Tudca: youtu.be/boTzigj646Q - Cure Parkinson's

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Tudca

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youtu.be/boTzigj646Q

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akgirlsrock
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Bolt_Upright profile image
Bolt_Upright

Alaska Girls do Rock! SilentEchoes Tauroursodeoxycholic acid in the treatment of patients with amyotrophic lateral sclerosis 2015 ncbi.nlm.nih.gov/pmc/articl...

I may need to add this back to my stack.

akgirlsrock profile image
akgirlsrock in reply toBolt_Upright

Hello, have you tried it? Thank you, Maria😄

Bolt_Upright profile image
Bolt_Upright in reply toakgirlsrock

I have taken it. It fell by the wayside but I still have some. Trying to figure out a good dose now. (any advice on dosing Hidden ?)

Bolt_Upright profile image
Bolt_Upright in reply toBolt_Upright

So the trial for UDCA for PD is using 50 mg/kg: sciencedirect.com/topics/ne...

for me, 70 kg, that would be 3.5 grams a day.

Bolt_Upright profile image
Bolt_Upright in reply toBolt_Upright

This web site that sells TUDCA says 500 mg a day, up to 1750 mg a day under medical supervision up to a month: bodybio.com/products/tudca

"The suggested dosage is take 2 capsules per day or use as directed by your Healthcare Professional. 1750 mg is the tolerable upper limit for most and can be used as a therapeutic dose for as long as one month. TUDCA is suitable for those without a gallbladder."

Bolt_Upright profile image
Bolt_Upright in reply toBolt_Upright

This paper says 2 grams a day for ALS: ncbi.nlm.nih.gov/pmc/articl...

Bolt_Upright profile image
Bolt_Upright in reply toBolt_Upright

Looks like I worked out the dosing 8 months ago. 1000 mg twice a day: healthunlocked.com/cure-par...

I don't think I can afford that.

TheRealness profile image
TheRealness in reply toBolt_Upright

A good dose is 500 mg and in an enteric capsule or delayed release capsule. I buy the powder version on Amazon and buy the capsules too and fill them myself. It’s a lot cheaper and when they’re put into a acid resistant capsule studies have shown that it’s far more effective. I can’t find any companies that put I TUDCA into a acid resistant capsules. I notice a huge difference doing it this way.

Bolt_Upright profile image
Bolt_Upright in reply toTheRealness

Thanks! Very interesting.

Bolt_Upright profile image
Bolt_Upright

Unraveling the neuroprotective role of TUDCA in Parkinson´s disease 2015 run.unl.pt/bitstream/10362/...

"Accumulating evidence suggests that mitochondrial dysfunction play a central role in Parkinson’s disease (PD). Evidence is based on the identification of PD-associated mutations in genes that affect mitochondrial function, such as phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1) and parkin. This was further reinforced by the discovery that exposure to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a mitochondrial complex I inhibitor, leads to clinical symptoms similar to sporadic PD. Thus, one therapeutic approach that has recently arisen in PD research is the selective clearance of damaged mitochondria by mitophagy. The bile acid tauroursodeoxycholic acid (TUDCA) is an anti-apoptotic molecule shown to interfere with the mitochondrial pathway of cell death. Importantly, TUDCA was demonstrated to protect against MPTP-induced neurodegeneration in mice, but the mechanisms involved are still unknown. Herein we investigate whether autophagy/mitophagy and mitochondrial biogenesis are part of TUDCA-mediated neuroprotection and discuss the molecular mechanisms involved, using two different models of PD, C57B/L6 mice and SH-SY5Y neuroblastoma cells treated with TUDCA and/or MPTP/MPP+. Our preliminary results reveal that in mice brain, TUDCA induced microtubule-associated protein 1 light chain 3 (LC3) lipidation, and increased voltage-dependent anion channel (VDAC), full length PINK1 and parkin protein expression, thereby suggesting that autophagy/mitophagy and mitochondrial biogenesis are part of TUDCA-mediated neuroprotection. In SH-SY5Y cells, TUDCA prevents MPP+-induced cell death and mitochondrial damage. Moreover, this bile acid was also shown to modulate parkin phosphorylation, and parkin expression levels in the presence of MPP+. Importantly, modulation of parkin was accompanied by increased levels of autophagy. Impaired mitochondrial turnover has been associated to PD, thus, mitochondrial protective agents represent an attractive direction for the development of new therapeutic drugs. Our results point to the pharmacological up-regulation of mitochondrial turnover by TUDCA as a novel neuroprotective mechanism of this molecule, and contribute to the validation of TUDCA clinical application in PD."

