ライフサイエンスコーパス: lipofuscin

1 estion the rationale of treatments targeting lipofuscin.

2 , as previously surmised, the damage product lipofuscin.

3 ilar to the bisretinoids that constitute RPE lipofuscin.

4 1 nm excitation, were similar to that of RPE lipofuscin.

5 particles were identified as the age pigment lipofuscin.

6 aneuronal ubiquitin-positive autofluorescent lipofuscin.

7 o play a key role in the formation of ocular lipofuscin.

8 e effects of retinal pigment epithelial cell lipofuscin.

9 and iso-A2E, major bis-retinoid pigments of lipofuscin.

10 cytoplasmic swellings containing undigested lipofuscin.

11 lammation, oxidative damage, drusen, and RPE lipofuscin.

12 s derivatives, in the photoreactivity of RPE lipofuscin.

13 ducts, called the retinyl pigment epithelium-lipofuscin.

14 y reflect dysfunction before accumulation of lipofuscin.

15 ntly lower than that induced by photoexcited lipofuscin.

16 t elicited in the yellow-orange range by RPE lipofuscin.

17 cellular accumulation of the aging biomarker lipofuscin.

18 estation of altered behavior, and buildup of lipofuscin.

19 that the albipunctate spots do not represent lipofuscin.

20 in detecting macular edema and deposition of lipofuscin.

21 to prevent the formation of the retinotoxic lipofuscins.

22 The effect of lipofuscin, a photoinducible intracellular generator of

23 Evidence includes the accumulation of lipofuscin, a pigment resulting from oxidative damage, a

24 nor components of retinal pigment epithelium lipofuscin, A2E isomers with cis olefins at positions ot

25 l unmasking) in hypopigmented choroid and no lipofuscin abnormality.

26 fuscin precursors, which after conversion to lipofuscin accumulate in the lysosomes of the retinal pi

27 Lipofuscin accumulates in human retinal pigment epitheli

28 d an animal model that manifests accelerated lipofuscin accumulation (ABCA4-/- mutant) to evaluate th

29 we explore the possible relationship between lipofuscin accumulation and complement activation in viv

30 Fundus AF can be used to monitor lipofuscin accumulation and melanin-related changes in v

31 that treatment with isotretinoin may inhibit lipofuscin accumulation and thus delay the onset of visu

32 The model predicted lipofuscin accumulation as a key and early component of

33 we tested a therapeutic strategy to inhibit lipofuscin accumulation in a mouse model of recessive St

34 ly, we tested the effects of isotretinoin on lipofuscin accumulation in abcr(-/-) knockout mice.

35 ar weight ubiquitin conjugates and premature lipofuscin accumulation in brains of young TAX1BP1 knock

36 ferent extents of photoreceptor/RPE loss and lipofuscin accumulation in different regions of the reti

37 kyphosis, osteoporosis, testicular atrophy, lipofuscin accumulation in renal proximal tubule and tes

38 as for monitoring effects aimed at lowering lipofuscin accumulation in the retinal pigment epitheliu

39 tinal or macular dystrophies associated with lipofuscin accumulation in the retinal pigment epitheliu

40 Despite pronounced lipofuscin accumulation in the RPE of Abca4(-/-) mice, E

41 Abca4(PV/PV) mice showed substantial A2E and lipofuscin accumulation in their RPE cells but no retina

42 We propose that excess neuronal lipofuscin accumulation in young patients with FLE repre

43 Retinal pigment epithelium lipofuscin accumulation indicated that rods had existed

44 ent of forms of macular degeneration wherein lipofuscin accumulation is an important risk factor.

45 Increased lipofuscin accumulation is assumed to be an important fa

46 Intracellular lipofuscin accumulation may have important effects on au

47 ber, or markers of cellular ageing including lipofuscin accumulation or ROS production.

