ライフサイエンスコーパス: atrophy

1 egions undergo the greatest rate of cortical atrophy.

2 erized by vision loss due to central retinal atrophy.

3 xtremities or pelvic bones, 73% had muscular atrophy.

4 ctive GC while soleus muscle showed expected atrophy.

5 by amyloid plaques and progressive cerebral atrophy.

6 hondria to induce inflammation and dendritic atrophy.

7 ed with pigmented paravenous retinochoroidal atrophy.

8 ar whether the same pathway mediates cardiac atrophy.

9 mentia with Lewy bodies, and multiple system atrophy.

10 tofluorescence corresponding to the areas of atrophy.

11 adaptive mechanisms to reduce disuse muscle atrophy.

12 ree diet to evaluate improvements in villous atrophy.

13 degeneration, capillary loss, fibrosis, and atrophy.

14 to identify potential etiologies of villous atrophy.

15 n and dimension were spatially mapped to RPE atrophy.

16 sarcolemma and skeletal muscle necrosis and atrophy.

17 elated to the patients' total, bilateral ATL atrophy.

18 ase, Lewy body dementia, and multiple system atrophy.

19 h greater bilateral inferomedial hippocampal atrophy.

20 l-subcortical dysfunction in multiple system atrophy.

21 ild myopathic changes with selective type II atrophy.

22 oing muscle weakness and the onset of muscle atrophy.

23 high ARMS2 and ECM GRS, RPD, and extrafoveal atrophy.

24 impairment in patients with multiple system atrophy.

25 etween FAM222A and AD-related regional brain atrophy.

26 ously observed to precede the development of atrophy.

27 extensive cortical encephalitis evolving to atrophy.

28 amic vacuolation and Purkinje cell dendritic atrophy.

29 oid-beta have all been linked to hippocampal atrophy.

30 onnexin45 hemichannels, which promote muscle atrophy.

31 (cPLA(2)) derived LOOHs in neurogenic muscle atrophy.

32 ubiquitination, and cortical and hippocampal atrophy.

33 ression from intermediate AMD to MMI-defined atrophy.

34 sorders involving white matter hypoplasia or atrophy.

35 ar regression model, independently from cord atrophy.

36 cristae biogenesis and fusion protein optic atrophy 1 (Opa1), retinal ganglion cell (RGC) dysfunctio

37 Atrophy (1.52 (1.08 to 2.15)) and severe leucoaraiosis (

38 %), isolated optic neuritis (19%), and optic atrophy (12%).

39 P < 0.0001), higher proportion with macular atrophy 2 years earlier (26.8% vs. 12.3%; P = 0.003), hi

40 eneration (5.2% versus 0.1%), and geographic atrophy (2.0% versus 0%).

41 Strikingly, severe pancreatic atrophy accompanied tumor progression in Ddr1(-/-); KPC

42 nd baseline grey matter volumes and rates of atrophy across phenotypes.

43 expected to target the cortex, understanding atrophy across this region is essential.

44 els, 1-year death was associated with severe atrophy (adjusted odds ratio [aOR] = 2.54, 95% confidenc

45 In autosomal dominant optic atrophy (ADOA), caused by mutations in the mitochondrial

46 disability stabilization, and reduced brain atrophy after 3 years of PA intake.

47 Incident macular atrophy after nAMD was examined by Kaplan-Meier analysis

48 The rate of incident macular atrophy after untreated nAMD is relatively high, increas

49 The cumulative risks of incident macular atrophy after untreated nAMD were 9.6% (standard error,

50 s associated with an increased risk of brain atrophy, aging-related diseases, and mortality.

51 s insufficient, but drawbacks include muscle atrophy, alveolar damage, and reduced mobility.

52 heimer's disease, 17 with posterior cortical atrophy and 22 with logopenic progressive aphasia) that

53 ctional brain volumes, faster rates of brain atrophy and acceleration of atrophy rates, more than a d

54 ase, Lewy body dementia, and multiple system atrophy and animal disease models; 2) provide mechanisti

55 ulosclerosis, interstitial fibrosis, tubular atrophy and arteriolosclerosis.

56 Muscle atrophy and cachexia are common comorbidities among pati

57 urth decade of life, followed by hippocampal atrophy and changes in cognition in the fifth decade of

58 isease, over and above MRI measures of brain atrophy and demographic data.