Bolt_Upright profile image
Bolt_Upright

TUDCA ALS Trial: tudca.eu/news-events-media/

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Bolt_Upright

Nrf2 activation by tauroursodeoxycholic acid in experimental models of Parkinson's disease 2017 pubmed.ncbi.nlm.nih.gov/285...

"Parkinson's disease (PD) is a progressive neurological disorder, mainly characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta. Although the cause of PD remains elusive, mitochondrial dysfunction and severe oxidative stress are strongly implicated in the cell death that characterizes the disease. Under oxidative stress, the master regulator of cellular redox status, nuclear factor erythroid 2 related factor 2 (Nrf2), is responsible for activating the transcription of several cytoprotective enzymes, namely glutathione peroxidase (GPx) and heme oxygenase-1 (HO-1). Nrf2 is a promising target to limit reactive oxygen species (ROS)-mediated damage in PD. Here, we show that tauroursodeoxycholic acid (TUDCA) prevents both 1-methyl-4-phenylpyridinium (MPP+)- and α-synuclein-induced oxidative stress, through Nrf2 activation, in SH-SY5Y cells. Additionally, we used C57BL/6 male mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to elucidate the effect of TUDCA in this in vivo model of PD. In vivo, TUDCA treatment increases the expression of Nrf2, Nrf2 stabilizer DJ-1, and Nrf2 downstream target antioxidant enzymes HO-1 and GPx. Moreover, we found that TUDCA enhances GPx activity in the brain. Altogether, our results suggest that TUDCA is a promising agent to limit ROS-mediated damage, in different models of PD acting, at least in part, through modulation of the Nrf2 signaling pathway. Therefore, TUDCA should be considered a promising therapeutic agent to be implemented in PD. "

Bolt_Upright profile image
Bolt_Upright

scienceofparkinsons.com/201...

"There is one potential concern regarding TUDCA: it increases glucose-induced insulin release (via the cAMP/PKA pathway), which in turn could increase insulin sensitivity (Click here to read more about this). This could affect people with diabetes or glucose intolerance – a common feature of Parkinson’s (Click here to read a previous SoPD post on this topic)."

Trailing profile image
Trailing

Tudca is an ingredient in Restore Gold, a product that many on this blog take.

healthunlocked.com/cure-par...

I posted about it last year too under a different user name. I can look for it if you want. I’ve been taking it for about a year with sodium butyrate

akgirlsrock profile image
akgirlsrock

Hello, do you feel any benefits, their's so much stuff out there, it's so confusing what to take. Thank you, Maria

in reply toakgirlsrock

I’m doing very well but I’m doing so much I don’t know what to attribute it to. But the science behind its benefits is strong. I am taking the long view on all of this.

TheRealness profile image
TheRealness

TUDCA is an amazing supplement that works in so many different ways from healing our liver, gallbladder, our gi tract, it’s antibacterial, anti fungal, anti viral, it’s shown to work as effective as antivirals and works to fight COVID v very effectively. I’ve studied this compound and haven’t found anything as versatile in the medical literature before. I would suggest that people buy it in powder form and also buy enteric capsules or delayed release capsules because TUDCA is far more effective if we can get it past our stomach and into the small intestine because it’s far more absorbed that way and studies have shown it’s far more effective this way.

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