ライフサイエンスコーパス: atrophy

1 entia with Lewy bodies, and multiple systems atrophy.

2 esults with MRI measures of gray matter (GM) atrophy.

3 the putamen of patients with multiple system atrophy.

4 sex and hypertension independent from brain atrophy.

5 etinal atrophy, and incomplete outer retinal atrophy.

6 left dorsal anterior insula and frontal pole atrophy.

7 value for clinical HD progression and brain atrophy.

8 vated in several settings of skeletal muscle atrophy.

9 n highly myopic eyes with advanced choroidal atrophy.

10 ls reveals delay in myelination and cerebral atrophy.

11 ts and mice with inflammation-induced muscle atrophy.

12 erve, present in 2 of the eyes, demonstrated atrophy.

13 -like peptide-1 analogues in multiple system atrophy.

14 no visual symptoms despite temporal macular atrophy.

15 e strategy in treating human spinal muscular atrophy.

16 ificance of P </= 0.001 after disuse-induced atrophy.

17 ere independent of global and regional brain atrophy.

18 ic intervention during muscle regrowth after atrophy.

19 ncludes wasting, hepatosteatosis, and thymus atrophy.

20 y-onset dysmyelination and progressive brain atrophy.

21 ssive supranuclear palsy, or multiple system atrophy.

22 a therapeutic option to improve vulvovaginal atrophy.

23 HAM/TSP and progressive MS show spinal cord atrophy.

24 ion of inflammation-mediated skeletal muscle atrophy.

25 could serve as a remedy for age-related skin atrophy.

26 -cell responses promote development of brain atrophy.

27 se steroids are also known to trigger muscle atrophy.

28 hagy-lysosome pathways, resulting in myotube atrophy.

29 nd the organ developed either hyperplasia or atrophy.

30 muscle undergoing regrowth after a period of atrophy.

31 cued memory deficits and reduced hippocampal atrophy.

32 from symptom onset) were associated with CA3 atrophy.

33 elow 50%) in detection of persistent villous atrophy.

34 acterized by distal limb muscle weakness and atrophy.

35 ar volume was computed as a measure of brain atrophy.

36 and cervical spinal cord lesions (T2LV) and atrophy.

37 %), intrachoroidal cavitation (2.2%), patchy atrophy (0.9%), and end-stage MD (0.2%).

38 le of the mitochondrial fusion protein optic atrophy 1 (OPA1) in differentiated skeletal muscle by re

39 %) and cerebellar variant of multiple system atrophy (11%).

40 Correlation of areas 1 (complete atrophy), 2 (FS in the central millimeter), and 3 (FS in

41 Five subjects with posterior cortical atrophy, 4 subjects with the logopenic variant of primar

42 y atrophy (7.0%), staphyloma (5.7%), diffuse atrophy (6.4%), lacquer cracks (2.6%), intrachoroidal ca

43 efractive error and amblyopia (12.1%), optic atrophy (6.4%), phthisis bulbi (6.4%), aphakia (5.6%) an

44 (31.7%), tilted disc (28.1%), peripapillary atrophy (7.0%), staphyloma (5.7%), diffuse atrophy (6.4%

45 Skeletal muscle ageing is characterised by atrophy, a deficit in specific force generation, increas

46 epressor, cause dentatorubral-pallidoluysian atrophy, a neurodegenerative disease.

47 uropathy (LHON) and Autosomal dominant optic atrophy (ADOA) are caused by mutant mitochondrial protei

48 ) are associated with significant urogenital atrophy, affecting quality of life and drug compliance.

49 latory networks that control skeletal muscle atrophy after denervation have been established, the tra

50 clerosis, interstitial fibrosis, and tubular atrophy) all increase with age.

51 ng inflammation within areas of fibrosis and atrophy and acceptance of transplant arteriolopathy with

52 play a causative role in the development of atrophy and contractile weakness of the diaphragm in cri

53 ritically ill patients displayed significant atrophy and contractile weakness, but lacked impaired mi

54 amic-pituitary-adrenal axis leads to splenic atrophy and contraction of NK cell numbers in the periph

55 aimed to investigate patterns of spinal cord atrophy and correlations with clinical markers.

56 r organization, bringing about terminal cell atrophy and degeneration.