59 f neuronal morphology demonstrated dendritic atrophy and dendritic spine loss in dorsal striatum D1-M

60 Atrophy and fat accumulation are debilitating aspects of

61 oth for therapeutic interventions for muscle atrophy and for further investigative areas into insulin

62 Unavoidable periods of disuse lead to muscle atrophy and functional decline.

63 isease who are seronegative but have villous atrophy and genetic risk factors for celiac disease must

64 hagy plays a role in alcohol-induced adipose atrophy and how altered adipocyte autophagy contributes

65 Others (p-tau205 and t-tau) increase with atrophy and hypometabolism closer to symptom onset.

66 and tau deposition in the brain, hippocampal atrophy and increased rates of hippocampal atrophy over

67 nd were resistant to alcohol-induced adipose atrophy and liver injury.

68 , genetic reduction of NLK exacerbates brain atrophy and loss of DARPP32 in HD mice.

69 sympathetic hyperreflexia-associated splenic atrophy and loss of leukocytes to dramatically improve t

70 in vivo mitigates LOOH production and muscle atrophy and maintains individual muscle fiber size while

71 trum of Parkinson's disease, multiple system atrophy and other proteinopathies.

72 n of an additive interaction between gastric atrophy and poor oral health was observed (relative exce

73 ckade was associated with choroidal vascular atrophy and retinal pigment epithelial (RPE) changes inc

74 irments of neuroplasticity, such as neuronal atrophy and synaptic loss in the medial prefrontal corte

75 Chronic stress induces neuronal atrophy and synaptic loss in the medial prefrontal corte

76 We aimed to test whether gastric atrophy and, further, its interaction with poor oral hea

77 d CNV, 9 eyes (12.7%) had large areas of RPE atrophy, and 2 eyes (2.8%) developed cystoid macular deg

78 sfunction-focal cerebral blood volume, focal atrophy, and evidence of elevated glutamate concentratio

79 ty, hypotonia, cerebellar ataxia, cerebellar atrophy, and facial dysmorphisms.

80 subgroup 2 generally showed low GRS, foveal atrophy, and few drusen (any type); and subgroup 3 showe

81 ve regeneration, neural angiogenesis, muscle atrophy, and functional recovery.

82 All studies confirmed the occurrence of atrophy, and when available, longitudinal data from the

83 ath or dependence was associated with severe atrophy (aOR = 3.67, 95% CI = 1.71-7.89, p = 0.001) and

84 Canine progressive retinal atrophies are a group of hereditary retinal degeneration

85 The causes of thalamic atrophy are not fully understood.

86 Muscle wasting and atrophy are regulated by multiple molecular processes, i

87 icant differences in enlargement rate of new atrophy area (P = 0.479, square-root transformed) or tim

88 udies were not designed or powered to assess atrophy as a primary outcome.

89 All affected individuals presented optic atrophy, associated with foveopathy in half of the cases

90 rize the rates of atrophy, risk factors, and atrophy-associated visual outcomes in patients with neov

91 than 42% of Alzheimer's disease patients had atrophy at any given location across these datasets.

92 were found to contribute to the prognosis of atrophy at the 36-month visit (P = 0.010).

93 and Parkinson's disease or multiple systems atrophy (AUC=81.90%).

94 lored for their potential as multiple system atrophy biomarkers.

95 evalence of cervical spinal cord lesions and atrophy, brain pathology seems more strongly related to

96 Pancreatic Bap1 deficiency causes acinar atrophy but combines with oncogenic Ras to produce pancr

97 we hypothesized that ATF4 may promote muscle atrophy by forming a heterodimer with another bZIP famil

98 tor neuron death, and muscle degradation and atrophy can also be recapitulated in this system.

99 rted 22-37% of patients with multiple system atrophy can develop cognitive impairment.

