Neuroinflammation and HD

Posted: March 19, 2013 in Uncategorized
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One important, and often overlooked, aspect of health that plays a role in almost every disease is inflammation. Neurodegenerative disorders such as Alzheimer’s and Parkinson’s have strong ties to inflammation. This is also true of depression, anger, anxiety, and other behavioral issues. During the inflammation process, protein messangers called cytokines are released. These cytokines can cross the blood brain barrier and suppress cell functioning in the brain. This is where the neurodegeneration and behavioral problems can be seen.

So how does this relate to Huntington’s Disease (HD). HD is a neurodegenerative disease that is accompanied by psychological symptoms so why would we not think that inflammation plays a key role? One marker studies look at for inflammatory damage is an increase in peripheral type benzodiazepine binding sites (PTBBS). PTBBS are found in higher numbers when neuronal damage is present (http://brain.oxfordjournals.org/content/123/11/2321.short). High levels of PTBBS were found in the putamen and moderate levels were found in the frontal cortex of patients with HD (http://www.sciencedirect.com/science/article/pii/S0304394097009671). This is what is seen in patients with other forms of neurodegeneration.

Two specific inflammatory markers I want to discuss are IL-6 and TNF-alpha. These two inflammatory cytokines are found in increased levels in the striatum, a part of the brain seriously affected in HD. Research has also shown that this increase in IL-6 leads to immune cell hyperactivity in the cells containing the abnormal HUntington protein. The exciting part is that these markers can be found in patients with the HD gene years before any symptoms begin (http://hdresearch.ucl.ac.uk/our-results/inflammation/). This may lead to other treatments that can help delay the age of onset, but also may give us a look into the pathology of the disease.

Perhaps the body produces an inflammation response to the abnormal Huntington protein. Inflammation does not do its damage immediately. It takes time for it to take its toll. Perhaps it is this continued inflammation response that damages neurons and leads to the onset of symptoms? The other interesting concept is the role of stress and our neurotransmitter GABA.

GABA is like our body’s valium. During high stress times we release GABA to cal ourselves down. Over time GABA can become depleted and this can lead to an imbalance. Chorea is another symtpom of HD and it is caused by a decrease in GABA in the basal ganglia. This leads to a lack of inhibition for dopamine and excessive movement. This is one area I am going to look into more. In the meantime manage your stress, with or without a HD diagnosis!

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Comments
  1. Andy says:

    Another great post!

    Have you come across any studies that also show an increase in peripheral inflammation along with intrathecal (central nervous system) inflammation in realation to HD?

    I am trying to locate studies that show this relationship in FTLD.

    Thanks,

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