Pokaż wątki

witam,

https://www.neals.org/for-people-with-als-caregivers/educational-webinars/results-from-the-immunosuppression-in-als-trial

pozdrawiam

Witam,

Ja mam SLA od trzech lat i mam niedowład czterokończynowy, opuszkowa forme choroby.
I ja biore od 2 tygodni nowy lek Edaravone i moja kinaza kreatynowa spadła z 500 do 180 czyli do normy z przed choroby. Badania aktywności kinazy kreatynowej w surowicy wykorzystuje się w diagnostyce medycznej. Podwyższony poziom CK świadczy przede wszystkim o uszkodzeniu tkanek, szczególnie mięśni. Moge przyjąć, że moja choroba sie zatrzymała

A czy jest ktos kto jeszcze probowal tego leku i badal sobie kinaze kreatynowa?
Pozrawiam

Witam , mam artykuł , że witamina B3 a dokładnie jej formy pomagają w chorobach  neurodegeneracyjnych          

This is the main reason I take nicotinamide, Niagen and nicotinic acid (all types of vitamin B3). Overactivation of the enzyme called PARP-1 leads to rapid depletion of its substrate NAD. NAD depletion causes mitochondrial dysfunction and cell death. High dose B3 boosts NAD synthesis, thereby preventing neuronal cell death.

Semin Cell Dev Biol. 2016 Nov 17. pii: S1084-9521(16)30395-0. doi: 10.1016/j.semcdb.2016.11.007. [Epub ahead of print]
Poly(ADP-ribose)Polymerase-1 hyperactivation in neurodegenerative diseases: the death knell tolls for neurons.
Narne P1, Pandey V1, Simhadri PK1, Babu PP2.
Author information
Abstract
Neurodegeneration is a salient feature of chronic refractory brain disorders like Alzheimer's, Parkinsons, Huntington's, amyotropic lateral sclerosis and acute conditions like cerebral ischemia/reperfusion etc. The pathological protein aggregates, mitochondrial mutations or ischemic insults typifying these disease conditions collude with and intensify existing oxidative stress and attendant mitochondrial dysfunction. Interlocking these mechanisms is poly(ADP-ribose) polymerase (PARP-1) hyperactivation that invokes a distinct form of neuronal cell death viz., 'parthanatos'. PARP-1, a typical 'moonlighting protein' by virtue of its ability to poly(ADP-ribosyl)ate a plethora of cellular proteins exerts diverse functions that impinge significantly on cellular processes. In addition, its interactions with various nuclear proteins like transcription factors and chromatin modifiers elicit varied transcriptional outcomes that wield pathological cellular responses. Further, emerging leitmotifs like mitochondrial and nucleolar PARPs and the novel aspects of gene expression regulation by PARP-1 and poly(ADP-ribosyl)ation can provide a holistic view of PARP-1's influence on cell vitality. In this review, we discuss the pathological underpinnings of PARP-1, with a special emphasis on mitochondrial dysfunction and cell death subroutines, in the realm of neurodegeneration. This would provide a deeper insight into the functions of PARP-1 in neurodegenerative conditions that would enable the development of more effective therapeutic strategies.

pozdrawiam

Witam , poniżej artykuł

https://alsnewstoday.com/2017/02/27/study-shows-meditation-improves-qualtity-of-life-and-psychological-well-being-of-als-patients/

Pozdrawiam

Witam
Pomaga na objawy opuszkowe poniżej link z trialem


http://link.springer.com/article/10.1007%2Fs13311-016-0508-5

Nuedexta
kapsułki twarde, 0,023g+9mg, 60 kaps.