57 stic criteria for WFS2 also consist of optic atrophy and diabetes mellitus, but unlike WFS1, this phe

58 d protein degradation and rescued the muscle atrophy and dysfunction in a Duchenne muscular dystrophy

59 use of mechanical ventilation (MV) leads to atrophy and dysfunction of the major inspiratory muscle,

60 e diagnostic criteria for posterior cortical atrophy and eight for logopenic variant primary progress

61 mast cell-depleted mice displayed less organ atrophy and fibrosis than did wild-type mice during the

62 e muscle fibre adaptations to ageing-induced atrophy and functional impairment is still unsettled.

63 (ii) muscle fibres went through significant atrophy and impairment of specific force (isometric forc

64 by loss of spinal cord motor neurons, muscle atrophy and infantile death or severe disability.

65 led midperipheral retinal pigment epithelial atrophy and intraretinal pigment migration.

66 for the optimal detection and measurement of atrophy and its associated features.

67 evented onset of photoreceptor apoptosis and atrophy and maintained near-normal levels of electroreti

68 pe I receptor (ALK4) as a mediator of muscle atrophy and muscle regeneration.

69 P301S/E4 mice develop markedly more brain atrophy and neuroinflammation than P301S/E2 and P301S/E3

70 er of 240 rapid decliners had 2-fold greater atrophy and progressed to dementia at almost 5 times the

71 , we showed that AKG rescues skeletal muscle atrophy and protein degradation through a PHD3/ADRB2 med

72 y cortical volume decline is consistent with atrophy and reabsorption of globally sclerotic glomeruli

73 These data show that molecular mechanisms of atrophy and regeneration are affected and contribute to

74 uscle biopsies of patients were analyzed for atrophy and regeneration by measuring fiber size and by

75 Vaginal atrophy and sexual interest and dysfunction improved for

76 cur without retinal pigment epithelium (RPE) atrophy and that atrophy can undergo an evolution of dif

77 d skeletal muscle atrophy; persistent muscle atrophy and weakness are major complications that hamper

78 atients have manifest diaphragm muscle fiber atrophy and weakness in the absence of mitochondrial dys

79 link between hyposialylation and the muscle atrophy and weakness.

80 disease manifesting with progressive muscle atrophy and weakness.

81 such as cancer, neurodegeneration and tissue atrophy, and in accelerated aging.

82 uter retinal atrophy, complete outer retinal atrophy, and incomplete outer retinal atrophy.

83 nvolving cortical demyelination, gray matter atrophy, and meningeal inflammation.

84 hypotonia, early-onset seizures, cerebellar atrophy, and osteopenia.

85 es, Parkinson's disease, and Multiple System Atrophy are age-related neurodegenerative disorders char

86 e of which interstitial fibrosis and tubular atrophy are dominant features.

87 Quantitative measurements of spinal cord atrophy are important in fully characterizing these and

88 scle homeostasis is best known during muscle atrophy, as the cullin-1 substrate adaptor atrogin-1 is

89 med to investigate which retinal layers show atrophy associated with neurodegeneration in multiple sc

90 ns of gray matter (GM) and white matter (WM) atrophy at presentation were assessed and tested as pred

91 orrelated with poor cognition and AD-related atrophy (at baseline and longitudinally) and with brain

92 s later-onset encephalopathy with cerebellar atrophy, ataxia and dystonia.

93 sensus terminology and criteria for defining atrophy based on OCT findings in the setting of age-rela

94 ume, cerebellar Lobules VI, Crus I and VIIIa atrophy being independent predictors of 9-HPT, SDMT, BVM

95 beta-zone parapapillary atrophy (betaPPA) has been reported as a risk factor for

96 ents with a dominant form of spinal muscular atrophy, but how these mutations cause disease is unknow

97 ce exercise is effective to attenuate muscle atrophy, but the underlying mechanism has not been fully

98 e channel (RyR1) display muscle weakness and atrophy, but the underlying mechanisms are unclear.

99 been shown to play a role in skeletal muscle atrophy, but their role is not completely understood.

100 stress response that locally induces muscle atrophy, but via secretion of FGF21 acts distally to mod

101 Recognizing that photoreceptor atrophy can occur without retinal pigment epithelium (RP

102 al pigment epithelium (RPE) atrophy and that atrophy can undergo an evolution of different stages, 4

103 nal capacity (r=-0.289, p=0.0264), and brain atrophy (caudate r=0.178, p=0.0087; whole-brain r=0.602,

104 tinal pigment epithelium (RPE) deposits, RPE atrophy, choroidal neovascularisation and photoreceptor

105 Atrophy colocated with cerebellar areas implicated for m

106 nsive cortical and subcortical brain volumes atrophy compared with controls.