48 ss could cause myofibrillar degeneration and lipofuscin accumulation resulting in LV contractile dysf

49 Excessive lipofuscin accumulation was observed in abnormal dysmorp

50 In the brain, lipofuscin accumulation, alpha-synuclein aggregation and

51 from that of Best1(-/-) mice with regard to lipofuscin accumulation, and changes in the LP and ATP C

52 rrogate measures of retinoid cycle kinetics, lipofuscin accumulation, and rod and cone photoreceptor

53 dystrophy such as reduced electro-oculogram, lipofuscin accumulation, and vision impairment.

54 It has been suggested that lipofuscin accumulation, as measured by increased fundus

55 as well as enlarged electron-dense vesicles, lipofuscin accumulation, fingerprint-like profiles and g

56 neration, subretinal neovascularization, RPE lipofuscin accumulation, oxidative stress, and complemen

57 en key factors of AMD pathogenesis including lipofuscin accumulation, photooxidative damage, compleme

58 ure of retinal pigment epithelium damage and lipofuscin accumulation, respectively.

59 e-active neurons, temporally coinciding with lipofuscin accumulation.

60 ARE defects and the pathological hallmark of lipofuscin accumulation.

61 nt reference to measure qAF as surrogate for lipofuscin accumulation.

62 inal or macular degeneration associated with lipofuscin accumulation.

63 in vivo and ex vivo estimates of the rate of lipofuscin accumulation.

64 upcoming treatment trials that aim to modify lipofuscin accumulation.

65 o NIR-AF, indicated by the colocalization of lipofuscin-AF and NIR-AF under the fluorescence microsco

66 r acute exposure of healthy RPE cells to A2E-lipofuscin affects oxidative stress and expression of CR

67 ptic vesicle trafficking contribute to early lipofuscin aggregation in these cases, compared to suppr

68 , eHsp70 treatment decreased accumulation of lipofuscin, an aging-related marker, in the brain and en

69 r study was to correlate the distribution of lipofuscin and A2E across the human RPE.

70 he agreement between the emission spectra of lipofuscin and A2E is fortuitous, and the collective dat

71 Lipofuscin and A2E levels in the RPE increased with age

72 and the levels and rates of increase of RPE lipofuscin and A2E were not different between dark-reare

73 ole of light exposure in the accumulation of lipofuscin and A2E, we analyzed RPEs and isolated rod ph

74 Accumulation of indigestible lipofuscin and decreased mitochondrial energy production

75 neration, associated with elevated levels of lipofuscin and its bis-retinoid components, such as N-re

76 de of this line may be attributable to lower lipofuscin and melanin content per unit area, possibly r

77 Later, lipofuscin and melanin granules decreased in number, whe

78 and blue light-illuminated Abca4(-/-) mice, lipofuscin and melanolipofuscin granules were found to c

79 ce of several blue-absorbing chromophores in lipofuscin and show A2E is not the dominant yellow-emitt

80 inal neovascularization, accumulation of RPE lipofuscin and sub-RPE deposits, and RPE/photoreceptor d

81 he qAF method enables measurement of in vivo lipofuscin and the detection of genotype and age-associa

82 wells precoated with bisretinoid pigments of lipofuscin and their oxidized forms.

83 triggering the formation of the majority of lipofuscin and transcriptional dysregulation of genes as

84 ctors that influence the accumulation of RPE lipofuscin and/or modulate the observed AF signal in fun

85 ulate in retinal pigment epithelial cells as lipofuscin are associated with inherited and age-related

86 Efforts to clarify the composition of RPE lipofuscin are important because these compounds are tar

87 Most of the constituents of RPE lipofuscin are inadvertent products of the retinoid visu

88 We elaborate on the usefulness of lipofuscin as a marker of cumulative oxidative stress in

89 and methylglyoxal (MG)), we investigated RPE lipofuscin as a source of the reactive species that cova

90 that correlates to focal RPE accumulation of lipofuscin as well as subretinal fluid, particularly on

91 relation between the distribution of A2E and lipofuscin, as the levels of A2E were highest in the far

92 were examined histologically, and levels of lipofuscin-associated bisretinoids were measured.

