Caption: FIGURE 3: CNV at Bruch's membrane
rupture sites is decreased in Flt3- deficient animals.
In normal ageing, the increased thickness of Bruch's membrane
[17, 18], the deposition of normal and abnormal ECM material , increased cross-link formation (oxidative and nonenzymatic glycosylation leading to advanced glycation end-products, AGEs, and ALEs) , and the accumulation of lipid-rich debris [20, 21] are changes that implicate a disturbance in the ECM turnover of the membrane.
Microscopic analysis of eyes donated by patients with AMD revealed lipid deposits within Bruch's membrane
and apoptosis of RPE cells as features of the disease that are distinct from normal aging.
Drusen are the focal deposits of extracellular debris located between the basal lamina of the RPE and Bruch's membrane
(2) They result from a rupture of the elastic tissue in the Bruch's membrane
of the retina.
Using aged submacular human Bruch's membrane
explants in organ culture, we reproduced the incomplete and aberrant RPE resurfacing seen in AMD patients following CNV excision .
A breakdown in the Bruch's membrane
usually occurs near drusen deposits, and this is where the new blood vessel growth occurs (neovascularization).
The wet form of the disease involves the growth of blood vessels from the choriocapillaris through the Bruch's membrane
and into the RPE and sub-retinal spaces.
Calcium deposits can build up in the Bruch's membrane
(a membrane between retinal tissues and its blood supply), blocking nutrients and oxygen to the eyes' photoreceptors and preventing the elimination of debris that contributes to macular degeneration.
Statins may prevent the accumulation of basal linear deposit in Bruch's membrane
, which occurs in patients with high cholesterol levels.
Statins may prevent accumulation of basal linear deposit in Bruch's membrane
, which occurs when cholesterol levels are high.
It has been postulated that in old age, this material is released from the RPE and renders the overlying Bruch's membrane
The TIMP3 mutations may promote excessive growth of blood vessels through Bruch's membrane
, which lies below the retina, they speculate.
The etiopathogenesis of pachychoroid spectrum diseases involves microtrauma to the Bruch's membrane
from the enlarged pachy-veins in the Haller's layer.
The diameter of Bruch's membrane
opening is larger in patients with papilloedema than in those without papilloedema.