Wednesday, December 23, 2015

misc PD ursolic acid, TUDCA, taurine, vibrations

taurine is unable to cross the blood-brain barrier. In addition of injured taurine transport systems under pathological conditions, CNS supplementation of taurine is almost null. Taurine is a potent antioxidant and anti-inflammatory semi-essential amino acid extensively involved in neurological activities, acting as neurotrophic factor, binding to GABA A/glycine receptors and blocking the excitotoxicity glutamate-induced pathway leading to be a neuroprotective effect and neuromodulation. Taurine deficits have been implicated in several CNS diseases, such as Alzheimer's, Parkinson's, epilepsy and in the damage of retinal neurons. This review describes the CNS physiological functions of taurine and the development of new derivatives based on its structure useful in CNS disease treatment.   (FULL)
The plasma taurine levels of PD patients were decreased when compared with controls and negatively associated with motor severity but not NMS (non-motor)
Strikingly, hydrophilic ursodeoxycholic acid (UDCA), and its taurine-conjugated form (TUDCA), show profound cytoprotective properties.   (FULL)
Taken together, these results strongly suggest that cysteamine is the neuroactive metabolite of cystamine and may further support its therapeutic use in neurodegenerative diseases, particularly in HD and PD.
Glycerol, trimethylamine-N-oxide, Betaine, and Taurine induced partially folded conformation and in turn enhanced the aggregation of alpha-synuclein.
taurine (FULL)

In patients with Parkinson's disease, it was found that the CSF level of  taurine had an
Prof. Jürgen Götz and Gerhard Leinenga of the Clem Jones Centre for Ageing Dementia Research, Queensland, Australia have pioneered the use of ultrasound at higher intensity to break up the beta amlyloid plaques in the brain, with dramatic benefits in mice
NSAIDs and curcumin offer some of the best protection against Alzheimer’s risk that we currently have available.
What you can do to lower your long-term risk of AD
?Regular and sufficient sleep
?Anti-inflammatories: NSAIDs, fish oil, curcumin=turmeric
?Weight control
?Mental and emotional engagement
?Yoga and meditation
?Vigorous exercise
?mega-doses of Vitamin D
?Melatonin at bedtime
?DHEA, Vit B12 and SAMe, especially for people with MTHFR genetic risk
?Low carb diet

Ursolic acid, could not confirm same as Ursocholanic acid.  UA lowers cholesterol and blood sugar and prevents muscle wasting. good for aging mice
It is particularly concentrated in apple peel but is also found in cranberries and prunes and in basil, oregano and thyme

usolic acid is also in a peruvian flower

Requested info from indian chemical supplier:
Dehydro (11,12)ursolic acid lactone (DUA)
ursodeoxycholic acid, ursodiol, UDCA, TUDCA (licensed drug)
Oxoursolic acid acetate
ursolic acid (natural compound in some plants)

coca tea
It works "primarily by blockade of the dopamine, serotonin or norepinephrine transporters". Blocking the transporters makes more of them available, primarily dopamine. Interestingly to me, it makes one more social.

Cocaine increases number of dendrite connections that are lost in PD, probably because more dopamine is being produced. The dopamine signals the connections to be maintained. A larger number of the dendritic spines with lower dopamine available to activate them might make "withdrawel" worse. The dendritic growth improves memory and occurs for up to 2 days after a single dose.

Unlike amphetamines, cocaine was not associated with an increased risk of PD

Saturday, December 19, 2015

parkinson's: MRI techniques

Early MRI studies of Parkinson’s disease used T2-weighted images to delineate the SN (, ), and researchers interpreted the hypointense region to result from iron in the SN pars reticulata (SNr) (). However, Rutledge et al. () and Mänz et al. () have observed that the correlation between this hypointense region and the SN was imperfect. Since T2-weighted images do not accurately depict the SN, others have employed additional MR imaging techniques, including diffusion weighted imaging (), inversion recovery imaging (, ), quantitative T1 mapping (), and susceptibility weighted imaging ().
Recently, Sasaki et al. (, ) used a T1-weighted fast spin echo sequence to visualize the SN and locus ceruleus. They referred to this technique as neuromelanin-sensitive MRI, arguing that the contrast results from neuromelanin as a byproduct of dopamine and noradrenalin metabolisms. They applied this technique to distinguish patients with schizophrenia and depression from healthy controls (). They found increased signal intensity in the SN in patients with schizophrenia, which is consistent with elevated levels of dopamine, and reduced signal intensity in the locus ceruleus in patients with depression, which is consistent with dysfunction of the noradrenergic system. To image the SN in patients with Parkinson’s disease, Schwarz et al. () recently used a T1-weighted fast spin echo sequence with additional magnetization transfer contrast pulses. They found smaller regions of hyperintensity with reduced contrast in the SN in patients compared to controls, consistent with the loss of dopamine neurons in the SN pars compacta (SNc). Because neuromelanin is a byproduct of dopamine and noradrenalin synthesis, alterations to these catecholamines or loss of dopaminergic neurons could have an effect on images sensitive to neuromelanin.

Monday, December 7, 2015

parkinson's: Michael Faraday had mercury poisoning like Pascal and Newton

update:  it appears Faraday had mercury poisoning like Newton, Pascal, and Alfred stock:

from a biography:

His tragic weakness was recurring “ill health connected with my head,” as he put it. Even as a young man, he had memory problems, and as he grew older he suffered from bouts of depression and headaches. “When dull and dispirited, as sometimes he was to an extreme degree,” his niece Constance Reid recalled, “my aunt used to carry him off to Brighton, or somewhere, for a few days, and they generally came back refreshed and invigorated.” These symptoms increased in severity and frequency until, in 1840, at age forty-nine, Faraday had a major nervous breakdown. Brighton vacations were no longer curative, and for four years he avoided most of his research activities. One can glimpse his desperate condition in a letter to his friend Christian Scho¨nbein, in 1843: “I must begin to write you a letter, though feeling, as I do, in the midst of one of my low nervous attacks, with memory so treacherous, that I cannot remember the beginning of a sentence to the end—hand disobedient to the will, that I cannot form the letters, bent with a certain crampness, so I hardly know whether I shall bring to a close with consistency.”

Although he returned to his research in 1845, he was still plagued by periods of memory loss, headaches, giddiness, and depression. He tells about his struggle against increasing mental frailty in letters written to his colleague and close friend Christian Scho¨nbein. In these letters, as nowhere else, Faraday reveals his affliction. Here are some extracts, written between 1845 and 1862, in chronological order: My head has been so giddy that my doctors have absolutely forbidden me the privilege and pleasure of working or thinking for a while, and so I am constrained to go out of town, be a hermit, and take absolute rest. My dear friend, do you remember that I forget, and that I can no more help it than a sieve can help water running out of it. I have been trying to think a little philosophy (magnetical) for a week or two, and it has made my head ache, turned me sleepy in the day-time as well at nights, and, instead of being a pleasure, has for the present nauseated me. Even if I go away for a little general health, I am glad to return home for rest in the company of my dear wife and time is to be quiet and look on, which I am able to do with great content and satisfaction. In his last letter to Scho¨nbein, in 1862, he said good-bye: “Again and again I tear up my letters, for I write nonsense. I cannot spell or write a line continuously. Whether I shall recover—this confusion—do not know. I will not write any more. My love to you.”