Progress and Prospects in Parkinson's Research/Causes/Infection

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Background
The ‘Causes’ page on this wiki states categorically that Parkinson’s Disease is not contagious, and most neurologists would agree with this. However, perversely, the disease can sometimes appears as a set of secondary symptoms of another disease which is contagious. The most noteworthy example of this was an outbreak of a disease with extreme PD symptoms called Encephalitis Lethargica. This was first described by Von Economo in 1912 and, following a pandemic of cases, which lasted from 1916 to 1926, he produced a monograph. The victims found it impossible to achieve any cognitive movement and were condemned to exist as living statues for decades.

Dr. Oliver Sachs describes the outbreak in his book “Awakenings” (1973), which includes the moving account of his rescue of the victims from their plight by administering massive doses of the newly discovered drug levodopa.

The outbreak disappeared as mysteriously as it first appeared. There was an unproven hypothesis that it was somehow linked to the devastating pandemic of flu in 1919, which killed more people than the combined casualties of World War One.

Research
2003

Wharton reviewed all literary references to encephalitis lethargica and identified the diagnostic criteria. He then set about reviewing modern diagnoses to see whether any met the criteria and turned up 19 cases since 1982. His paper suggest that a further widespread outbreak is real possibility.

2006

Field et al produced evidence that prenatal depression in a mother induced a biochemical/physiological profile in the foetus that mimics their mothers' prenatal biochemical/physiological profile including elevated cortisol,  lower levels of dopamine  and serotonin, greater relative right frontal EEG activation and lower vagal tone.

2012

H.V. et al studied patients in Belgrade during the period 2001-2005, comprising 110 subjects diagnosed for the first time as PD cases, and 220 controls chosen among patients with degenerative joint disease and some diseases of digestive tract.

"According to logistic regression analysis PD was significantly related to mumps (Odds ratio adjusted on occupation and family history of PD - aOR = 7.86, 95% confidence interval - CI = 3.77-16.36), scarlet fever (aOR = 12.18, 95%CI = 1.97 -75.19), influenza (aOR = 8.01, 95% CI = 4.61 -13.92), whooping cough (aOR = 19.90, 95% CI = 2.07 -190.66) and herpes simplex infections (aOR = 11.52, 95% CI = 2.25 -58.89). Tuberculosis, measles and chicken pox were not associated with PD. Other infectious diseases we asked for were not reported (12 diseases), or were too rare (4 diseases) to be analysed."

De Chiara et al evaluated connections between infective conditions and neurodegenerative diseases.

"The activation of inflammatory processes and host immune responses cause chronic damage resulting in alterations of neuronal function and viability, but different pathogens can also directly trigger neurotoxic pathways. Indeed, viral and microbial agents have been reported to produce molecular hallmarks of neurodegeneration, such as the production and deposit of misfolded protein aggregates, oxidative stress, deficient autophagic processes, synaptopathies and neuronal death. These effects may act in synergy with other recognized risk factors, such as aging, concomitant metabolic diseases and the host’s specific genetic signature. "

2013

Tome et al have carried out a comprehensve review of the role of inflammation and alpha synuclein in the development of PD and their conclusions were:-

"Although α-syn aggregation appears to be central to the development and progression of PD pathology, inflammation also plays an important role in this disease. Immune activation in the GI tract or in the olfactory system via chemical or virus exposure might trigger α-syn misfolding, subsequent aggregation, and propagation to the brain. It is also possible that neuroinflammation promotes the prion-like transfer of α-syn by increasing its release, increasing its uptake, or both. However, further studies are needed to support this hypothesis. If correct, it will open up new avenues for early detection and therapeutic intervention. For example, one could speculate that it will be possible to develop therapies which slow down the progression of PD by reducing the underlying inflammation and mitigating its effects on cell-to-cell α-syn transfer. In addition, it is conceivable that it would be possible to adopt a preventive strategy and lower the risk of developing PD by treating the triggers of inflammation in the olfactory or gastrointestinal system."