Well, Huntington’s disease is a neurodegenerative disease, is a genetic neurodegenerative disease, which the cause of the disease is pretty well known, and apparently it has nothing to do with tau pathology. Huntington’s results as a consequence of a CAG repeat expansion, an abnormal expansion that alters the configuration of a protein called Huntingtin. However, we know many things about the toxicity of Huntingtin and how it disrupts several structures in the brain, etc...
Well, Huntington’s disease is a neurodegenerative disease, is a genetic neurodegenerative disease, which the cause of the disease is pretty well known, and apparently it has nothing to do with tau pathology. Huntington’s results as a consequence of a CAG repeat expansion, an abnormal expansion that alters the configuration of a protein called Huntingtin. However, we know many things about the toxicity of Huntingtin and how it disrupts several structures in the brain, etc. Huntington’s is extremely heterogeneous by means of age at onset, by means of clinical phenotype, etc. So, in this study, we attempted to know a bit more about all the other mechanisms that may be contributing to the clinical heterogeneity of Huntington’s disease beyond all these things explained by the genetic mutation. So, we used this tau PET tracer to see in pre-manifest people who are carrying the genetic mutation that confirms that they will develop the disease in the future, but they are not exhibiting symptoms. And in early symptomatic HD patients, we administered this tau PET tracer to see if something relevant is happening by means of tau pathology in the brain of these people. Not because we think it’s a tau pathology, but because we think that even in a genetically-determined neurodegenerative disease, things are not the result of a single protein or problem. Things are the result of a complex constellation of neurobiological events. And we identified that already in an important subset of pre-manifest individuals, around 60% of them, we can detect tau PET binding in the striatum and in different cortical regions, and that this pattern of tau activity progressively spreads to the whole brain along the progression of the disease. So it confirms that tau copathology is happening in Huntington’s. Our results also show a clear association between the location and the extent and the magnitude of the signal and a series of clinical symptoms of Huntington’s disease. So there is a clear association between tau activity and the clinical phenotype and the clinical aspects of the disease. And this is quite important because we have anti-tau molecules being used in other diseases, so in our attempt to correct or to do something good for people experiencing or having Huntington’s disease, our results go in the direction of the need to consider a multi-target treatment strategy in an attempt to solve this kind of problem.
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