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    Researchers glimpse Parkinson’s in rats’ eyes

    Retinal changes might serve as a marker for Parkinson’s disease, an experiment in mice suggests. And the therapy also points to a potential treatment.

    Retinal changes may serve as a marker for Parkinson’s disease, an experiment in mice suggests. And the therapy also points to a potential treatment.

    “We show that rosiglitazone can efficiently protect retinal neurons from the rotenone insult, and that systemic administration of liposome-encapsulated rosiglitazone has an enhanced neuroprotective effect on the retina and central nervous system,” wrote Eduardo Maria Normando of Imperial College London, UK, and colleagues.

    They published their finding in Acta Neuropathologica Communications.

    Their line of inquiry began with the observation that intracytoplasmic inclusions called Lewy bodies characteristic of Parkinson’s disease appear not just in the brain, where they damage cells that produce dopamine, but throughout the central nervous system, including the retina.

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    Patients often experience reduced visual acuity, low contrast sensitivity, and disturbed colour vision. The inner retinal layer thins as the disease progresses. Studies are underway to see whether such changes can serve as biomarkers in treatment trials.

    In other trials, investigators have created conditions similar to Parkinson’s in animals. One approach is to administer rotenone, which selectively damages dopaminergic cells, creating cytoplasmic inclusions similar to Lewy bodies. Rats poisoned this way show signs of Parkinson’s, such as parkinsonian bradykinesia and rigidity.

    On the other hand, rosiglitazone, a member of the thiazolidinedione drug family, has shown promise in protecting against the effects of rotenone in these animals. It appears to promote an anti-inflammatory response and to reverse inhibition of monoamine oxidase, a crucial enzyme for dopamine metabolism.

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    Originally used to counter insulin resistance in type 2 diabetes, thiazolidinedione reduced the incidence of Parkinson’s in patients with diabetes by 28% in one study. But in another, it failed to slow disease progression in patients already diagnosed with Parkinson’s. Some investigators theorise that it can protect cells but not restore their function.

    Dr Normando and colleagues wanted to see whether they could measure signs of retinal change in rats treated with rotenone, and whether they could also measure the effects of rosiglitazone in these eyes.

    They treated eight different groups of rats with rotenone, rosiglitazone, the vehicles for these drugs, or various combinations.

    Study results


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