multifocal leukoencephalopathy caused by JC papovavirus after autol

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

94 Survivors with leukoencephalopathy demonstrated reduced cognitive fluen

95 Acute leukoencephalopathy during chemotherapy treatment, witho

96 , 1 patient developed progressive multifocal leukoencephalopathy during the observation period, with

97 ria were used to identify cystic infarction, leukoencephalopathy, encephalomalacia, or atrophy.

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

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

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

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

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

103 Cases of progressive multifocal leukoencephalopathy have occurred following monoclonal a

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

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

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

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

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

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

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

111 emyelinating disease, progressive multifocal leukoencephalopathy in immunocompromised individuals.

112 demyelinating disease progressive multifocal leukoencephalopathy in immunocompromised patients.

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

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

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

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

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

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

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

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

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

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

123 Progressive multifocal leukoencephalopathy is a currently untreatable infection

124 Progressive multifocal leukoencephalopathy is a deadly demyelinating disease of

125 Progressive multifocal leukoencephalopathy is a demyelinating disease of the hu

126 Immunosuppressive-associated leukoencephalopathy is a significant complication of cyc

127 Immunosuppressive-associated leukoencephalopathy is a unique entity that can usually

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

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

130 Leukoencephalopathy is observed in some children undergo

131 Progressive multifocal leukoencephalopathy is the most common clinical presenta

132 d from a patient with progressive multifocal leukoencephalopathy, is characterized by lacking the 23-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 prolonged survival in progressive multifocal leukoencephalopathy patients.

156 ipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL).

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

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

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

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

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

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

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

164 s system (CNS) called Progressive Multifocal Leukoencephalopathy (PML) in immunosuppressed individual

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

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

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

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

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

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

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

172 demyelinating disease progressive multifocal leukoencephalopathy (PML) in patients with neurologic co

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

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

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

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

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

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

179 Progressive multifocal leukoencephalopathy (PML) is a demyelinating disorder of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

198 Progressive multifocal leukoencephalopathy (PML) is associated with natalizumab

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

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

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

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

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

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

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

206 rimary infections and progressive multifocal leukoencephalopathy (PML) upon reactivation of a latent

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

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

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

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

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

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

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

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

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

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

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

218 he causative agent of progressive multifocal leukoencephalopathy (PML), has a hypervariable regulator

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

220 al after diagnosis of progressive multifocal leukoencephalopathy (PML), we analyzed data from an obse

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

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

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

224 demyelinating disease progressive multifocal leukoencephalopathy (PML).

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

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

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

228 demyelinating disease progressive multifocal leukoencephalopathy (PML).

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

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

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

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

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

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

235 demyelinating disease progressive multifocal leukoencephalopathy (PML).

236 come in patients with progressive multifocal leukoencephalopathy (PML).

237 emyelinating disease, progressive multifocal leukoencephalopathy (PML).

238 ting disease known as progressive multifocal leukoencephalopathy (PML).

239 rker of the course of progressive multifocal leukoencephalopathy (PML).

240 lbeit associated with progressive multifocal leukoencephalopathy (PML).

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

242 demyelinating disease progressive multifocal leukoencephalopathy (PML).

243 gliomas] and two with progressive multifocal leukoencephalopathy [PML]) with thallium-positive, galli

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

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

246 Fifty cases of immunosuppressive-associated leukoencephalopathy reported in the literature in organ

247 Toxic leukoencephalopathy results from damage to the white mat

248 Progressive multifocal leukoencephalopathy results from lytic infection of the

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

250 osed adult patients referred to a specialist leukoencephalopathy service.

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

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

253 hemorrhage (n = 2), and reversible posterior leukoencephalopathy syndrome (n = 3).

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

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

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

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

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

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

260 hthalmoplegia, gastrointestinal dysmotility, leukoencephalopathy, thin body habitus, and myopathy.

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 of white matter volume, encephalomalacia, or leukoencephalopathy was identified.

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

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

269 and biopsy-confirmed progressive multifocal leukoencephalopathy were randomly assigned to receive on

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

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

272 a causative agent of progressive multifocal leukoencephalopathy which results from lytic infection o

273 emyelinating disease, progressive multifocal leukoencephalopathy, which usually occurs in individuals

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

275 nfected patients with progressive multifocal leukoencephalopathy who are treated with the antiretrovi

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

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

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

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

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

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

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

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

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

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

286 koencephalopathies are an important cause of leukoencephalopathy with calcifications.

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

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

289 Infants with Alexander disease develop a leukoencephalopathy with macrocephaly, seizures and psyc

290 Hereditary diffuse leukoencephalopathy with neuroaxonal spheroids (HDLS) is

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

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

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

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

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

296 some 3 in some patients, and megalencephalic leukoencephalopathy with subcortical cysts whose gene ha

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.