breakdown of the myelin that depends on it. That, consecutively, upsets cell signalling, which results in the neuron's death.
The problem is compounded by the recurrent production of other cells that carry on making myelin. In HD, increasing numbers of these cells, called oligodendrocytes, are created in an effort to remyelinate axons whose myelin sheaths have broken down. This results in markedly elevated numbers of oligodendrocytes years before the appearance of HD symptoms.
Such elevation is damaging because oligodendrocytes are rich with iron, which, while required for myelination, is also a recognized catalyst of free-radical-induced tissue damage. Iron accumulates during normal aging, and abnormal iron metabolism is believed to be involved in many human disorders.
To spot myelin destruction, neuron death and iron accumulation in the brains of HD subjects, Bartzokis used two magnetic resonance imaging (MRI) machines operating at different field strengths. Measurements of myelin breakdown and iron content were taken from the brains of 11 HD subjects and compared to a control group of 27 subjects. Bartzokis found that both the breakdown and the iron accumulation matched the typical progression of the disease from early to late myelinating regions.
Thus, according to Bartzokis, earlier myelinated axons, such as the ones controlling movement, take the strain of damage from the mutant gene in the disease. "And the early symptoms of Huntington's are problems with controlling movement, behavior and eventually thinking," Bartzokis said.
The implications of this are significant, Bartzokis noted, since there is a decades-long period during which therapeutic interventions could alter the course of the disease, long before clinical evidence - such as behavioral, cognitive and motor problems - appear. Thus, it may be achievable to build up medication that could be controlled in the very early stages using noPage: 1 2 3 Related medicine news :1
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