D-serine treatment

[Mnd0vrmnky]

ncbi.nlm.nih.gov/pubmed/217...

Has anyone any knowledge on the success of using d-serine?

It ties in with the research from ethnomedicine regarding serine and the toxin BMAA.

[silvestrov]

I don't have full internet to give you a link but can suggest an internet search. Google cycloserine aka brand name Seromycin & Parkinson's. It is a second line TB antibiotic and has similar action to serine. It blocks the NMDA receptors thus preventing toxicity which kills nerve cells. Glutamate toxicity is associated with PD, schizophrenia, Huntington's.... and PD is genetically related to schizophrenia.

[silvestrov]

PS. If you want to give D-serine a try Smart Powders sells it plus do an internet search you may be able find a less expensive brand.

[Mnd0vrmnky in reply to silvestrov]

They found that the neuro toxin BMAA has a similar structure to serine and the theory is that the BMAA replaces the serine in the amino acid chain as it forms. Serine is used the the manufacture of membranes.

BMAA has been found in samples taken from ppl who had parkinsons, Alzheimers, Psp, picks disease, ALS and more.

ethnomedicine.org/neurodege...

12/12 lochs/lakes/reservoirs in the uk tested positive in a study performed by Dundee uni.

dailymail.co.uk/news/articl...

Dr Paul Alan Cox was part of the team who found the treatment for hiv in tree bark.

He has now set his sights on ALS, PD, AD and his team are the first scientists to replicate the brain tangles and plaques in the lab.

They are trialing l-serine on ALS patients and are on phase two.

Also BMAA is a chelator of zinc but too much zinc is also bad for the brain.

There is no evidence this treatment will work as of yet.

[Mnd0vrmnky]

Previous studies into the Guamian ALS-Parkinson's Dementia complex has identified β-methylamino-L-alanine (BMAA), as a potential neurotoxin responsible for this disease. BMAA is a non-essential amino acid and is produced by a cyanobacterium which is present in all ecosystems. Subsequently several groups have identified high concentrations of BMAA in brain tissues of patients from North America and Europe with several neurodegenerative diseases including ALS, Parkinson's Disease and Alzheimer's Diseases. It has been hypothesized that chronic intake of BMAA in the diet leads to mis-incorporation of the amino acid into brain proteins, where it produces slow neuronal damage and recent evidence has shown that BMAA is mis-incorporated into proteins in neuronal cell lines via seryl tRNA synthetase, thereby producing protein mis-folding and protein aggregates, leading to cell death. It has been demonstrated in mammalian neuronal cell cultures that exogenous L-serine could prevent the BMAA neurotoxin from being mis-incorporated into proteins, thereby preventing cell death and that very high doses of L-serine may compete with the transport of a number of non-essential amino acids across the blood-brain barrier via the y+ transporter. These findings have led us to believe that high doses of L-serine could possibly stop the mis-incorporation of BMAA into brain proteins which in turn would slow or even abate the progression of ALS. This study will determine the safety of different doses of L-serine given to ALS subjects at 0.5 gm twice daily (BID), 2.5gm BID, 7.5g BID or 15 grams BID for six months.