107 hy (cRORA), incomplete RPE and outer retinal atrophy, complete outer retinal atrophy, and incomplete

108 loid retention, cognitive decline, and brain atrophy, controlling for neuronal metabolism.

109 (18)F-flortaucipir binding and GM atrophy correlated similarly to cognitive test performan

110 ere proposed: complete RPE and outer retinal atrophy (cRORA), incomplete RPE and outer retinal atroph

111 h celiac disease who have persistent villous atrophy despite a GFD.

112 Skeletal muscle fiber atrophy develops in response to severe sepsis, but it is

113 prevent diaphragm atrophy, to strengthen an atrophied diaphragm, and mitigate the harms of mechanica

114 es are recognised, including spinal muscular atrophy, distal hereditary motor neuropathy and LMN vari

115 utamine disease dentatorubral-pallidoluysian atrophy (DRPLA), progressive acquirement of an ataxic ph

116 alopathy characterized by extreme cerebellar atrophy due to almost total granule neuron loss.

117 Skeletal muscle atrophy due to excessive protein degradation is the main

118 aging modalities used to detect and quantify atrophy due to late-stage non-neovascular and neovascula

119 ecline, and drives amyloid-independent brain atrophy during the earliest stage of disease.

120 To compare the enlargement rate of macular atrophy (ERMA) in eyes treated with ranibizumab monthly

121 nerves results in muscle regeneration and in atrophy especially in the case of slow muscle fibers.

122 s and show predominant ataxia and cerebellar atrophy features on imaging.

123 ty due to bone marrow failure and intestinal atrophy featuring stem and progenitor cell depletion, a

124 n 2009, older age, worse vision, presence of atrophy/fibrosis, pigment epithelium detachment, and geo

125 igment epithelium detachment, and geographic atrophy/fibrotic scar/neovascular AMD in the fellow eye.

126 mpared between late AMD subtypes; geographic atrophy (GA) and choroidal neovascularization (CNV).

127 dies have shown premalignant lesions gastric atrophy (GA) and intestinal metaplasia (IM) influence ga

128 To correlate the area of geographic atrophy (GA) and residual foveal sparing (FS), and to id

129 cidence, size, and growth rate of geographic atrophy (GA) during 5 years of follow-up among participa

130 dence, and rate of progression of geographic atrophy (GA) in eyes with neovascular age-related macula

131 Geographic atrophy (GA) is an advanced form of age-related macular

132 Appearance of geographic atrophy (GA) on color photography (CP) is preceded by sp

133 (RPE) defects not attributable to geographic atrophy (GA) or RPE-tears with overlying preserved photo

134 s 2 and 3, neovascularization and geographic atrophy (GA) were present, ranging from 0.4% to 6% in ey

135 luded neovascular AMD (nvAMD) and geographic atrophy (GA).

136 d vitelliform lesions (AVLs), and geographic atrophy (GA); and ultrastructural and staining character

137 Hippocampal-sparing and the no atrophy group showed less aggressive disease progression

138 ications, and the problem of long term graft atrophy have been roadblocks to its wider application.

139 h responded with reduced body weight, kidney atrophy, hyperphosphatemia, and increased bone turnover.

140 Interstitial fibrosis and tubular atrophy (IFTA) associated with interstitial inflammation

141 This same region was the point of maximal atrophy in 100% of individual patients in both semantic

142 ze the contribution of immune cells to brain atrophy in a system where persistent virus infection and

143 subgroups and even individual patients share atrophy in anterior cingulate, frontoinsula, striatum, a

144 an accurate timeline of incipient geographic atrophy in clinic populations and for quantifying anatom

145 ore, expression of ASYN resulted in neuronal atrophy in DIV7 cortical cultures of either from E18 tra

146 detect fibrotic tissue deposition and fiber atrophy in dystrophic strains.

147 A multifactorial model of white matter atrophy in focal epilepsy is proposed.

148 XR cause a novel mitochondriopathy and optic atrophy in humans.

149 not associated with the rate of hippocampal atrophy in individuals with a low likelihood of having A

150 ggers more severe and sustained muscle fiber atrophy in limb muscles when compared with respiratory m

151 y reduced the annualised rate of whole brain atrophy in patients with secondary progressive multiple

152 Brain atrophy in picornavirus-infected FVB mice is dependent o

153 Together, these results indicate that brain atrophy in presymptomatic carriers of common frontotempo

154 easant and unpleasant odours correlated with atrophy in right ventral mid-insula and right amygdala.

