THE origin of the mysterious filaments that clog the brains of people with Parkinson鈥檚 and other neurodegenerative diseases may have been identified.
It seems that the barrier enclosing the nucleus inside cells grows leakier with age, admitting proteins from outside. One, called tubulin, forms long filaments that clog up the nucleus and may damage chromosomes.
Lead researcher Martin Hetzer of the Salk Institute for Biological Sciences in La Jolla, California, says that in people with Parkinson鈥檚, tubulin filaments abound in the substantia nigra, the part of the brain affected by the disease.
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Finding a way to reverse nuclear 鈥渓eakiness鈥� could lead to new treatments as well as slowing ageing more generally, he says.
The barrier between nucleus and cytoplasm is usually policed by nuclear pore complexes, molecular sentinels regulating passage of molecules in and out. Hetzer and his colleagues investigated the fate of these complexes as cells age. They showed that Caenorhabditis elegans, a roundworm whose cells do not divide in adulthood, retains the same complexes for life. This was also true in non-dividing rat neurons (Cell, ).
But these pore scaffolds gradually break down with age, admitting proteins. 鈥淲e think the age-dependent deterioration of pores might lead to defects in nuclear function,鈥� Hetzer says. 鈥淲e are now investigating the possibility of plugging the leaky pores and preventing breakdown of cell compartmentalisation.鈥