100 Muscle wasting, or muscle atrophy, can occur with age, injury, and disease; it aff

101 worse muscle function and predominant muscle atrophy compared with those with HF with reduced ejectio

102 However, the MRI-derived atrophy component and demographic variables were exclude

103 with Parkinson's disease and multiple system atrophy correspond to different conformational strains o

104 retinal pigment epithelium and outer retinal atrophy (cRORA) and (2) hypertransmission through Bruch'

105 tion (measured by 11C-PK11195 PET) and brain atrophy (derived from structural MRI) predicted longitud

106 le drusen), and features conferring risk for atrophy development (e.g., hyperreflective foci, drusen,

107 Atrophy diagnosis criteria were consistent with those pr

108 ography of longitudinal tau accumulation and atrophy differed across phenotypes, with key regions of

109 In addition, unique regional atrophy differences were evident in each of the structur

110 Central macular atrophy does not develop universally in eyes receiving l

111 eatures included components of outer retinal atrophy (e.g., ellipsoid zone disruption), components of

112 sion), features frequently seen in eyes with atrophy (e.g., refractile drusen), and features conferri

113 l pigment epithelium (RPE) and outer retinal atrophy (e.g., RPE perturbation with associated hypotran

114 Geographic atrophy enlargement in these eyes was significantly slow

115 Geographic atrophy enlargement in these eyes was similar (0.31 mm/y

116 ed with an increased risk of CNV and macular atrophy, even after adjustment for age.

117 cal trials targeting AMD stages earlier than atrophy expansion.

118 ions in SSBP1 cause a form of dominant optic atrophy frequently accompanied with foveopathy brings in

119 , dementia with Lewy bodies, multiple system atrophy, frontotemporal dementia, progressive supranucle

120 among enlargement rates (ERs) of geographic atrophy (GA) and choriocapillaris (CC) flow deficits (FD

121 conventional clinical endpoint of geographic atrophy (GA) as defined on color fundus photography (CFP

122 Geographic atrophy (GA) in the fellow eye was associated with incre

123 bstructures independently predict geographic atrophy (GA) onset secondary to age-related macular dege

124 Geographic atrophy (GA) secondary to age-related macular degenerati

125 ere assessed in participants with geographic atrophy (GA) secondary to AMD (GATHER1 Study).

126 The cause of geographic atrophy (GA), a progressive dry form of age-related macu

127 factor (anti-VEGF) treatments or geographic atrophy (GA).

128 of fatty acid oxidation, glucose metabolism, atrophy genes, and proteins as well as inflammatory biom

129 ither Parkinson's disease or multiple system atrophy hallmarks in vivo.

130 h as Parkinson's disease and multiple system atrophy have been postulated to stem from unique strains

131 as associated with increased risk of macular atrophy (hazard ratio [HR], 1.70; 95% confidence interva

132 ot associated with increased risk of macular atrophy (HR, 1.03; 95% CI, 0.90-1.17; P = 0.67).

133 e of intellectual disability and optic nerve atrophy/hypoplasia.

134 l stenosis and interstitial fibrosis/tubular atrophy (IF/TA) of the cortex.

135 of superficial "polka dots" pattern iridian atrophy in 360 degrees secondary to anterior uveitis due

136 superficial white circular spots of iridian atrophy in 360o, some with deeper atrophy where the stro

137 cause of poor vision appeared to be macular atrophy in 60% and subretinal fibrosis in 40%.

138 as present in 148 patients (49%) and retinal atrophy in 71 patients (24%).

139 atic and semantic processing, underpinned by atrophy in a thalamo-cortico-striatal network.

140 indings of vascular brain injury or cerebral atrophy in adult American Indians.

141 s of visual acuity lagged behind central RPE atrophy in AF images.

142 on in PGE(2) signaling contributed to muscle atrophy in aged mice and results from 15-PGDH-expressing

143 n effects on cognitive performance and brain atrophy in Alzheimer's disease (AD), little is understoo

144 re associated with early or late hippocampal atrophy in Alzheimer's disease and primary age-related t

145 trajectories of hippocampal and neocortical atrophy in Alzheimer's disease and primary age-related t

146 esis and progressive cortical and cerebellar atrophy in an effort to determine the genetic aetiology

147 ontrols at the group level, but locations of atrophy in CBS were heterogeneous outside of the perirol

148 iew the application of brain and spinal cord atrophy in clinical practice in the management of MS, co

149 h grey/white matter volume loss; grey matter atrophy in cognitively unimpaired was specific to APOE e

150 rirolandic cortex and it remains unknown why atrophy in different locations would cause the same CBS-

151 cause-specific subhazard ratios for nAMD and atrophy in either eye.

152 selectively in muscle cells caused muscular atrophy in larval stages and pupal lethality.

153 sociated with chronic weight loss and muscle atrophy in mice.

154 Dementia (CAIDE) risk score and longitudinal atrophy in middle-aged subjects.

155 ntiation and prevented dexamethasone-induced atrophy in myotubes in vitro.

