Basal linear deposit in the human macula

Löffler, K. U.; Lee, William R.

doi:10.1007/bf02154735

Cited by 143 publications

(64 citation statements)

References 24 publications

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“…Basal laminar deposits (BLamD) that accumulate between the RPE basal plasma membrane and its basal lamina (Figures 21, 24 and 28) do not appear to be specific to or 'diagnostic' for AMD; however, there is a strong relationship between macular BLamD and exudative AMD, disciform scarring, and visual loss (74,84,(108)(109)(110)(111)(112)(113)(114). BLamD-like deposits are also seen in other macular disorders with a clinical appearance similar to what is observed in AMD.…”

Section: Morphological Correlates Of Early Amdmentioning

confidence: 99%

Age‐related macular degeneration—emerging pathogenetic and therapeutic concepts

et al. 2006

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Today, the average life expectancy in developed nations is over 80 years and climbing. And yet, the quality of life during those additional years is often significantly diminished by the effects of age-related, degenerative diseases, including age-related macular degeneration (AMD), the leading cause of blindness in the elderly worldwide. AMD is characterized by a progressive loss of central vision attributable to degenerative and neovascular changes in the macula, a highly specialized region of the ocular retina responsible for fine visual acuity. Estimates gathered from the most recent World Health Organization (WHO) global eye disease survey conservatively indicate that 14 million persons are blind or severely visually impaired because of AMD. The disease has a tremendous impact on the physical and mental health of the geriatric population and their families and is becoming a major public health burden.Currently, there is neither a cure nor a means to prevent AMD. Palliative treatment options for the less prevalent, late-stage 'wet' form of the disease include anti-neovascular agents, photodynamic therapy and thermal laser. There are no current therapies for the more common 'dry' AMD, except for the use of antioxidants that delay progression in 20%-25% of eyes. New discoveries, however, are beginning to provide a much clearer picture of the relevant cellular events, genetic factors, and biochemical processes associated with early AMD. Recently, compelling evidence has emerged that the innate immune system and, more specifically, uncontrolled regulation of the complement alternative pathway plays a central role in the pathobiology of AMD. The complement Factor H gene-which encodes the major inhibitor of the complement alternative pathway-is the first gene identified in multiple independent studies that confers a significant genetic risk for the development of AMD. The emergence of this new paradigm of AMD pathogenesis should hasten the development of novel diagnostic and therapeutic approaches for this disease that will dramatically improve the quality of our prolonged lifespan.

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Section: Morphological Correlates Of Early Amdmentioning

confidence: 99%

Age‐related macular degeneration—emerging pathogenetic and therapeutic concepts

et al. 2006

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“…Basal laminar deposit (BlamD), between the RPE and its basement membrane, forms small pockets in many older normal eyes or a continuous layer as thick as 15 µm in eyes with ARMD ( 58,65,66 ). Ultrastructurally, BlamD resembles basement membrane material and contains laminin, fi bronectin, and type IV and VI collagen (67)(68)(69)(70). Thick BlamD, associated with risk for advanced ARMD ( 65 ), is more heterogeneous, containing vitronectin, MMP-7, TIMP-3, C3, and C5b-9 ( 66 ) and histochemically detectable EC and UC.…”

Section: Epidemiology and Risk Factorsmentioning

confidence: 99%

Apolipoprotein B-containing lipoproteins in retinal aging and age-related macular degeneration

Curcio

Johnson

Huang

et al. 2010

Journal of Lipid Research

169

145

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“…A subsequent production of vesicular and eosinophilic, PAS-positive amorphous material, together with an increasing amount of LSC, accumulate first in the inner collagenous zone of Bruch's membrane but progressively also extend into the elastic and outer collagenous zones, the boundaries of which then disappear. These prominent age-related changes of Bruch's membrane are considered to play a role in the pathogenesis of age-related macular degeneration (AMD) [Hogan, 1972;Sarks, 1976;Löffler and Lee, 1986;van der Schaft et al, 1992;Green and Harlan, 1999;Guymer and Bird, 2001]. With the increasing thickness of BlamD throughout life, the distance between the RPE and its nutritional source the choriocapillaries also increases.…”

Section: Introductionmentioning

confidence: 99%

New Components of ‘Basal Laminar Deposits’ in Age-Related Macular Degeneration

Reale

Groos

Eckardt

et al. 2008

Cells Tissues Organs

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Two new components of basal laminar deposit (BlamD) occurring in samples of submacular neovascular membranes surgically removed from patients with a wet (exudative) form of age-related macular degeneration are described. They are: (1) minute ribbon-like structures which occur singly and/or in a bunch and extend from the inner surface of the BlamD layer into the extracellular matrix (ECM) beneath the retinal pigment epithelium (RPE). The ribbons are composed of polarized molecules, aggregating in parallel, aligned transversally in register, morphologically similar to isolated collagen molecules of the short-chain type. Deeper in the BlamD but always close to its inner surface, aspects suggesting a transition between ribbons and (2) long-spacing collagen (LSC)-like aggregates characterized by periods bordered by a single dense band were observed. This band could arise from the globular domains of the polarized monomers, which assemble in parallel and display all their terminal extensions at the same end of each period resulting in the single dense band. The presence of ribbons and of LSC-like aggregates in the BlamD layer and the concomitant choroidal neovascularization (CNV) suggest that the events might be correlated. The newly formed vessels crossing Bruch’s membrane and invading the BlamD layer could induce physicochemical changes in the ECM of the RPE, providing the required environmental conditions for the polymerization of collagen molecules into aggregates with the LSC-like pattern. With the deposition of new components, the thickness of BlamD increases and further impairs the supply of nutrients and oxygen, thus sustaining CNV.

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Basal linear deposit in the human macula

Cited by 143 publications

References 24 publications

Age‐related macular degeneration—emerging pathogenetic and therapeutic concepts

Age‐related macular degeneration—emerging pathogenetic and therapeutic concepts

Apolipoprotein B-containing lipoproteins in retinal aging and age-related macular degeneration

New Components of ‘Basal Laminar Deposits’ in Age-Related Macular Degeneration

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