Nazwa międzynarodowa:Quinine sulphatePodmiot odpowiedzialny:JENSON PHARMACEUTICAL SERVICESDostępność:Pełna odpłatność, na receptę

Pozdrawiam

Od paru dni zaczalem czytac o propofolu jest to srodek usypiajacy stosowany podczas operacji i malych zabiegow.
Pacjenci z SLA ktorzy mieli podawane podczas tych zebiegow ten srodek mieli poprawe i objawy choroby sie im cofnely na pewien czas, ale nigdy nie bylo zadnych trialow potwierdzajacych, jedynie opis pacjentow i ich wlasnych doswiadczen i badan.
Znalazlem badania naukowe o dzialaniu tego leku i jego wplywie na organizm i cos jest na rzeczy.
Dziwne jest to, ze nigdy nie slyszalem o tym leku a wy?

Ponizej zalaczam to co znalazlem:

Pozdrawiam

http://link.springer.com/content/pdf/10.1007%2Fs005400050040.pdf

http://pvangels.com/news/1525/affordable-safe-propofol-treatments-for-als-patients-in-puerto-vallarta

http://www.tandfonline.com/doi/pdf/10.3109/21678421.2013.826469

http://www.alsforums.com/forum/als-research-news/22130-propofol-reverses-symptoms.html

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2438270/


Here is some BioChemical evidence of why this molecule/compound might be working on PALS.

Quote:
Note that the existence of defective inhibitory GABA-A alpha-1 receptor in ALS patients is not a hypothesis. It is an actual research finding. The inhibitory glycine alpha-1 receptors are also known to be defective in ALS patients. What really makes this interesting is that those receptors are used for inhibition by both the CNS and the immune system. In other words they are responsible for both hypnosis (sleep) and the suppression of inflammation. This is the reason that Propofol is such a powerful anti-inflammatory substance: it directly activates those specific inhibitory receptors and suppresses the elevated inflammatory response in the brain and spinal cord.

But Propofol appears to be doing much more than that. It seems to be able to restore the receptors to their normal inhibitory function and this reversal of symptoms can last a few weeks if the abnormal inflammation is completely suppressed in an ALS patient, the patient may see a complete remission of symptoms for a longer period, possibly years.

As an aside, why does Propofol reduce ALS-caused inflammation in the brain and spinal cord and not some of the other powerful anti-inflammatory drugs? The answer is that there are many types of inflammation. It all has to do with activating the correct receptors. This is why Propofol works and why the arthritis drugs do not.

I know this explanation might be over your head to understand it but...in terms of layman, this molecule may show some promise on treating the symptoms of MND/ALS.






The experimental and clinical pharmacology of propofol, an anesthetic agent with neuroprotective properties.
Kotani Y, Shimazawa M, Yoshimura S, Iwama T, Hara H.

Department of Biofunctional Evaluation, Molecular Pharmacology, Gifu Pharmaceutical University, Gifu 502-8585, Japan.

Abstract

Propofol (2,6-diisopropylphenol) is a versatile, short-acting, intravenous (i.v.) sedative-hypnotic agent initially marketed as an anesthetic, and now also widely used for the sedation of patients in the intensive care unit (ICU). At the room temperature propofol is an oil and is insoluble in water. It has a remarkable safety profile. Its most common side effects are dose-dependent hypotension and cardiorespiratory depression. Propofol is a global central nervous system (CNS) depressant. It activates gamma-aminobutyric acid (GABA A) receptors directly, inhibits the N-methyl-d-aspartate (NMDA) receptor and modulates calcium influx through slow calcium-ion channels. Furthermore, at doses that do not produce sedation, propofol has an anxiolytic effect. It has also immunomodulatory activity, and may, therefore, diminish the systemic inflammatory response believed to be responsible for organ dysfunction. Propofol has been reported to have neuroprotective effects. It reduces cerebral blood flow and intracranial pressure (ICP), is a potent antioxidant, and has anti-inflammatory properties. Laboratory investigations revealed that it might also protect brain from ischemic injury. Propofol formulations contain either disodium edetate (EDTA) or sodium metabisulfite, which have antibacterial and antifungal properties. EDTA is also a chelator of divalent ions such as calcium, magnesium, and zinc. Recently, EDTA has been reported to exert a neuroprotective effect itself by chelating surplus intracerebral zinc in an ischemia model. This article reviews the neuroprotective effects of propofol and its mechanism of action.