Vitreous fluid levels of β-amyloid(1–42) and tau in patients with retinal diseases

Yoneda, Shinji; Hara, Hideaki; Hirata, Akira; Fukushima, Mikiko; Inomata, Yasuya; Tanihara, Hidenobu

doi:10.1007/s10384-004-0156-x

Cited by 160 publications

(128 citation statements)

References 7 publications

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“…The vitreous humor has functional interactions with the lens and retina. No changes in these chambers have been reported in AD to date, but a change in Aβ42 and tau protein levels in the vitreous humor has been linked to retinal diseases such as diabetic retinopathy and "glaucoma concurrent with other ocular diseases" [107]. This change in protein levels is similar to that observed in the CSF in AD.…”

Section: (Figure 3)mentioning

confidence: 53%

“…This high protein concentration, along with the optical accessibility of the lens, makes it ideal for the optical investigation of protein aggregation in disease, in vivo. The Aβ protein involved in the pathogenesis of AD in the brain has also been found to exist in the lens (Aβ40 and Aβ42), aqueous humor (Aβ40) and vitreous humor (Aβ42) of the normal human eye [106][107].…”

Section: The Ocular Lens and Vitreous Humor In Alzheimer's Diseasementioning

confidence: 99%

“…This change in protein levels is similar to that observed in the CSF in AD. Given the retinal degeneration observed in AD [119][120][121][122][123] and the recently reported common features between AD and glaucoma [61,107,[121][122][123][124][125][126][127][128][129][130], the vitreous humor is an interesting focus for future research into ocular protein changes in AD.…”

Section: (Figure 3)mentioning

confidence: 99%

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Ocular Biomarkers for Early Detection of Alzheimer's Disease

Frost

Martins

Kanagasingam

2010

JAD

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Alzheimer's disease (AD) is the most common form of dementia and is characterized clinically by a progressive decline in memory, learning and executive function and neuropathologically by the presence of cerebral amyloid deposits. Despite a century of research, there is still no cure or conclusive pre-mortem diagnosis for the disease. A number of symptom-modifying drugs for AD have been developed, but their efficacy is minimal and short-lived. AD cognitive symptoms arise only after significant, irreversible neural deterioration has occurred, hence there is an urgent need to detect AD early, before the onset of cognitive symptoms. An accurate, early diagnostic test for AD would enable current and future treatments to be more effective, as well as contribute to the development of new treatments.While most AD related pathology occurs in the brain, the disease has also been reported to affect the eye, which is more accessible for imaging than the brain. AD-related proteins exist in the normal human eye and may produce ocular pathology in AD. There is some homology between the retinal and cerebral vasculatures and the retina also contains nerve cells and fibers that form a sensory extension of the brain. The eye is the only place in the body where vasculature or neural tissue is available for non-invasive optical imaging. This article presents a review of current literature on ocular morphology in AD and discusses the potential for an ocular based screening test for AD.

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Section: (Figure 3)mentioning

confidence: 53%

Section: The Ocular Lens and Vitreous Humor In Alzheimer's Diseasementioning

confidence: 99%

Section: (Figure 3)mentioning

confidence: 99%

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Ocular Biomarkers for Early Detection of Alzheimer's Disease

Frost

Martins

Kanagasingam

2010

JAD

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“…Other authors have investigated possible changes in retinal anatomy in patients with AD, reporting an abnormal reduction of retinal thickness (by OCT) [75] associated with defective blood flow [76]. This retinal damage appears to be associated with increased amounts of b-amyloid and tau proteins in the vitreous body [77]. Finally, a reduction in the number of optic nerve fibers, probably due to the toxicity on RGCs of β-amyloid, has been detected in some studies [78][79][80].…”

Section: Alzheimer' Disease and Eye Pathologiesmentioning

confidence: 99%

“…The Tau protein has also been suggested as a possible common etiopathogenic factor, since it is present both in the CSF of AD patients [98] and in the horizontal cells in the retina of glaucoma patients [99]. However, the most promising studies indicate the amyloid-β protein as the common pathogenetic factor for both diseases [77,90,10,100,11]. In fact, this aberrant protein was found in the vitreous humor of patients with glaucoma and seems to be involved in RGC death.…”

