Ocular amyloidosis and secondary glaucoma

Nelson, Gregory A.; Edward, Deepak P.

doi:10.1016/s0161-6420(99)00726-5

Cited by 45 publications

(21 citation statements)

References 11 publications

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“…Although intracellular A␤ deposition has been detected in both ganglion and lens fiber cells of patients with glaucoma, AD, or Down's syndrome, [22][23][24][25] other typical hallmarks of AD have not yet been demonstrated. Interestingly, thioflavine-S-positive A␤ plaques were recently found in the retinal strata of APPswe/PS1⌬E9 transgenic mice 26 but not in the other animal models of AD.…”

mentioning

confidence: 99%

Amyloid-Peptide Vaccinations Reduce β-Amyloid Plaques but Exacerbate Vascular Deposition and Inflammation in the Retina of Alzheimer’s Transgenic Mice

Liu

Rasool

Yang

et al. 2009

The American Journal of Pathology

162

176

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confidence: 99%

Amyloid-Peptide Vaccinations Reduce β-Amyloid Plaques but Exacerbate Vascular Deposition and Inflammation in the Retina of Alzheimer’s Transgenic Mice

Liu

Rasool

Yang

et al. 2009

The American Journal of Pathology

162

176

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“…The deposition of perivascular amyloid in conjunctival and episcleral tissue may contribute to the elevation in episcleral venous pressure, resulting in an elevation in intraocular pressure. 12 Another possibility is that the deposition of ocular amyloid leads to a resultant obstruction in the aqueous outflow route. 27 We believe that the glaucoma associated with FAP is caused by these 2 mechanisms.…”

Section: Commentmentioning

confidence: 99%

Secondary Glaucoma in Patients With Familial Amyloidotic Polyneuropathy

Kimura

Ando

Fukushima³

et al. 2003

Arch Ophthalmol

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To elucidate the clinical features and surgical outcomes of the treatment of secondary glaucoma associated with transthyretin (TTR)-related familial amyloidotic polyneuropathy (FAP).Design: Retrospective case study.Participants: Forty-nine Japanese patients with FAP.Methods: For all patients, measurement of bestcorrected visual acuity, intraocular pressure, and visual fields as well as slitlamp and ocular fundus examinations were conducted and compared. In addition, the exact mutation of the amyloidogenic TTR variants was analyzed for all 49 patients with FAP. The TTR mutations included amyloidogenic TTR (ATTR) Val30Met in 41 patients, ATTR Tyr114Cys in 6, ATTR Ser50Ile in 1, and a compound heterozygous mutation of ATTR Val30Met + Arg104His in 1. Results:The onset of secondary glaucoma was defined as elevation of intraocular pressure and glaucomatous changes in visual field defects. Secondary glaucoma was detected in 12 (24%) of the 49 patients. The incidence of secondary glaucoma in patients with the Val30Met mutation (17%) was lower than for the other FAP genotypes (P=.02 using the 2 test). Of 20 glaucomatous eyes,

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“…Ocular tissues are one type of tissue in which several different types of amyloid precursor proteins deposit as amyloid fibrils (Lee et al, 2000;Nelson et al, 1999). Most of these amyloid precursor proteins have been identified for systemic amyloidoses in ocular tissues (Ando et al, 1997a;Campos et al, 1980;Ratnakar and Mohan, 1976;Rodrigues and Zimmerman, 1971;Sandgren, 1995).…”

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confidence: 99%

A Novel Localized Amyloidosis Associated with Lactoferrin in the Cornea

Ando

Nakamura

Kai

et al. 2002

Laboratory Investigation

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SUMMARY:We report a novel localized amyloidosis associated with lactoferrin. To elucidate the precursor protein of corneal amyloidosis associated with trichiasis, we analyzed amyloid deposits from three patients by histopathology and biochemistry. Amyloid deposits showed immunoreactivity, confirmed by electron microscopy, for only anti-human lactoferrin antibody. Electrophoresis of amyloid fibrils revealed lactoferrin with and without sugar chains; N-terminal sequence analysis revealed full-length lactoferrin and a truncated tripeptide of N-terminal amino acids, Gly-Arg-Arg. Carboxymethylated wild-type lactoferrin formed amyloid fibrils in vitro. Lactoferrin gene analysis in the three patients revealed a Glu561Asp mutation in all of the patients and a compound heterozygote of Ala11Thr and Glu561Asp mutations in one patient. A heterozygotic Glu561Asp mutation appeared in 44.8% of healthy Japanese volunteers, suggesting that the mutation may not be an essential mutation for amyloid formation (p ϭ 0.104). Results thus suggest that lactoferrin is this precursor protein. (Lab Invest 2002, 82:757-765).

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Ocular amyloidosis and secondary glaucoma

Cited by 45 publications

References 11 publications

Amyloid-Peptide Vaccinations Reduce β-Amyloid Plaques but Exacerbate Vascular Deposition and Inflammation in the Retina of Alzheimer’s Transgenic Mice

Amyloid-Peptide Vaccinations Reduce β-Amyloid Plaques but Exacerbate Vascular Deposition and Inflammation in the Retina of Alzheimer’s Transgenic Mice

Secondary Glaucoma in Patients With Familial Amyloidotic Polyneuropathy

A Novel Localized Amyloidosis Associated with Lactoferrin in the Cornea

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