Study Links 'Leaky' Brain Cells to Ageing

As we age, the barrier between the nucleus and the rest of the brain cell grows leakier, says a new study, which claims that reversing this leakiness could lead to new treatments

As we age, the barrier between the nucleus and the rest of the brain cell grows leakier, says a new study, which claims that reversing this "leakiness" could lead to new treatments for Parkinson's, and overturn the effects of ageing.

The barrier between nucleus and cytoplasm is usually controlled by cellular gateways called nuclear pores, which selectively import and export the molecular ingredients for life to and from the nucleus.

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For the study, the researchers used Caenorhabditis elegans, a roundworm that consists entirely of non-dividing cells as an adult.

They found that the scaffold begins to break down in ageing cells as a result of oxidative stress, which allows other cell proteins to start invading the nucleus.

"We think that the age-dependent deterioration of pores might be an ageing mechanism that leads to defects in nuclear function," New Scientist quoted Martin Hetzer at the Salk Institute of Biological Sciences in La Jolla, California as saying.

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"We are now investigating the possibility of plugging the leaky pores and thereby preventing the breakdown of cell compartmentalisation," he added.

The team found that tubulin, proteins that make up the microtubule filaments normally found only out in the cytoplasm, accumulate in nuclei with such leaky pores.

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This tubulin forms long filaments that may damage the chromosomes. In Parkinson's patients, tubulin filaments are particularly prevalent in part of the brain linked to production of the neurotransmitter dopaminem, and is damaged by the disease.

The study appears in journal Cell.

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