Glad you asked that question
First, the route was predicted by a German scientist named Braak a few years ago based on Lewy bodies. This is the first time it has actually been seen to happen.

Personally, I think PD, autism, and even schizophrenia are part of a spectrum so I would not be surprised.

While it is important, to me the virus isn't the story. The real story is the inflammation and microglial activation leading to alpha-synuclein and so on. And what makes that even more important is that it is mirrored by what happens in the womb when a fetus is exposed to bacterial toxins. Several researchers have shown that that rat pup will be born with an immune system sensitized to further encounters with the toxin. That encounter will lead to the same inflammatory mess that the flu virus triggered. In short, it looks like that, as suspected, the microglial response is at the heart of PD and we have two different examples of triggers for it.

Now is when it gets more interesting and begins to explain the wide range of symptoms in individual PWP. If a virus can cause PD then it can do it at various ages, start the process, and 5, 10, 15 years later your hand starts to shake. You might be 80 years old or 40, remember nothing of the virus, and have no other risk factors.

On the other hand, you may have been born with a time bomb in your skull that eventually is activated after puberty and ticks away another 20 0r 30 years so that at 40 you notice the first symptoms. But there is a big difference between these two scenarios. The fetal toxin one leaves you open to a dozen things that can accelerate the process. I am going to paste an excert from a book I wrote a couple of years ago listing things that linked PD with this second scenario. LPS is the bacterial toxin. The links don't work but I have abstracts for each point. It all fits like a glove.




Chapter Seven
And Now the Stage is Set

The youngster looks normal enough with little sign of endocrine problems or immune systems waiting for a trigger. But within his body things are already going awry. For example, informal polling of adult PWPs revealed that fully fifty percent remembered constipation as a factor in their childhood. Cortisol can cause constipation. Systemic inflammation can cause the intestinal wall to become more permeable. In a constipated child with a leaky intestinal wall, toxins intended for elimination can be reabsorbed into the system. An ornament is added to the tree.

Those toxins can include LPS which can find its way into the bloodstream. The same inflammatory chemicals that caused the breach of the gut wall can also open the similar barrier in the brain and allow toxins such as LPS to enter and damage directly by contact or indirectly by activating the microglia.

Any hypothesis explaining PD should be able to account for the “anomalous” features of the disorder – the “weird” things that don’t make sense. The more they begin to fit into a coherent picture the stronger the hypothesis. PD has many such anomalies for us to explore and use as a gauge to evaluate this model before you. In fact, this combination of LPS, cortisol and endocrine, microglia and immune, gut and neuron, can account for more of these known facts about Parkinson’s than any other hypothesis offered to date. While the list will be somewhat long, I will provide the “facts” and their explanations in light of this model for your consideration. This is not the time for brevity but rather for testing the idea against the reality.

Fact 1- PD was little known until two hundred years ago.
Explanation - See Chapter One.

F2- Until recently, PD has been a disease of the aged.
Ex- Microglia normally become more active with age, thus increasing the age of onset of PD. <Link>

F3- Only a relatively small portion of a population develop PD.
Ex- Only a low percentage are exposed to maternal stress. Only a smaller subset of that group is also exposed to LPS. A still smaller subset is sensitized to it. And a still smaller group encounters it in their environment. And so on. Unlike an infectious process where the pool of the afflicted widens with time, this process instead narrows over time.

F4- PD appears to be increasing in incidence and affecting a younger population.
Ex- See Chapter Two.

F5- Although little acknowledged, the leading problem reported in the younger PD population is not with movement but with stress related problems.
Ex- A hyperstressed system such as described here is walking a tightrope and can collapse easily.

F6- Anti-inflammatory drugs such as NSAIDs are believed to lower the risk of PD.
Ex- Since the immune response we propose is itself an inflammatory reaction, this would be expected.

F7- Manganese exposure is believed to increase the odds of PD.
Ex- Manganese and LPS combine synergistically to damage nerve tissues. <Link>

F8- Agricultural work seems to increase the odds of developing PD.
Ex- Agricultural dust such as from seed and hay storage has an unusually high LPS content. <Link>

F9- Mercury exposure also seems causal.
Ex- Like manganese, LPS increases the neuronal damage from mercury. <Link>

F10- The “Parkinson’s Personality” is not entirely a myth and younger PWPs are particularly likely to be “responsible” sorts who occupy positions reflecting this.
Ex- Pre-natal LPS exposure produces anxiety-like behavior in the adult. One possible response to anxiety is to “take charge” in the time-honored “if you want it done right…” approach. <Link>

F11- More men than women develop PD.
Ex- Estrogen reduces the immune response to LPS exposure. <Link>

F12- Societies that consume large amounts of green tea have lower rates of PD.
Ex- EGCG, a polyphenol in green tea, strongly inhibits microglial action and inflammation. <Link>

F13- Excess levels of iron in the substantia nigra are thought to contribute to cell death and PD.
Ex- Introducing LPS into this area of the brain leads to iron accumulation there. <Link>

F14- The antibiotic minocycline is thought to be of value in treating PD.
Ex- Minocycline blocks or reduces many of the effects of LPS. <Link>

F15- The pesticide rotenone is linked to increased PD.
Ex- Rotenone and LPS combine synergistically and increase degenerative effects. <Link>

F16- Sleep disturbances in PD are extremely common.
Ex- LPS is a potent disruptor of sleeping patterns. <Link>

F17- Unexplained, generalized muscle pain is common in PD.
Ex- There are reports of similar pain resulting from LPS exposure. <Link>

F18- Milk consumption has been linked to developing PD later in life.
Ex- Milk often has a high LPS content due to the toxin’s resistance to heat and due to the fact that it is common in dairy herds. <Link>

F19- Tobacco use has been linked to reduced PD rates.
Ex- Nicotine counters the inflammatory effects of LPS. <Link>

F20- Coffee consumption has been linked to lowered PD risk.
Ex- Caffeine counters LPS inflammatory action. <Link>