"We know that there is a natural process that is actually stimulated in the diseased brain for the brain to try and repair itself," said Faull. "We need to harness the natural processes."

Forget embryonic stem cell therapy for neurodegenerative diseases like Huntington's, says a New Zealand neurologist. The stem cells are already there in diseased brains, he notes, it's just a question of harnessing their potential. "We have evidence to suggest that stem cells in the basal ganglia of the human brain have the potential to proliferate and possibly repair in disease," said Richard Faull, co-director of the Neurodegenerative Diseases of the Brain section at the University of Auckland. "No-one's shown it in diseases before," he told BioMedNet News.

The first discovery of neurogenesis in the adult human brain was made in 1998 in sections of healthy brain from patients with cancer of the larynx. Faull has now found that not only does this process occur in the brains of patients with Huntington's disease, but that it increases with disease severity.

Faull looked for signs of cell proliferation in the brains of patients who had died with Huntington's disease. He probed sections of the subependymal region (SEP) with an antibody against a proliferating-cell marker, called proliferating cell nuclear antigen (PCNA).

The data revealed a band of dividing cells in the SEP, which increased in thickness relative to increasing symptom severity.

So, says Faull, the normal process of neurogenesis is amplified in patients with Huntington's disease, but appears not to be switched on fast enough or directed correctly.

"We know that there is a natural process that is actually stimulated in the diseased brain for the brain to try and repair itself," said Faull. "We need to harness the natural processes."

Not everyone is so enthused by the findings. "It's nothing," said Yvan Arsenijevic, research fellow at the Oculogenetic Unit of Lausanne University in Switzerland. "Those could be any cells dividing," he told BioMedNet News. "They could be glial cells."

Faull rejects the criticism. He says that he also probed the SEP tissue sections for neuron-specific markers, including beta tubulin and microtubule associated protein (MAP). Some of the cells in the band of dividing cells stained for both these markers, he claims, although he did not show these data in today's presentation. He also probed for the glial marker GFAP, and concedes that there are glial cells among those in the proliferative band.

Data collected in rats show that there are multipotential cells in the SEP, says Faull. Those cells can become glial cells or neurons under different conditions, he adds, suggesting that the same may be true in humans. "We need to work out what it is that's going to induce differentiation into neurons."

Faull also has evidence of neuronal proliferation in this brain region in patients with epilepsy, he says, and suggests that the same could be true for patients with Parkinson's disease and even Alzheimer's.

"There's a common principle here," he said. "These cells do proliferate in this area, in a disease of the brain."

Source: ISDN 2002 - Day 3 by Bea Perks 03-Feb-2002

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