User:Reverett123

I will assume that this is the appropriate place to provide some background information on myself and what I hope to see from this project. If I am in error just let me know.

Born in 1953, it has been twenty years (1992) since I first noted symptoms, in my case a tremor in my right hand. Initial diagnosis was essential tremor. Eight years later (2000) difficulty in walking brought a revised diagnosis of Parkinson's Disease. At this point (2012) I am able to walk most of the day and appear normal during the mid-day period. However, there is an ever-present sense of fragility that must always be allowed for. Having gone through most of the pharmaceutical options, I rely on a high-dose monotherapy of 22 mg daily of levodopa-carbidopa.

My educational background consists of two years at university in an engineering curriculum. As to Parkinson's I am self-taught. Actually, that is a bit of an understatement. I struck up a collaborative friendship with a French surgeon

(http://translate.google.com/translate?hl=en&sl=fr&u=http://gp29.net/%3Fp%3D60&prev=/search%3Fq%3Danne%2Bfrobert%26hl%3Den%26client%3Dfirefox-a%26hs%3DMwa%26rls%3Dorg.mozilla:en-US:official%26prmd%3Dimvnso&sa=X&ei=goBwUMegJJPg8wTMpoCQAg&ved=0CC4Q7gEwAQ)

who was herself recentlt diagnosed with PD and attempting to make sense of it all. Using Skype, we worked together two to four hours each day for approximately three years. In effect, we used the OC aspects of PD against the disease itself. As a result I know far more about the disorder than I ever wanted.

In my view, PD is a maddening puzzle and quite fascinating. We don't know cause or cure despite our best efforts. We can only address symptoms. Rather than go into detail here, I will direct the reader to a blog that I maintained for a while-

http://amatterofbalance.wordpress.com/ Reverett123 (talk) 03:21, 11 October 2012 (UTC)

Beginning to catch glimpses of daylight about wikis. I can't help but notice that there is no discussion of matters PD. Is this just a reflection of the small size of our little band or is there a discussion venue that I have missed?

Also, I know that many of my ideas run counter to the prevailing mindset that says PD is about dead neurons and neurologists. My argument is that it is more a autotoxic immune response arising from fetal immune challenge paired with a dysfunction of the endocrine "fight or flight" response. These two systems, in turn, produce cytokines and hormones which damage the nervous system. Here are a few abstracts to give you the way it runs.

1. Curr Pharm Des. 2007;13(18):1925-8.

Inflammation in Parkinson's diseases and other neurodegenerative diseases: cause and therapeutic implications.

Wilms H, Zecca L, Rosenstiel P, Sievers J, Deuschl G, Lucius R.

Department of Neurology, Christian-Albrechts-Universität Kiel, Germany. h.wilms@neurologie.uni-kiel.de

Agents suppressing microglial activation are attracting attention as candidate drugs for neuroprotection in Parkinson s disease (PD): While different mechanisms including environmental toxins and genetic factors initiate neuronal damage in the substantia nigra and striatum in PD, '''there is unequivocal evidence that activation of neuroinflammatory cells aggravates this neurodegenerative process.''' It was shown that following an acute exposure to the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and other toxins the degenerative process continues for years in absence of the toxin. Reactive microglia has been observed in the substantia nigra of patients with PD, indicating that this inflammatory process might aggravate neurodegeneration. By r'''eleasing various kinds of noxious factors such as cytokines or proinflammatory molecules microglia may damage CNS cells.''' The stimuli triggering microgliosis in Parkinsonian syndromes are unknown so far: However, analysis of neuronal loss in PD patients shows that it is not uniform but that neurons containing neuromelanin (NM) are predominantly involved. We hypothesized that extraneuronal melanin might trigger microgliosis, microglial chemotaxis and microglial activation in PD with subsequent release of neurotoxic mediators. The addition of human NM to microglial cell cultures induced positive chemotactic effects, activated the pro-inflammatory transcription factor nuclear factor kappa B (NF-kappaB) via phosphorylation and degradation of the inhibitor protein kappaB (IkappaB), and led to an upregulation of TNF-alpha, IL-6 and NO. These findings demonstrate a crucial role of NM in the pathogenesis of Parkinson's disease by augmentation of microglial activation, leading to a vicious cycle of neuronal death, exposure of additional neuromelanin and chronification of inflammation. '''Antiinflammatory drugs may be one of the new approaches in the treatment of PD.'''

PMID: 17584117 [PubMed - indexed for MEDLINE]

1. Front Biosci. 2003 Sep 1;8:s826-37.

Prenatal exposure to the bacteriotoxin lipopolysaccharide leads to long-term losses of dopamine neurons in offspring: a potential, new model of Parkinson's disease.

Carvey PM, Chang Q, Lipton JW, Ling Z.

Department of Pharmacology and Neurological Sciences1, Rush-Presbyterian-St. Luk'e Medical Center, 2242 West Harrison St. (Suite 260), Chicago, IL 60612, USA. pcarvey@rush.edu

The cause of Parkinson's disease (PD) is currently unknown. Although a genetic cause has been implicated in familial PD, the vast majority of cases are considered idiopathic. Environmental toxins have been implicated as a cause for PD by many investigators. Unfortunately, the magnitude of this exposure would likely need to be very high and as a result, would likely have been identified by the many epidemiological studies performed to date. Recently, we inadvertently realized that '''exposure to neurotoxins while still in utero may also represent a risk factor. 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. The DA neuron loss is accompanied by reductions in striatal DA, increases in DA activity, and increased production of the pro-inflammatory cytokine Tumor Necrosis Factor alpha (TNF-alpha). These are also characteristics of the PD brain. This model therefore shares many of the same characteristics with PD, and most importantly exhibits a slow, protracted loss of DA neurons - a characteristics of this animal model not found in other models. Interestingly, a '''common complication of pregnancy is a condition known as bacterial vaginosis (BV), which is known to produce increased levels of LPS and pro-inflammatory cytokines in the chorioamniotic environment of the fetus'''. This raises the interesting possibility that BV may be a risk factor for PD. The possibility that prenatal toxin exposure may contribute to the development of a neurodegenerative disease of the aged raises interesting new pathogenic questions and draws attention to the possibility that in utero exposure to neurotoxins may represent a here to fore unrecognized cause of PD.

PMID: 12957870 [PubMed - indexed for MEDLINE]

1. Infant Behav Dev. 2006 Jul;29(3):445-55. Epub 2006 May 30.

Prenatal depression effects on the fetus and newborn: a review.

Field T, Diego M, Hernandez-Reif M.

Touch Research Institutes, University of Miami, School of Medicine, P.O. Box 016820, Miami, Florida, 33101, United States. tfield@med.miami.edu

A review of research on prenatal depression effects on the fetus and newborn suggests that they experience prenatal, perinatal and postnatal complications. Fetal activity is elevated, prenatal growth is delayed, and prematurity and low birthweight occur more often. Newborns of depressed mothers then show a biochemical/physiological profile 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. Elevated prenatal maternal cortisol is the strongest predictor of these neonatal outcomes.''' Moderate pressure massage can alleviate these effects including reducing prematurity.

PMID: 17138297 [PubMed - indexed for MEDLINE]

Well, you get the idea. Reverett123 (talk) 03:21, 11 October 2012 (UTC)

I would be interested in working this up into pages in the Causes section of the wiki. Can do this via my e-mail hape@waitrose.com if you communicate directly.