In Parkinson’s Disease, age of onset of symptoms provides a dividing line of sorts between two subgroups. If symptoms first appear after the approximate age of sixty, then the influences of age and the insults that come with it are the predominant factors. generating a destructive neuroinflammatory response including the activation of microglia. This appropriately named “Senior Onset” can be triggered by pathogens such as influenza but with a latency period of twenty years or more. Aging tends to sensitize the microglia, as well. The combination of past exposures and the effects of aging can trigger the “slow burn” which ultimately leads to SOPD.
Young Onset, however, arises from a more complicated field and, while the microglial role is similar to that in SOPD, the complexity of additional factors overshadows it to a certain extent. At a minimum, the following must be considered:
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The role of the bacterial endotoxin lipopolysaccharide (LPS), both as it impacts the fetal environment and its effect upon the adult;
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The role of the maternal endocrine system and the effect of her stress hormones upon the fetus;
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The effect of both LPS and maternal stress upon the young endocrine system;
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The synergistic relationship between the sensitized immune system and the poorly regulated endocrine system and its impact upon the nervous system;
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The influence of the gastrointestinal tract in an inflammatory environment;
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The impact of these three systems upon the central nervous system;
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The role of the environment, both chemical and situational.
We will examine these various aspects of PD, one by one, but it must be kept in mind that the problem exists as a whole and it is only as a whole that it will be understood. As a result, it does not lend itself to a description of its parts and must, instead, be examined in “layers” which preserve the connections between the components. We begin with a brief overview with no attempt to justify our statements. That will come at the next stage.
Young Onset Parkinson’s Disease is not Senior Onset and its origins are its own. The two share a common path in terms of the damage done by the activity of the microglia and the problems of the resulting motor symptoms, it is true. However, YOPD has other aspects to consider:
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A hypersensitivity to exposure to the bacterial toxin lipopolysaccharide (LPS).
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A vulnerability to certain environmental factors that results from that hypersensitivity.
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A poorly regulated endocrine system that yields a host of symptoms even more debilitating than the motor problems.
It is this complex interweaving of factors that will be examined in the weeks to come.