ライフサイエンスコーパス: lipofuscin

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

2 estation of altered behavior, and buildup of lipofuscin.

3 aneuronal ubiquitin-positive autofluorescent lipofuscin.

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

5 e effects of retinal pigment epithelial cell lipofuscin.

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

7 cytoplasmic swellings containing undigested lipofuscin.

8 cellular accumulation of the aging biomarker lipofuscin.

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

10 s derivatives, in the photoreactivity of RPE lipofuscin.

11 ducts, called the retinyl pigment epithelium-lipofuscin.

12 y reflect dysfunction before accumulation of lipofuscin.

13 ntly lower than that induced by photoexcited lipofuscin.

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

15 case of mtDNA, the vacuoles associated with lipofuscin.

16 that the albipunctate spots do not represent lipofuscin.

17 in detecting macular edema and deposition of lipofuscin.

18 estion the rationale of treatments targeting lipofuscin.

19 , as previously surmised, the damage product lipofuscin.

20 ilar to the bisretinoids that constitute RPE 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 e mechanisms by which retinoids modulate RPE lipofuscin accumulation have not been elucidated.

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

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

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

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

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

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

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

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

59 upcoming treatment trials that aim to modify lipofuscin accumulation.

60 inal or macular degeneration associated with lipofuscin accumulation.

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

62 of Rpe65 knockout mice did not contribute to lipofuscin accumulation.

63 impairment of retinoid metabolism alters RPE lipofuscin accumulation.

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

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

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

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

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

69 Lipofuscin and A2E levels in the RPE increased with age

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

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

72 Accumulation of indigestible lipofuscin and decreased mitochondrial energy production

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

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

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

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

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

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

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

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

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

82 A2E, the major fluorophore of lipofuscin, and its precursors, A2PE-H(2) and A2PE, were

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

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

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

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

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

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

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

90 orescence imaging permits measurement of RPE lipofuscin at specific sites.

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

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

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

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

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

96 Lipofuscin bisretinoids (exemplified by N-retinylidene-N

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

98 Because accumulation of lipofuscin bisretinoids and abnormal cholesterol homeost

99 Synthesis of lipofuscin bisretinoids depends on the influx of retinol

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

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

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

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

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

105 gangliosides and preventing their storage in lipofuscin bodies.

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

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

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

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

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

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

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

113 ified two related but previously unknown RPE lipofuscin compounds.

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

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

116 Lipofuscin contained in the retinal pigment epithelium (

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

118 suggest that the age-related increase in RPE lipofuscin content results from an imbalance in the rate

119 RPE lipofuscin content was also estimated with quantitative

120 Lipofuscin content was classified independently by 2 mas

121 detection of true retinal pigment epithelial lipofuscin content.

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

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

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

125 Lipofuscin deposition is increased in both DRG neurons a

126 Lipofuscin deposition was increased in cardiomyocytes of

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

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

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

130 luorescence imaging device was used to study lipofuscin distribution associated with individual druse

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

132 te autofluorescent lysosomal storage bodies (lipofuscin) during senescence.

133 Lipofuscin fluorescence increased linearly until age 70,

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

135 Lipofuscin fluorescence was imaged in flat-mounted RPE f

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

137 The lipofuscin fluorophore A2E has been shown to mediate blu

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

139 In the Rpe65(-/-) mice, RPE lipofuscin fluorophore accumulation was almost abolished

140 RPE lipofuscin fluorophore content was compared in 12- to 13

141 Lipofuscin fluorophore content was determined using quan

142 Indeed, at least one RPE lipofuscin fluorophore is derived in part from vitamin A

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

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

145 The major lipofuscin fluorophore, A2E, is a pyridinium bisretinoid

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 ockout mice drastically reduced formation of lipofuscin fluorophores in these animals.

152 hese findings indicate that formation of RPE lipofuscin fluorophores is almost completely dependent o

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

154 ion, a significantly reduced accumulation of lipofuscin fluorophores was also observed in the Rpe65(+

155 visual cycle retinoids and ocular levels of lipofuscin fluorophores.

156 nt results from an imbalance in the rates of lipofuscin formation and disposal rather than from a com

157 Increased lipofuscin formation is characteristic of LC cells from

158 RPE-retina complex play a major role in RPE lipofuscin formation.

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

160 The spatial distribution of lipofuscin generally matches that of rods and reflects,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 dominant blue-absorbing chromophores within lipofuscin granules.

176 oved recovery of dark adaptation and reduced lipofuscin granules.

177 RPE lipofuscin had strong autofluorescent emissions that wer

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

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

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

181 characterize the age-related accumulation of lipofuscin in a population of normal subjects, resolve d

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

183 Increased accumulation of lipofuscin in cells of the retinal pigment epithelium (R

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

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

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

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

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

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

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

191 and characterize the spatial distribution of lipofuscin in the normal fundus.

192 Accumulation of lipofuscin in the retina is associated with pathogenesis

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

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

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

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

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

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

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

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

201 93C) mice exhibited enhanced accumulation of lipofuscin in the RPE, and a significant deposition of d

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

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

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

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

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

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

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

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

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

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

212 Although lipofuscin is considered a hallmark of Stargardt disease

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

214 Excessive accumulation of lipofuscin is observed in numerous degenerative retinal

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

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

217 A major fluorophore of lipofuscin is the toxic bis-retinoid, N-retinylidene-N-r

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

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

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

221 Lipofuscin levels were determined by fluorescence imagin

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

223 1 result in an increased accumulation of the lipofuscin-like fluorescent aging pigment, shortened lif

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

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

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

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

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

229 cells were filled with membranous profiles, lipofuscin-like material, and pigment.

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

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

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

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

234 ous albinism, bleeding tendency and a ceroid-lipofuscin lysosomal storage disease result from defects

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

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

237 High RPE lipofuscin may not adversely affect retinal structure or

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

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

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

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

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

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

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

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

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

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

248 In contrast to lipofuscin, photoexcited melanosomes did not substantial

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

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

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

252 The autofluorescent lipofuscin pigment A2E accumulates in retinal pigment ep

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

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

255 This lipofuscin pigment is a fluorescent compound with absorb

256 Lipofuscin pigment-granules were also visible in abcr+/-

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

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

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

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

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

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

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

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

265 Bisretinoid lipofuscin pigments that accumulate in retinal pigment e

266 Lipofuscin pigments were significantly increased by bioc

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

268 ere analyzed biochemically for retinoids and lipofuscin pigments.

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

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

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

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

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

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

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

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

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

278 and melanosomes approached that observed in lipofuscin samples.

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

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

281 Aerobic photoreactivity of RPE lipofuscin substantially increases with aging.

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

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

284 The autofluorescent lipofuscin that accumulates in retinal pigment epithelia

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

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

287 Lipofuscin, the formation of which is driven by reactive

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

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

290 ggesting additional mechanisms beyond direct lipofuscin toxicity.

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

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

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

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

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

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

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

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

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

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

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