Stories about: glaucoma

Drug-eluting contact lens offers hope in glaucoma

Daniel Kohane drug-eluting contact lens
Contact lenses ringed with a drug-bearing polymer film provided gradual, sustained drug release in this preclinical study, potentially offering an alternative to eye drops.

Daily medicated eye drops are the first line of treatment for glaucoma, the leading cause of irreversible blindness. The drops relieve pressure in the eye, a significant risk factor for glaucoma. But they’re not ideal: their delivery is imprecise, they can cause stinging and burning and patients often struggle to administer them. Adherence is poor: in one study based on insurance claims data, nearly half of patients who had filled a glaucoma prescription stopped topical glaucoma therapy within six months.

Engineered contact lenses dispensing glaucoma medication gradually could vastly improve adherence, helping hang onto their eyesight longer. In a pre-clinical study of glaucoma published online this week in the journal Ophthalmology, slow-release lenses lowered eye pressure at least as well as daily eye drops containing the drug latanoprost — and, in a higher-dose form, possibly more so.

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Stopping blindness: The drug-eluting contact lens

drug-eluting contact lens
(John Earle Photography)

Growing up, my grandmother’s eyes were always a problem. For years, she was losing her central vision to glaucoma, and numerous surgeries and treatments did not seem to help. Later in life, she could not see my face but could always tell who I was when I was close.

Glaucoma is the leading cause of irreversible blindness worldwide. While FDA-approved medications such as latanoprost can prevent vision loss by reducing pressure in the eye, their beneficial effects are limited by poor patient compliance: At six months of treatment, compliance is estimated to be little more than 50 percent.

Why? First, the medications are typically delivered as eye drops, and the drops themselves can cause stinging and burning. The drops also contain preservatives that can cause ocular surface disease.

Perhaps most importantly, latanoprost and other glaucoma drugs halt the disease’s progression but do not reverse it. Taking the drugs does not provide positive feedback that will motivate patients, such as relieving pain.

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Immune cells “sculpt” brain circuits — by eating excess connections

The above movie shows an immune cell caught in the act of tending the brain—it’s just eaten away unnecessary connections, or synapses, between neurons.

That’s not something these cells, known as microglia, were previously thought to do. As immune cells, it was thought that their job was to rid the body of unwanted pathogens and debris, by engulfing and digesting them.

The involvement of microglia in the brain’s development has started to be recognized only recently. The latest research finds that microglia tune into the brain’s cues, akin to the way they survey their environment for invading microbes, and get rid of excess synapses the same way they’d dispatch these invaders—by eating them.

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First light: Vision restored in blind mice

Regenerating nerve fibers from the retina (shown in red) are seen coming into the dorsal lateral geniculate nucleus, a principal visual relay area of the brain.

Some kinds of vision loss are reversible: Lucentis and Avastin can restore some visual acuity in macular degeneration, and gene therapy in the eye has had success in genetic forms of blindness like Leber’s hereditary neuropathy, affecting light receptors in the retina. But when the optic nerve is damaged – from a traumatic injury or from glaucoma — all bets are off. The eyes may take in visual information, but it can’t get to the brain. It’s the end of the road.

Larry Benowitz, PhD, and other neurobiologists at Boston Children’s Hospital and elsewhere have tried for years to rebuild that road. Regeneration of the optic nerve, and in the central nervous system in general, was once thought impossible. But through patient tinkering to coax natural growth signals and silence growth-inhibiting signals, neurons in the retina – known as retinal ganglion cells — began to grow a bit into the optic nerve. Then a bit more.

In a 2010 paper, Benowitz’s team combined their top three interventions, and showed a synergistic effect – the greatest growth of optic nerve fibers (axons) to date. But no one had been able to demonstrate recovery of vision after severe optic nerve damage – until now.

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