155 atients and is associated with greater brain atrophy in secondary progressive disease over a period o

156 the most prominent and consistent region of atrophy in semantic variant primary progressive aphasia

157 to assess patterns of cerebellar grey matter atrophy in seven neurodegenerative conditions (Alzheimer

158 zures, and global insults each contribute to atrophy in specific tracts.

159 Mild atrophy in the left upper and lower limbs without pain,

160 e changes in host gene expression as well as atrophy in the mandible muscles of its ant host, but it

161 fication system and criteria for OCT-defined atrophy in the setting of AMD has been proposed based on

162 atibility complex class I molecules to brain atrophy in Theiler's murine encephalomyelitis virus (TME

163 c hypertrophy, while excessive IL-22 induced atrophy in these lymphoid organs.

164 The treatment of vulvovaginal atrophy includes administration of estrogens.

165 s were accompanied by pronounced hippocampal atrophy, including subfields cornu ammonis 2/3 (CA2/3) a

166 in three large families with isolated optic atrophy, including the two families that defined the OPA

167 hippocampal cingulum and anterior commissure atrophy, indicating an effect of the underlying patholog

168 rophy while inhibition of miR-29b attenuates atrophy induced by denervation and immobilization.

169 s, and conversely, its inhibition attenuates atrophy induced by dexamethasone (Dex), TNF-alpha and H2

170 represent a therapeutic approach for muscle atrophy induced by different stimuli.

171 Qki5 prevented cardiac apoptosis and cardiac atrophy induced by doxorubicin and improved cardiac func

172 In mice, during the rapid muscle atrophy induced by fasting, the desmin cytoskeleton and

173 bolic response in muscles regrowing after an atrophy-inducing event.

174 The areas of atrophy involved the inner retinal layers and were assoc

175 Geographic atrophy is a blinding form of age-related macular degene

176 Brain atrophy is a common feature of numerous neurologic disea

177 generative disorder of which skeletal muscle atrophy is a common feature, and multiple lines of evide

178 Spinal muscular atrophy is an untreatable potentially fatal hereditary d

179 e tested the hypothesis that multiple system atrophy is associated with brain insulin resistance and

180 cytopathological hallmark of multiple system atrophy is the accumulation of alpha-synuclein aggregate

181 3 with atypical variants (posterior cortical atrophy, logopenic variant primary progressive aphasia,

182 women with symptoms of vaginal and/or vulvar atrophy, lubricants in addition to vaginal moisturizers

183 as well as analyze risk factors for macular atrophy (MA) development and progression.

184 s of 2 consensus meetings (Classification of Atrophy Meeting [CAM]) on conventional and advanced imag

185 As part of the Classification of Atrophy Meetings (CAM) program, an international group o

186 eased rates of TDP-43-associated hippocampal atrophy might occur at least 10 years before death.

187 We measured hippocampal atrophy morphometrically, and all brains were examined h

188 Multiple system atrophy (MSA) is a progressive neurodegenerative disorde

189 hic lateral sclerosis (ALS), multiple system atrophy (MSA), progressive supranuclear palsy (MSP)).

190 nefits, but its potential anabolic effect on atrophied muscle has not been investigated.

191 arkinson disease (n = 6), or multiple system atrophy (n = 6).

192 ampal TDP-43 had faster rates of hippocampal atrophy (n=17, annual volume change -4.05%, 95% CI -5.09

193 r's disease including age-dependent cortical atrophy, neuron loss, dendritic degeneration, and memory

194 OCT) imaging can identify nascent geographic atrophy (nGA) in eyes with intermediate age-related macu

195 months; at 24 months, the reduction in brain atrophy no longer reached statistical significance.

196 syndrome characterized by body weight loss, atrophy of adipose tissue (AT) and systemic inflammation

197 the symptom complex of hypomyelination with atrophy of basal ganglia and cerebellum (H-ABC).

198 dent lymphoid follicle, and degeneration and atrophy of brain microvasculature with visual evoked pot

199 volume loss in the hippocampus in humans and atrophy of CA3 pyramidal cells and suppression of adult

200 ities: e.g., disrupted lung alveolarization, atrophy of intestinal villus and colon-resident lymphoid

201 he beta-amyloid (Abeta) and tau proteins and atrophy of medial temporal lobe (MTL) structures crucial

202 HS-TLE subjects had lateralized atrophy of most temporal lobe tracts, and hippocampal vo

203 miR-29b promotes atrophy of myotubes differentiated from C2C12 or primary

204 uronal overexpression of TG2 resulted in the atrophy of neurons and reduced levels of TrkB in the PFC

205 ration of lower motor neurons and subsequent atrophy of proximal skeletal muscles.