93 tinoids and arrested accumulation of A2E and lipofuscin autofluorescence in the RPE.

94 ing and emitting secondary probe to mitigate lipofuscin autofluorescence, facilitated the detection o

95 y rats, exhibiting substantial age-dependent lipofuscin autofluorescence, were used to characterize t

96 using spectral imaging and dotdotdot to mask lipofuscin autofluorescence.

97 ll tight junctions, accumulation of RPE cell lipofuscin, basal laminar and linear-like deposit materi

98 ed RBP4 antagonist, can significantly reduce lipofuscin bisretinoid formation in the retinas of Abca4

99 Lipofuscin bisretinoids (exemplified by N-retinylidene-N

100 Accumulation of lipofuscin bisretinoids (LBs) in the retinal pigment epi

101 Because accumulation of lipofuscin bisretinoids and abnormal cholesterol homeost

102 Synthesis of lipofuscin bisretinoids depends on the influx of retinol

103 A1120 significantly reduces accumulation of lipofuscin bisretinoids in the Abca4(-/-) animal model.

104 Accumulation of cytotoxic lipofuscin bisretinoids may contribute to atrophic age-r

105 ation on serum RBP4, visual cycle retinoids, lipofuscin bisretinoids, and retinal visual function was

106 r degeneration identify a mechanism by which lipofuscin bisretinoids, visual cycle metabolites that p

107 etinol to the retina and reduce formation of lipofuscin bisretinoids.

108 ogliosis, neuroinflammation, accumulation of lipofuscin bodies, and memory loss, whereas their cortic

109 gangliosides and preventing their storage in lipofuscin bodies.

110 nules that had features typical of lysosomal lipofuscin by electron microscopy.

111 reducing the accumulation of the retinotoxic lipofuscin by inhibiting visual cycle function.

112 s and retinal degeneration without improving lipofuscin, C1q, and microglial accumulation.

113 tion from normal age-related accumulation of lipofuscin can be challenging.

114 rared and shortwave-infrared fluorescence of lipofuscin can be used to monitor the progression and re

115 Large amounts of autofluorescent lipofuscin, characteristic of the neurodegenerative dise

116 function of RPE cells loaded or not with the lipofuscin component A2E and inhibiting or not mitochond

117 inal pigment epithelial cells accumulate the lipofuscin component, A2E.

118 The amount of A2E, a major lipofuscin component, increased 10- to 12-fold in 6- to

119 ified two related but previously unknown RPE lipofuscin compounds.

120 ately quantify the FAF intensities, thus the lipofuscin concentration, is to compensate the light att

121 portant step toward accurately assessing RPE lipofuscin concentrations by FAF.

122 ymes and develop accelerated accumulation of lipofuscin, consistent with a senescence-like phenotype

123 in retinal pigment epithelial (RPE) cells as lipofuscin constituents are considered to be responsible

124 Lipofuscin contained in the retinal pigment epithelium (

125 Exposure of lipofuscin-containing cells to visible light caused an i

126 Lipofuscin content was classified independently by 2 mas

127 detection of true retinal pigment epithelial lipofuscin content.