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confidence: 99%

Critical Review on the Relationship between Glaucoma and Alzheimer's Disease

Pescosolido¹,

Pascarella²,

Buomprisco³

et al. 2014

AOVS

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two distinct pathologies, despite similar pathophysiology and demographic distribution. Both diseases are neurodegenerative, chronic and progressive in nature, with irreversible neuronal cell loss. Furthermore, both POAG and AD disease primarily affect the elderly, with a strongly age-dependent incidence. The progressive debilitating course of both diseases has tremendous implications on an aging population [1]. For years Glaucoma has been associated with high IOP [2], although scientists had accepted this etiology with caution, since it was known that POAG could develop in subjects with normal or even low IOP. In fact, one out of three POAG patients has normotensive or low tension glaucoma [3]. This observation has led the scientific community to look for other possible causes of this slowly debilitating pathogenesis.The hallmark of neurodegenerative diseases is the death of specific neuron populations, and of those other neurons that are inter-connected and depend for their survival on the inputs from the main population (trans-synaptic degeneration). In Parkinson's disease accumulation of alfa-synuclein [4] causes the degeneration of dopaminergic neurons of the substantia nigra, in the midbrain, thus leading to the classic symptoms of Parkinson's such as tremor, akinesia, bradykinesia, and stiffness [5]. In AD there is a loss of neurons in the cerebral cortex and certain subcortical regions. This loss results in gross atrophy of the affected regions, including degeneration in the temporal lobe and parietal lobe, and parts of the frontal cortex and cingulate gyrus [6]. Both amyloid plaques and neurofibrillary tangles are AbstractA third of people affected by primary open angle glaucoma (POAG) have normal or even low intraocular pressure (IOP), such as in the case of normotensive glaucoma and low pressure glaucoma. Therefore, high IOP, while remaining the most important risk factor for POAG development, is not the only one. POAG has been recognized to belong to the class of neurodegenerative diseases, such as Alzheimer's (AD) and Parkinson's, and several recent studies have suggested possible links between Alzheimer's and glaucoma both from an epidemiological and a pathogenetic point of view. In fact, several pathogenetic factors are common between the two diseases: the diffuse axonal degeneration of ganglion cells, the presence of specific markers (such as amyloid-β) in the aqueous humor, the activation of caspases and the abnormal processing of amyloid precursor protein in retinal ganglion cells, the reduction of the intracranial pressure of the cerebrospinal fluid, the mutations of the gene that encodes for optineurine. Conflicting data have been reported concerning apolipoprotein E. Finally, numerous publications affirm the utility of molecules traditionally used in the treatment of neurodegenerative diseases (e.g. forskolin, L-carnosine, homotaurine, folic acid, acetylcholinesterase inhibitors, antioxidant vitamins, glatiramer acetate, etc.) also in the treatment of glaucoma.In the present research we ana...

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Activated VEGF Receptor Shed Into the Vitreous in Eyes With Wet AMD

Davuluri¹

2009

Arch Ophthalmol

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To examine whether phosphorylated vascular endothelial growth factor (VEGF) receptors shed into the vitreous reflect the ongoing retinal and choroidal signal pathway activity in wet age-related macular degeneration (AMD).Methods: Vitreous samples obtained immediately prior to anti-VEGF injection from 11 patients with choroidal neovascularization were analyzed using reverse-phase microarrays. Two patients had samples collected at the time of injection and 1 month later. Samples from 5 patients were collected prior to vitrectomy for macular hole, epiretinal membrane, or retinal detachment.Results: Phosphorylated forms of VEGF receptor (VEGFR Y996 and Y1175), platelet-derived growth factor receptor ␤ (PDGFR␤ Y716 and Y751), and c-KIT (Y703) were present in the vitreous. A significant difference in PDGFR␤ Y751 (PϽ.002), VEGFR Y996 (PϽ.04), and VEGFR Y1175 (P Ͻ .006), but not c-KIT Y703 (P Ͻ.05) or PDGFR␤ Y716 (PϽ .96), was noted for the responders to treatment (n = 5) compared with nonresponders (n=6) and controls (n=5).Conclusions: Vitreous levels of activated receptors constitute a new class of biomarkers. Activated forms of VEGF and PDGF receptors, previously not known to exist in the vitreous, correlate with response to anti-VEGF therapy. These findings could provide the basis for the development of individualized treatment and discovery of new therapeutic targets.

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Vitreous fluid levels of β-amyloid(1–42) and tau in patients with retinal diseases

Abstract: Our findings indicate the possibility of a role for Abeta42 and tau in the pathogenesis of some retinal diseases.

Cited by 160 publications

References 7 publications

Ocular Biomarkers for Early Detection of Alzheimer's Disease

Ocular Biomarkers for Early Detection of Alzheimer's Disease

Critical Review on the Relationship between Glaucoma and Alzheimer's Disease

Activated VEGF Receptor Shed Into the Vitreous in Eyes With Wet AMD

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