At the Institut Curie, CNRS and Inserm researchers have shown that cysteamine, which is already used to treat a rare disease called cystinosis, prevents the death of neurons in Huntington’s disease. Like Alzheimer’s and Parkinson’s, Huntington’s disease, is characterized by the abnormal death of neurons.
A protein that “releases” BDNF The nuclei in these two neuronal cells appear blue. The cell on the right has been treated with cysteamine, and so neuroprotective BDNF is progressively secreted from the Golgi apparatus, which appears yellow, and spreads around the nucleus within the cytoplasm. This reorganization results in better release of neuroprotective BDNF. © S. Humbert-F. Saudou/Institut Curie
A protein that “releases” BDNF BDNF (green) and clathrin (red), a marker of BDNF-containing vesicles, are abundant in the Golgi apparatus of neurons. © S. Humbert-F. Saudou/Institut Curie
Cysteamine raises neuronal levels of BDNF protein, a trophic factor which is depleted in Huntington’s disease, and by assaying BDNF in the blood it is possible to evaluate the effect of treatment. If other studies confirm these results, cysteamine could soon be used to treat Huntington’s disease, and BDNF could serve as a biomarker of its efficacy.
Huntington’s disease is a rare (1 in 10 000 people) neurological condition whose onset occurs between the ages of 35 and 50. The most striking symptoms are involuntary abnormal movements of the limbs, head and neck. These are accompanied by mental symptoms (anxiety, irritability, depression) and intellectual deterioration leading to dementia. Death occurs 15 to 20 years after disease onset as a result of complications (pulmonary embolism, pneumonia, other infection).
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