128 The accumulation of lipofuscin depends on the severity of ABCA4 variants, pr

129 scattering, the emission spectrum of a thick lipofuscin deposit or intracellular lipofuscin resembles

130 riched vitamin A, C20-D(3)-vitamin A, on RPE lipofuscin deposition and eye function in a mouse model

131 in A dimerization and by extension, may slow lipofuscin deposition and the progression of common dege

132 Lipofuscin deposition is increased in both DRG neurons a

133 Lipofuscin deposition was increased in cardiomyocytes of

134 lated synucleinopathies, and accumulation of lipofuscin deposits characteristic of NCL, thus providin

135 all-trans-retinal often are associated with lipofuscin deposits in the retinal pigmented epithelium

136 y promoting the degradation of toxic retinal lipofuscin deposits, and cytotoxic, by triggering lysoso

137 Here, we show that the endogenous pigment lipofuscin displays strong near-infrared and shortwave-i

138 This phenotype includes lipofuscin, drusen, and basal laminar deposits, Bruch's

139 f A2E is not responsible for the increase in lipofuscin fluorescence observed in the central RPE with

140 Lipofuscin fluorescence was imaged in flat-mounted RPE f

141 HPLC measurements of the lipofuscin fluorophore A2E also revealed age-associated

142 This finding is supported by measurements of lipofuscin fluorophore A2E in the RPE using liquid chrom

143 The lipofuscin fluorophore A2E is known to be an initiator o

144 A2E, a major lipofuscin fluorophore that accumulated during AMD progr

145 ctural characterization of an additional RPE lipofuscin fluorophore that originates as a condensation

146 ssive Stargardt, we investigated the role of lipofuscin fluorophores (A2E-lipofuscin) on oxidative st

147 Consistent with this, the lipofuscin fluorophores A2PE, A2E, and A2PE-H(2), which

148 The accumulation of the lipofuscin fluorophores in retinal pigment epithelial (R

149 h with potential to halt the accumulation of lipofuscin fluorophores in the eye.

150 Accumulation of vitamin A-derived lipofuscin fluorophores in the retinal pigment epitheliu

151 se diseases is the accumulation of cytotoxic lipofuscin fluorophores such as A2E within the retinal p

152 visual cycle retinoids and ocular levels of lipofuscin fluorophores.

153 Increased lipofuscin formation is characteristic of LC cells from

154 Results support the notion that lipofuscin forms partly as a result of the aberrant reac

155 Accumulation of lipofuscin (granular deposits) in the retinal pigment ep

156 was to determine whether photoreactivity of lipofuscin granules also changes with the donor age.

157 ce of LRRK2, as indicated by accumulation of lipofuscin granules as well as altered levels of LC3-II

158 f the emission spectrum of a thick sample of lipofuscin granules dried on glass varies with excitatio

159 rst paralleled by an accumulation of typical lipofuscin granules in the retinal pigment epithelium (R

160 hagocytosed photoreceptor outer segments and lipofuscin granules in the subretinal space.

161 The emission properties of ocular lipofuscin granules isolated from human retinal pigment

162 In contrast, ChNS contents in lipofuscin granules significantly increased with aging.

163 Atomic force microscopy images show lipofuscin granules to be an aggregated structure.

164 ctivity of lipofuscin itself is age related, lipofuscin granules were isolated from human RPE and poo

165 ng-spaced collagen, and increased numbers of lipofuscin granules were seen on electron microscopy.

166 ted that when normalized to equal numbers of lipofuscin granules, aerobic photoreactivity of lipofusc

167 iferation of enlarged tertiary lysosomes and lipofuscin granules, indicating significant alterations

168 e vitelliform lesions themselves and contain lipofuscin granules, melanolipofuscin granules, and mela

169 oved recovery of dark adaptation and reduced lipofuscin granules.

170 dominant blue-absorbing chromophores within lipofuscin granules.