156 e human corpus callosum exhibits substantial atrophy in old age, which is stronger than what would be

157 matter (GM) in relapsing-remitting MS and GM atrophy in patients with progressive MS are the most rel

158 (DMTs) did not impact rates of retinal layer atrophy in PMS.

159 demonstrate a relationship between cortical atrophy in PTSD-relevant brain regions and shorter predi

160 -1a, the latter partially due to accelerated atrophy in the IFN beta-1a group.

161 lobes for all phenotypes and key regions of atrophy in the occipitotemporal regions for posterior co

162 activation despite a lack of cerebrocortical atrophy in the oldest animals studied.

163 rations were associated with faster rates of atrophy in the temporal lobe.

164 Last, we investigated whether atrophy in these ICNs could inform the differential diag

165 93, a known TRPM7 inhibitor, prevents kidney atrophy in UUO kidneys, retains tubular formation, and r

166 of i-IFTA and t-IFTA (tubulitis in areas of atrophy) in the first biopsy for cause after 90 days pos

167 included studies demonstrated an increase in atrophy incidence over time.

168 e primary meta-analytic classes: gray matter atrophy, increased function, and decreased function in p

169 sociated with significantly decreased muscle atrophy, increased myofiber diameter, and improved SFI.

170 PMS is associated with faster retinal atrophy independent of age.

171 The odds for future RPE atrophy involvement were reduced by a factor of 0.21 (95

172 Skeletal muscle atrophy is a highly-prevalent and debilitating condition

173 f virus-mediated GT to treat spinal muscular atrophy is a significant milestone, serving to accelerat

174 le sclerosis (MS) and the degree of thalamic atrophy is a strong predictor of disability progression.

175 Thalamic atrophy is among the earliest brain changes detected in

176 te to cognitive dysfunction, and grey matter atrophy is an early sign of potential future cognitive d

177 Our results show that progressive brain atrophy is associated with increased risk of future deme

178 D1-MSN atrophy is caused by cell-type specific upregulation of

179 Spinal muscular atrophy is caused by reduced levels of SMN resulting fro

180 se, yet the long-term trajectory of cortical atrophy is not well defined.

181 Although posterior cortical atrophy is often regarded as the canonical 'visual demen

182 Muscle atrophy is regulated by the balance between protein degr

183 Given the fact that cerebellar atrophy is seen in other IGDs, flow cytometry for GPI-AP

184 injury to a nerve and the associated muscle atrophy is unclear.

185 stics included interstitial fibrosis/tubular atrophy, larger cortical nephron size (but not nephron n

186 ipitotemporal regions for posterior cortical atrophy, left temporal lobe for logopenic progressive ap

187 hibition also attenuated DOX-induced cardiac atrophy, likely because of repression of muscle RING fin

188 Atrophy location and drusen type were the most relevant

189 Previous studies of macular atrophy (MA) in HARBOR analyzed color fundus photography

190 First, we defined single-subject atrophy maps by comparing cortical thickness in each Alz

191 ' to test the hypothesis that single-subject atrophy maps in patients with a clinical diagnosis of Al

192 network mapping" to localize single-subject atrophy maps to symptom-specific brain networks.

193 Single-subject atrophy maps were generated by comparing cortical thickn

194 esis of pigmented paravenous retinochoroidal atrophy may involve inflammatory-related precursors on a

195 ns in the junctional zone and future macular atrophy may represent progressive migration and loss of

196 he management of MS, considering the role of atrophy measures in prognosis and treatment monitoring a

197 he relationship between tau-PET and cortical atrophy measures, thus suggesting a modulatory effect of

198 ance to recently published Classification of Atrophy Meeting criteria as sharply demarcated hyperrefl

199 with those proposed by the Classification of Atrophy Meetings (CAM) group: hypertransmission of light

200 recently shown that T. gondii-induced muscle atrophy meets the clinical definition of cachexia.

201 r's disease, to what degree flortaucipir and atrophy mirror clinical phenotype in Alzheimer's disease

202 amilial PD, and six cases of multiple system atrophy (MSA) for their ability to induce alpha-synuclei

203 cleinopathies, which include multiple system atrophy (MSA), Parkinson's disease, Parkinson's disease

204 a with Lewy bodies (DLB) and multiple system atrophy (MSA).