206 Atrophy of specific cerebellar lobules explains differen

207 epsy, developmental problems and ataxia, and atrophy of the cerebellum or even the whole brain in abo

208 Both epilepsy groups had bilateral atrophy of the dorsal cingulum and corpus callosum fiber

209 decreased proliferation, thereby leading to atrophy of the esophageal epithelium.

210 0.11] vs Abeta+N+, 1.19 [0.11]), less severe atrophy of the lateral temporal lobe, and lower mean (SD

211 Atrophy of the macular ganglion cell layer and inner ple

212 ergo branching morphogenesis and progressive atrophy of the proximal lung endoderm with complete epit

213 y, enhanced muscle repair and did not induce atrophy or adipogenesis, and was associated with improve

214 e frontoparietal network, but not with brain atrophy or glucose hypometabolism.

215 ulate gene expression during skeletal muscle atrophy or recovery have yet to be investigated.

216 To avoid hyperplasia or atrophy, organ turnover demands strict equilibration of

217 o severe neurodevelopmental delay with brain atrophy (p.Ser94Arg) and extend the clinical outcomes to

218 nd presence of interstitial fibrosis/tubular atrophy (P=0.003) at diagnosis and changes in GFR (P<0.0

219 There was significantly less brain atrophy (p=0.037, adjusted for MCI status) in the IVIG g

220 and over two years; and (3) investigate how atrophy patterns and non-memory cognitive domains contri

221 These four atrophy patterns effectively define a 4-dimensional cate

222 Atrophy patterns on MRI can reliably predict three neuro

223 netic mutations, motor features, or striking atrophy patterns) and the results of a discriminant func

224 We identified four such atrophy patterns: (i) individuals with largely normal ne

225 pathy with oedema, hypsarrhythmia, and optic atrophy (PEHO) syndrome is an early childhood onset, sev

226 ere burns result in profound skeletal muscle atrophy; persistent muscle atrophy and weakness are majo

227 diagnosis of early-onset progressive retinal atrophy (PRA) was supported by reduced direct and consen

228 istered in the MCI stage of AD reduces brain atrophy, prevents cognitive decline in LMCI and delays c

229 hat BET proteins directly promote the muscle atrophy program during cachexia.

230 ceptible mice by preventing D1-MSN dendritic atrophy, reduced frequency of excitatory input and alter

231 n association with prominent Purkinje neuron atrophy, repetitive spiking is restored, although at a g

232 nigral degeneration and olivopontocerebellar atrophy, respectively.

233 ne, which leads to motor neuron loss, muscle atrophy, respiratory distress, and death.

234 VA; scar; geographic atrophy; retinal thickness, fluid; and number of anti-VE

235 Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease characterized

236 Of these 38 eyes, 23 (60%) had geographic atrophy secondary to age-related macular degeneration (A

237 ication system based on OCT was proposed for atrophy secondary to AMD.

238 eration (AMD) and 2 eyes (5%) had geographic atrophy secondary to pattern dystrophy.

239 ective Natural History of the Progression of Atrophy Secondary to Stargardt Disease (ProgStar) study.

240 Vaginal atrophy, sexual interest, and sexual dysfunction were im

241 detect, quantify, and monitor progression of atrophy should include color fundus photography (CFP), c

242 Spinal muscular atrophy (SMA) is a common and often fatal neuromuscular

243 Spinal muscular atrophy (SMA) is a devastating neuromuscular disorder ch

244 Spinal muscular atrophy (SMA) is a hereditary neurodegenerative disease

245 Spinal muscular atrophy (SMA) is a neurodegenerative disease characteriz

246 Spinal Muscular Atrophy (SMA) is a neuromuscular disorder caused by insu

247 Spinal muscular atrophy (SMA) is a progressive neurodegenerative disease

248 Spinal muscular atrophy (SMA) is an autosomal-recessive disorder charact

249 Spinal muscular atrophy (SMA) is caused by deficiency of SMN protein, wh

250 Spinal muscular atrophy (SMA) is caused by deletions or mutations of the

251 Spinal Muscular Atrophy (SMA) is caused by diminished Survival of Motor

252 o SMA.SIGNIFICANCE STATEMENT Spinal muscular atrophy (SMA) is caused by the loss of motor neurons, bu

253 Infantile-onset spinal muscular atrophy (SMA) is the most common genetic cause of infant

254 dystrophy type 1 (CDM1) and spinal muscular atrophy (SMA) patients.