171 RPE lipofuscin had strong autofluorescent emissions that wer

172 min A-based fluorophore (A2E) present within lipofuscin has been implicated in the death of RPE and p

173 To date, several bisretinoids of RPE lipofuscin have been isolated and characterized, and for

174 onverted into hydrogen peroxide, whereas for lipofuscin, hydrogen peroxide accounted for not more tha

175 l features of AMD, including accumulation of lipofuscin in and drusen beneath the retinal pigmented e

176 how a massive accumulation of hemoglobin and lipofuscin in renal tubules that account for the pigment

177 Bisretinoid adducts accumulate as lipofuscin in retinal pigment epithelial (RPE) cells of

178 id pigments, such as A2E, that accumulate as lipofuscin in retinal pigment epithelial (RPE) cells, co

179 diminished electrooculogram light peak (LP), lipofuscin in retinal pigment epithelial cells (RPE), an

180 ondegradable fluorophores that accumulate as lipofuscin in retinal pigment epithelium (RPE) cells con

181 as early as 2 months of age, accumulation of lipofuscin in retinal pigment epithelium (RPE), and subr

182 The accumulation of lipofuscin in the aged Brown Norway rat makes it a suita

183 older controls, which could imply a role for lipofuscin in the pathophysiology of epilepsy and possib

184 Accumulation of lipofuscin in the retina is associated with pathogenesis

185 ought to be the result of an accumulation of lipofuscin in the retina.

186 opathies associated with the accumulation of lipofuscin in the retina.

187 The age-dependent accumulation of lipofuscin in the retinal pigment epithelium (RPE) has b

188 Lipofuscin in the retinal pigment epithelium (RPE) is th

189 s characterized by premature accumulation of lipofuscin in the retinal pigment epithelium (RPE) of th

190 retinoid cycle and accelerated deposition of lipofuscin in the retinal pigment epithelium (RPE).

191 these mice were analyzed morphologically for lipofuscin in the retinal pigment epithelium and for deg

192 acterized by the accelerated accumulation of lipofuscin in the retinal pigment epithelium, degenerati

193 segment (POS) clearance and accumulation of lipofuscin in the retinal-pigmented epithelium (RPE) and

194 The accumulation of lipofuscin in the RPE is a hallmark of aging in the eye.

195 93C) mice exhibited enhanced accumulation of lipofuscin in the RPE, and a significant deposition of d

196 ed the slower, age-dependent accumulation of lipofuscin in wild-type mice.

197 mpus, and early formation of autofluorescent lipofuscins in the neurons throughout the entire brains.

198 RPE lipofuscin, including the fluorophore A2E, forms in larg

199 tion by the RPE of undigested phagosomes and lipofuscin, including the fluorophore, 2-[2,6-dimethyl-8

200 anules and phagosomes with outer segment and lipofuscin inclusions that may account for their autoflu

201 ofuscin granules, aerobic photoreactivity of lipofuscin increased with age.

202 ggesting that dispersal of drusen-associated lipofuscin is a marker of atrophic disease progression.

203 Lipofuscin is a nondegradable end-product of oxidative s

204 The best characterized component of lipofuscin is A2E, a bis-retinoid byproduct of the norma

205 ow-orange autofluorescence of RPE-associated lipofuscin is associated with AMD.

206 Excessive accumulation of lipofuscin is associated with pathogenesis of atrophic a

207 Although lipofuscin is considered a hallmark of Stargardt disease

208 have no FIAF abnormalities, suggesting that lipofuscin is not a major determinant of CNV.

209 Excessive accumulation of lipofuscin is observed in numerous degenerative retinal

210 A major component of lipofuscin is the bis-retinoid N-retinylidene-N-retinyle

211 The major fluorophore of lipofuscin is the bis-retinoid, N-retinylidene-N-retinyl

212 To determine whether the photoreactivity of lipofuscin itself is age related, lipofuscin granules we

213 Although iron increased ROS production and lipofuscin levels and sensitized TM cells to H(2)O(2), i

214 in certain subgroups may point to subnormal lipofuscin levels in the retinal pigment epithelium or,

215 Lipofuscin levels were determined by fluorescence imagin

216 ith the anatomic distribution of fluorescent lipofuscin, light-attenuating macular pigment (MP), cone

217 1 result in an increased accumulation of the lipofuscin-like fluorescent aging pigment, shortened lif

218 Both 11-cis- and all-trans-retinal generated lipofuscin-like fluorophores when added to metabolically

219 abnormal accumulation of lipid droplets and lipofuscin-like granules while demonstrating photorecept

220 h age and led to the formation of insoluble, lipofuscin-like lysosomal inclusions in microglia.