205 Our study supports atrophy network mapping as a method to localize clinical

206 Here, we use a similar technique termed "atrophy network mapping" to localize single-subject atro

207 Here, we use a new technique termed 'atrophy network mapping' to test the hypothesis that sin

208 Nascent geographic atrophy (nGA) describes features on OCT imaging previous

209 progressive uveitis, with retinal scars and atrophy observed in the chronic stage by fundoscopy.

210 The association between TDP-43 and brain atrophy occurred slightly later in time (~3 years) in ca

211 condary radiological findings such as muscle atrophy, oedema in peripheric soft tissue and bone marro

212 oved for the treatment of 5q spinal muscular atrophy of all types and stages in patients of all ages.

213 e brain, pathological findings reveal severe atrophy of cerebellar cortex in SCA1 patients.

214 saturation during sleep was associated with atrophy of cortical and subcortical brain areas known fo

215 ical stage, which is mediated by progressive atrophy of grey matter indicative of increased Alzheimer

216 This invariance related to exacerbated atrophy of lobule VI of the cerebellum and exacerbated d

217 tein is also associated with faster rates of atrophy of other brain regions and whether there is evid

218 Atrophy of the bilateral temporal poles and the fusiform

219 psy in adults is associated with progressive atrophy of the cortex at a rate more than double that of

220 0) showed the following characteristics: (1) atrophy of the foveal photoreceptor layer with or withou

221 nce imaging features are hypomyelination and atrophy of the striatum and cerebellum.

222 d by the presence of small intestinal villus atrophy on histopathology specimens during the years 196

223 as accounted for by pre-existing evidence of atrophy on OCT alone, the development of MA in areas of

224 lthy subjects, we found progressive cortical atrophy on vertex-wise analysis in TLE before surgery th

225 also protected muscles against aging-induced atrophy, our findings have implications for sarcopenia.

226 Studies including atrophy outcome(s) in patients with age-related macular

227 There is heterogeneity in the locations of atrophy outside the perirolandic cortex and it remains u

228 administration (0.9 g/kg per day) prevented atrophy over the first 2 weeks, and mitigated alteration

229 l atrophy and increased rates of hippocampal atrophy over time.

230 al muscle index and significant muscle fiber atrophy (P < 0.0001) in patients with cachexia, NMJ morp

231 trinsic networks relate to syndrome-specific atrophy patterns in primary progressive aphasia.

232 ' spatial distribution in HCs with patients' atrophy patterns, we identified ICNs associated with eac

233 However, it is unclear whether retinal atrophy persists in PMS, exceeds normal aging, or can be

234 imaging, but only baseline focal hippocampal atrophy predicted progression to syndromal psychosis.

235 sion of NLK in the striatum attenuates brain atrophy, preserves striatal DARPP32 levels and reduces m

236 seen in the larger context of outer retinal atrophy, previously suggested as a new form of advanced

237 indicate that there is markedly reduced RPE atrophy progression in areas co-localizing with quiescen

238 fficient) between predicted and observed RPE atrophy progression was evaluated to estimate the model

239 h overlap between predicted and observed RPE atrophy progression with a cross-validated Dice coeffici

240 d Foxo1 phosphorylation, eliminating FOXO1's atrophy-promoting effect.

241 he only significant predictor of whole brain atrophy rates (p=0.025) while age (p=0.009), sex (p=0.00

242 Atrophy rates did not differ between subjects with and w

243 r rates of brain atrophy and acceleration of atrophy rates, more than a decade prior to death, with d

244 tein-associated acceleration/deceleration of atrophy rates.

245 d review protocol including validated visual atrophy rating scales, and to consider volumetric analys

246 ohort of 21 patients with posterior cortical atrophy, referenced to 15 healthy age-matched individual

247 ter hyperintensities, microbleeds, and brain atrophy reflecting key structural changes.

248 Optic atrophy resulting from retinal ganglion cell (RGC) degen

249 To summarize the rates of atrophy, risk factors, and atrophy-associated visual out

250 s of cancer cachexia, including muscle fiber atrophy, sarcolemmal fragility, and impaired muscle rege

251 Spinal and bulbar muscular atrophy (SBMA) is a hereditary neuromuscular disorder ca

252 ssive microcephaly with brachycephaly, optic atrophy, seizures, and hypertonia with hyperreflexia.