255 ow that, in a mouse model of spinal muscular atrophy (SMA), a reduction in proprioceptive synaptic dr

256 Spinal muscular atrophy (SMA), an autosomal recessive neuromuscular dise

257 Spinal muscular atrophy (SMA), the leading genetic cause of infant morta

258 Homozygous SMN1 loss causes spinal muscular atrophy (SMA), the most common lethal genetic childhood

259 ards a potential therapy for spinal muscular atrophy (SMA).

260 lation of other factors implicated in muscle atrophy, such as angiotensin-II, activin and Acvr2b, in

261 tion at key time points after disuse-induced atrophy that corresponded with significantly increased g

262 tically studied tTreg cell generation in the atrophied thymus by utilizing both postnatal TEC-defecti

263 sting the contribution of cerebellar lobular atrophy to both motor and cognitive performances.

264 Analyzing the borders of atrophy to determine the origin of ORT provides new insi

265 ter may provide a means to prevent diaphragm atrophy, to strengthen an atrophied diaphragm, and mitig

266 of its previously identified role in disuse atrophy together with Trim63 (MuRF1), were confirmed by

267 stem sexuality subscales, changes in vaginal atrophy using a validated 4-point scale, and comparison

268 ities, abnormal cortical formation, cerebral atrophy, ventriculomegaly, hydrocephaly, and cerebellar

269 ce, neuropathology, and development of brain atrophy via T2-weighted MRI and subsequent 3-dimensional

270 -29b contributes to multiple types of muscle atrophy via targeting of IGF-1 and PI3K(p85alpha), and t

271 nted moderate or severe symptoms and villous atrophy (villous height:crypt depth ratio of </=2.0) wer

272 A fourth group with no atrophy was also identified (n = 30).

273 In addition, the muscle fiber atrophy was associated with high levels of inflammatory

274 Fourth, CA3 subfield atrophy was associated with severe episodic but not sema

275 analyses assessed neuropathology, and brain atrophy was detected by ex vivo magnetic resonance imagi

276 small hippocampi, but no focal white matter atrophy was detected, indicating a limited effect of gen

277 Across both samples the point of maximal atrophy was located in the same region of the left tempo

278 Iris stromal atrophy was noted in 26 patients (52%), progression or n

279 tal day 200, random appearance of testicular atrophy was noted in exposed offspring, and limited chan

280 Brain atrophy was observed at 1 mo postinfection and persisted

281 Atrophy was quantified in the diaphragm and tibialis ant

282 evated FTP signal, largely co-localised with atrophy, was evident on both visual inspection and quant

283 mitochondria, glial cell activation, muscle atrophy, weight loss, and reduced survival.

284 Across 54 studies, clusters of cerebellar atrophy were found for AD, ALS, FTD, MSA, and PSP.

285 uring cognition and function and hippocampal atrophy were observed.

286 ss is consistent with disuse-driven neuronal atrophy which may have clinical implications for disease

287 st the inflammation-mediated skeletal muscle atrophy which occurs in sarcopenia and cachexia.

288 ance imaging revealed symmetrical cerebellar atrophy, which appeared progressive, and a prominent cor

289 gnificantly attenuated tumor-mediated thymic atrophy, which is associated with immunosuppression in t

290 erexpression is sufficient to promote muscle atrophy while inhibition of miR-29b attenuates atrophy i

291 lesion volume [T1LV] to T2LV [T1:T2]), brain atrophy (whole brain and gray matter), and cervical spin

292 lled: (1) at least 1 well-demarcated area of atrophy with a minimum diameter of 300 microm, with the

293 ocal macular pigment mottling, chorioretinal atrophy with a predilection for the macular area, congen

294 aracteristics of this syndrome combine brain atrophy with clubfoot and arthrogryposis.

295 , focal lesion changes might precede diffuse atrophy with cortical thinning.

296 identified patients with persistent villous atrophy with high levels of specificity: 0.83 for the tT

297 However, they detected villous atrophy with low levels of sensitivity: 0.50 for the tTG

298 ortical development (MCD) or spinal muscular atrophy with lower extremity predominance (SMALED), as w

299 reditary motor neuropathies, spinal muscular atrophy with parkinsonism and the later stages can resem

300 (iii) individuals with a diffuse pattern of atrophy with relatively less pronounced involvement of t

301 associated with worse memory performance and atrophy within the MTL.