221 We aimed to compare the content of lipofuscin-like material and markers of autophagy in LC

222 l dominant disorder in which accumulation of lipofuscin-like material within and beneath the retinal

223 ells exhibit lysosomes containing ceroid and lipofuscin-like material.

224 sosomal Fe(2+) levels and an accumulation of lipofuscin-like molecules in TRPML1(-/-) cells.

225 op in myocardial NADH levels, the release of lipofuscin-like pigments, and the increase in diffuse re

226 n Ercc1(-/Delta) and old WT liver, including lipofuscin, lipid hydroperoxides and acrolein, as well a

227 phs revealed the cytoplasmic accumulation of lipofuscin-loaded lysosomes.

228 eased cytoplasmic poly-ubiquitin aggregates, lipofuscin material, damaged mitochondria and impaired m

229 ing this epilepsy; the early accumulation of lipofuscin may be disease driven, secondary to as-yet un

230 High RPE lipofuscin may not adversely affect retinal structure or

231 al cellular reductants, which, together with lipofuscin, may contribute to cellular dysfunction.

232 andidate drug target for type 2 diabetes and lipofuscin-mediated macular degeneration.

233 can be activated by various stimuli such as lipofuscin-mediated photooxidative damage to lysosomal m

234 t inflammasome activation by stimuli such as lipofuscin-mediated photooxidative damage.

235 rophages fully packed with pigment granules (lipofuscin, melanin, and melanolipofuscin).

236 e RPE/BM complex thickness could reflect the lipofuscin/melanolipofuscin accumulation in normal subje

237 uorophores; two of the compounds within this lipofuscin mixture are A2E and all-trans-retinal dimer.

238 Because bisretinoid constituents of the lipofuscin of retinal pigment epithelial (RPE) cells are

239 gradable fluorophores that accumulate as the lipofuscin of retinal pigment epithelium (RPE) are invol

240 ted the role of lipofuscin fluorophores (A2E-lipofuscin) on oxidative stress and complement activatio

241 Lipofuscin, or aging pigment, is accreted as red autoflu

242 The results suggest that lipofuscin originates from the free 11-cis-retinal that

243 , P = 0.01), and greater extent of overlying lipofuscin (P = 0.001).

244 An evaluation of these lipofuscin particles using Imaris(C) software allowed ro

245 In contrast to lipofuscin, photoexcited melanosomes did not substantial

246 ndings are indicative of a contribution from lipofuscin photooxidation in RPE.

247 responsible for the age-related increase in lipofuscin photoreactivity.

248 nd enabled IL-1beta secretion in response to lipofuscin phototoxicity, thus indicating inflammasome p

249 The autofluorescent lipofuscin pigment A2E accumulates in retinal pigment ep

250 ated in wells precoated with peroxy-A2E, the lipofuscin pigment all-trans-retinal dimer, and oxidized

251 upplementation with vitamin A may accelerate lipofuscin pigment formation in abca4(-/-) mice.

252 This lipofuscin pigment is a fluorescent compound with absorb

253 absence of serous retinal detachment, orange lipofuscin pigment, drusen, retinal pigment epithelial f

254 of A2E biochemically and the accumulation of lipofuscin pigments by electron microscopy.

255 a knockout mutation in abcr accumulate toxic lipofuscin pigments in ocular tissues, similar to affect

256 oducts of the photooxidation of bis-retinoid lipofuscin pigments in RPE cells could serve as a trigge

257 e to brown as a result of massive storage of lipofuscin pigments in the exocrine (but not islet) cell

258 ce exhibit buildup of bisretinoid-containing lipofuscin pigments in the retinal pigment epithelium (R

259 in the abca4 gene massively accumulate toxic lipofuscin pigments in the retinal pigment epithelium.

