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Prenatal Beginnings of Parkinson’s Disease

March 23, 2011

Fetal encounters with the bacterial waste products from maternal infections are common. However, in order for them to cause serious problems, these encounters must occur during the short time that critical structures are forming.      The  results of fetal exposure to the bacterial endotoxin lipopolysaccharide (LPS) can have several pro-parkinson’s effects.

Our results thus confirm that maternal immunological stimulation during early/middle pregnancy is sufficient to induce long-term changes in multiple neurotransmitter levels in the brains of adult offspring. This further supports the possibility that infection-mediated interference with early fetal brain development may predispose the developing organism to the emergence of neurochemical imbalances in adulthood, which may be critically involved in the precipitation of adult behavioural and pharmacological abnormalities after prenatal immune challenge.  (Meyer 2009)

Thus, exposure to the bacteriotoxin, lipopolysaccharide (LPS) during a critical developmental window in rats, leads to the birth of animals with fewer than normal dopamine (DA) neurons. This DA neuron loss is apparently permanent as it is still present in 16 months old animals (the longest period studied to date). Moreover, the loss of DA neurons seen in these animals increases with age thereby mimicking the progressive pattern of cell loss seen in human PD. (Carvey 2003)

One is a reduced density of dopaminergic neurons in the substantia nigra and another is hypersensitivity to further exposure – the system is “primed”. Future exposure to LPS, particularly after the changes of puberty, will trigger a greater reaction whose magnitude will vary with individual sensitivity.

Sensitivity to LPS is genetically determined, varying considerably among different species. The sensitivity of normal animals (mice) to endotoxin may be enhanced considerably under different experimental conditions that include treatment with live (infection) or killed Gram-negative and -positive bacteria. (Fruedenberg 1993)

We conclude that prenatal exposure to LPS produces a long-lived THir cell loss that is accompanied by an inflammatory state that leads to further DA neuron loss following subsequent neurotoxin exposure. The results suggest that individuals exposed to LPS prenatally, as might occur had their mother had bacterial vaginosis, would be at increased risk for Parkinson’s disease. (Carvey 2004)

Thus, this disrupted immune system can lead to chronic inflammation and microglial activation with elevated levels of cytokines and related pro-inflammatory chemicals leading to “cell death.

The twin roots (immune and endocrine) of Parkinson’s Disease reaching back to the earliest moments of existence represent the extreme of a spectrum of causal scenarios and produce the earliest onset of symptoms. The two arise together and interact to produce the disorder by means of a self-perpetuating immune-endocrine reaction.

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