Summary: Low dosages of carbon dioxide, related to levels experienced by smokers, does protect against aging in Parkinson’s illness models. Researchers found that carbon monoxide inhibited the oxidative stress-limiting pathways by activating the Parkinson ‘s-associated protein alpha-synuclein accumulation.
These studies point to the possibility that low-dose carbon monoxide may play a role in the slowing down of Parkinson’s disease. A scientific test to test this treatment in Parkinson’s patients is being planned.
Important Information:
- Low concentrations of carbon dioxide protected rabbits from Parkinson ‘s-like aging.
- It reduced alpha-synuclein formation and unlocked stress-reducing processes.
- A clinical trial for low-dose carbon dioxide in Parkinson’s individuals is planned.
Origin: Harvard
Paradoxically, earlier studies has shown that despite its natural health challenges, cigarette smoking is linked with a reduced risk of Parkinson’s disease. Until then, however, it was not obvious how.
Recent studies in laboratory types demonstrated that small doses of graphite monoxide, similar to those experienced by smoking, prevented neurodegeneration and stopped the formation of a crucial Parkinson ‘s-associated protein in the brain.
The studies are published in , npj Parkinson’s Disease , by researchers at Massachusetts General Hospital.
” Because tobacco has constantly been associated with a reduced risk of Parkinson’s disease, we wondered whether elements in cigar smoking may give neuroprotection”, said top author , Stephen Gomperts,  , an attending , physician , at , Massachusetts General Hospital and an associate professor of neuroscience at , Harvard Medical , School.
” Coconut was included in our analysis because it is produced endogenously in response to stress and has been demonstrated to have low-level protecting qualities. Moreover, overexpression of protein oxygenase-1, a stress-induced protein that produces intrinsic carbon dioxide, has been found to protect dopaminergic neurons from neurotoxicity in an animal type of Parkinson’s”.
In addition, smoking, a main constituent of cigar smoke, has been found to be inefficient at slowing the disease’s growth in a lengthy reported clinical trial.
These results led Gomperts and his colleagues to investigate the effects of low carbon dioxide doses on Parkinson’s mouse models.
They administered a low dose of carbon dioxide in the form of an oral medicine goods from Hillhurst Biopharmaceuticals, which they found to be comparable to the exposure of people who smoke, protecting the rodents against essence characteristics of the condition, including the formation of the Parkinson ‘s-associated proteins alpha-synuclein and the loss of cholinergic cells. Biologically, low-dose carbon dioxide activated signaling processes that limit oxidative stress and damage alpha-synuclein.
Additionally, the study found that smokers ‘ cerebrospinal fluid had a higher protein oxygenase-1 level than nonsmokers’. And in brain cells samples from patients with Parkinson’s, protein oxygenase-1 rates were higher in cells that were completely of alpha-synuclein disease.
These studies point to the possibility that low-dose carbon monoxide may activate molecular pathways that may decrease the onset and lessen the pathology of Parkinson’s disease. They support further research into the mechanisms that low-dose carbon dioxide modifies to slow the spread of disease,” Gomperts added.
A clinical trial of low-dose, orally administered carbon monoxide in patients with Parkinson’s disease is planned based on several Phase 1 and Phase 2 scientific studies in both good people and people with a variety of medical conditions showing safety of the small doses studied around.
Funding:  , This work was supported by the Farmer Family Foundation Parkinson’s Research Initiative, Michael J. Fox Foundation, National Institutes of Health, and the Challenger Foundation, with in-kind support from Hillhurst Biopharmaceuticals Inc.
About this Parkinson’s disease research news
Author: Brandon Chase
Source: Harvard
Contact: Brandon Chase – Harvard
Image: The image is credited to Neuroscience News
Original Research: Open access.
” Neuroprotection of low dose carbon monoxide in Parkinson’s disease models commensurate with the reduced risk of Parkinson’s among smokers” by Stephen Gomperts et al. npj Parkinson’s Disease
Abstract
Neuroprotection of low dose carbon monoxide in Parkinson’s disease models commensurate with the reduced risk of Parkinson’s among smokers
Paradoxically, cigarette smoking is associated with a reduced risk of Parkinson’s Disease ( PD). This led us to hypothesize that carbon monoxide ( CO ) levels, which are constitutively but modestly elevated in smokers, might contribute to neuroprotection.
We demonstrate that low-dose CO lessens neurodegeneration and lowers -synuclein ( Syn ) accumulation and oxidative stress by using rodent models of PD.
Oral CO administration activated signaling cascades mediated by heme oxygenase-1 ( HO-1 ), which have been implicated in limiting oxidative stress, and in promoting αSyn degradation, thereby conferring neuroprotection.
In accordance with the neuroprotective effect of smoking, HO-1 levels in cerebrospinal fluid were higher in humans smokers than nonsmokers.
Moreover, in PD brain samples, HO-1 levels were higher in neurons without αSyn pathology. Thus, CO in rodent PD models lowers pathology and causes oxidative stress responses, which may explain the potential protective effects of smoking in PD patients.
These findings highlight the potential for low-dose CO-modulated pathways to slow down symptom onset and slow down pathology in PD patients.