260 hetic pathways of retinal pigment epithelial lipofuscin pigments is critical to the development of th

261 Stargardt's disease is accumulation of toxic lipofuscin pigments such as N-retinylidene-N-retinyletha

262 Bisretinoid lipofuscin pigments that accumulate in retinal pigment e

263 Lipofuscin pigments were significantly increased by bioc

264 in retinal pigment epithelial (RPE) cells as lipofuscin pigments.

265 ere analyzed biochemically for retinoids and lipofuscin pigments.

266 For each strain, the levels of lipofuscin precursor fluorophores in dark-adapted rods a

267 It also prevented light-induced lipofuscin precursor formation, but it did not remove pr

268 of all-trans-retinol, all-trans-retinal, and lipofuscin precursors in real time in single isolated mo

269 outer segment components, sometimes forming lipofuscin precursors, which after conversion to lipofus

270 In Abca4(-/-) mice, lipofuscin-related 488 nm AF increased early in life wit

271 evels of GM2 and GM3 in lysosomes, decreases lipofuscin-related autofluorescence, and eliminates gian

272 These data do not support a role for lipofuscin-related cell death and call into question the

273 surements in this sample showed no increased lipofuscin-related fundus AF in patients with early and

274 a thick lipofuscin deposit or intracellular lipofuscin resembles that for A2E.

275 and melanosomes approached that observed in lipofuscin samples.

276 Cases with abnormal neuronal lipofuscin showed subtle magnetic resonance imaging cort

277 inoid pigments of retinal pigment epithelial lipofuscin, subsequent to photoactivation and cleavage,

278 Aerobic photoreactivity of RPE lipofuscin substantially increases with aging.

279 d within autophagosomes, increased levels of lipofuscin suggest that impairments in mitochondrial tur

280 urons containing Marinesco bodies (TH+MB) or lipofuscin (TH+lipo), markers of UPS or lysosomal activi

281 retinylethanolamine, a toxic form of retinal lipofuscin that accumulates in RPE lysosomes and drives

282 The debris within the cells is converted to lipofuscin, the antigen for the ED-1 antibody, and remai

283 Lipofuscin, the formation of which is driven by reactive

284 Indeed, a major constituent of RPE lipofuscin, the pyridinium bisretinoid A2E, is a diretin

285 in retinal pigment epithelial (RPE) cells as lipofuscin; these fluorophores are implicated in the pat

286 ggesting additional mechanisms beyond direct lipofuscin toxicity.

287 idene-N-retinylethanolamine) seem to mediate lipofuscin toxicity.

288 Hyperreflective specks may represent lipofuscin translocating inwardly within cones.

289 composition, absorption, and fluorescence of lipofuscin undergo age-related changes, the purpose of t

290 increasing cholesterol accumulation (but not lipofuscin) via upregulation of cholesterol biosynthesis

291 1), G85R SOD1YFP and G93A SOD1, little or no lipofuscin was detected in motor neuron cell bodies.

292 By histologic analysis, cone lipofuscin was found in outer retinal layers of 25% of h

293 Lipofuscin was noted in aged GRN(+/+) mice at levels com

294 After 2 wk, lipofuscin was now observed in motor neurons, and SQSTM1

295 osition of autofluorescent storage material (lipofuscin) was observed in the cerebellum and in neuron

296 deposits of lipoproteins, including immature lipofuscin, were observed.

297 ium bis-retinoid A2E is a major component of lipofuscin which accumulates in retinal pigment epitheli

298 Aging RPE accumulates lipofuscin, which includes N-retinylidene-N-retinylethan

299 xhibits hyperautofluorescence from overlying lipofuscin within RPE (orange pigment) and free fluoroph

300 isplays overlying hyperautofluorescence from lipofuscin within RPE and fresh subretinal fluid, but wh