253 ory subunit NDUFS4 develop early-onset optic atrophy, severe systemic mitochondrial dysfunction leads

254 tor and gait deficits with underlying muscle atrophy, similar to that observed in the constitutive iT

255 Spinal muscular atrophy (SMA) is a motor neuron disease.

256 otype.SIGNIFICANCE STATEMENT Spinal muscular atrophy (SMA) is a neurodegenerative disease, characteri

257 Spinal muscular atrophy (SMA) is a neuromuscular disorder caused by homo

258 Spinal muscular atrophy (SMA) is caused by mutation or deletion of survi

259 Spinal muscular atrophy (SMA) occurs as a result of cell-ubiquitous depl

260 MN1 and SMN2 copy numbers in spinal muscular atrophy (SMA) samples has not been reported.

261 cohort of 199 patients with spinal muscular atrophy (SMA) type III assessed using the Hammersmith Fu

262 rophic lateral sclerosis and spinal muscular atrophy (SMA), and 3 mutations of the ASC-1 gene TRIP4 h

263 tor neuron diseases, ALS and spinal muscular atrophy (SMA).

264 We report an optic atrophy spectrum disorder, including retinal macular dys

265 associated with large soft drusen and foveal atrophy; subgroup 2 generally showed low GRS, foveal atr

266 Here, we report FAM222A as a putative brain atrophy susceptibility gene.

267 Bosch-Boonstra-Schaaf optic atrophy syndrome (BBSOAS) has been identified as an auto

268 The neostriatal atrophy that pathologically defines Huntington's disease

269 ), we identified patterns of covarying brain atrophy that were represented across the diagnostic grou

270 Aside from right temporal atrophy, the imaging pattern showed volume loss of the r

271 Inactivity, as in disuse or aging, causes atrophy, the loss of muscle mass and strength, leading t

272 Muscle VDR-KD elicited atrophy through a reduction in total protein content, re

273 ntribute to the attenuation of disuse muscle atrophy through prolonged periods of immobility of hiber

274 hippocampal volume, and sulcal and ventricle atrophy using nested multivariate regression analyses.

275 ch Alzheimer's disease patient's location of atrophy using seed-based functional connectivity in a la

276 Patients with CBS had perirolandic atrophy versus controls at the group level, but location

277 ilepsy, polyneuropathy, cerebral gray matter atrophy), visual impairment, testicular dysgenesis in ma

278 Similar to KPC mice, tissue atrophy was a hallmark of both neoplasia and pancreatiti

279 In most models, organ atrophy was accompanied by increased fibrillar collagen

280 Progressive cerebellar atrophy was also noted.

281 tus in whom predominant right temporal lobar atrophy was identified based on blinded visual assessmen

282 Grey matter atrophy was not predicted by diffuse axonal injury at ba

283 Additionally, no atrophy was seen, muscle strength was generally preserve

284 ntify potential mechanisms underlying muscle atrophy, we studied the impact of VDR knockdown (KD) on

285 extent of angioid streaks and CNV or macular atrophy were investigated using regression analysis.

286 Another exception is denervation-atrophy where nuclei are not eliminated.

287 of iridian atrophy in 360o, some with deeper atrophy where the stroma fibers were visualized and only

288 a is required for the development of villous atrophy, which demonstrates the location-dependent centr

289 on of skeletal muscles induces severe muscle atrophy, which is preceded by cellular alterations such

290 al cord GM lesions may subsequently cause GM atrophy, which may contribute to evolution to PMS.

291 riability in the spatial pattern of cortical atrophy, which relates to genetic factors and motor and

292 n be limited in the setting of peripapillary atrophy, which was present in all but 2 participants.

293 rt a case of white circular spots of iridian atrophy, which we will call "polka dots" pattern, as a r

294 ith treatment-naive quiescent CNV (n=7), RPE atrophy with a history of exudative CNV (n=10), and RPE

295 thies with AUC=0.98 and from multiple system atrophy with AUC=0.94.

296 ified by estimation of brain and spinal cord atrophy with MRI.

297 ar history: retinal pigment epithelium (RPE) atrophy with treatment-naive quiescent CNV (n=7), RPE at

298 d samples from patients with multiple system atrophy, with an overall sensitivity of 95.4%.

299 l auditory dysfunction in posterior cortical atrophy, with implications for our pathophysiological un

300 h a history of exudative CNV (n=10), and RPE atrophy without evidence of coexisting CNV (n=81).