NeuroTalk Support Groups

NeuroTalk Support Groups (https://www.neurotalk.org/)
-   Parkinson's Disease (https://www.neurotalk.org/parkinson-s-disease/)
-   -   research examines connection between inflammatory stimulus and Parkinson's (https://www.neurotalk.org/parkinson-s-disease/187433-research-examines-connection-inflammatory-stimulus-parkinsons.html)

olsen 04-24-2013 01:10 AM

research examines connection between inflammatory stimulus and Parkinson's
 
New research examines connection between inflammatory stimulus and Parkinson's disease

University of Texas Health Science Center study suggests inflammation's role in the development of the disease...


The precise cause or causes of PD is unknown, but there is a consensus that an inflammatory event or episode is involved in the initiation of neurodegeneration, and that chronic neuroinflammation is a sustaining and exacerbating reason for the loss of the dopaminergic neurons. A new study conducted by a team of Texas researchers brings the understanding of inflammation's role a step further. They have found that a single, high-dose exposure of an experimental inflammatory agent in an animal model causes changes in brain tissue that are similar to those associated with the development of the disease...


In the study, the researchers examined inflammatory cell and cytokine production in brain tissue from a lipopolysaccharide (LPS)-treated rat model that mimics many of the neuropathologic changes associated with PD. Concurrently, they monitored the appearance of glial cell line-derived neurotrophic factor (GDNF), a neuronal protective agent, and circulating nitric oxide (NO) levels. They also examined the immune system associated cells in the olfactory bulb of the brain...

In general, the researchers found that a single injection of LPS elicited a systemic inflammatory response in the rats, as indicated by an elevation in certain circulatory cytokines. Tissue taken from the olfactory bulb showed the presence of immune associated cells. Individual cytokines within the olfactory bulb showed an increase in certain types of cytokines. Taken together, the complete analysis indicated that the single dose of LPS stimulated an inflammatory response that closely resembled the hallmarks of the development of the disease.

The results suggest an involvement of both the peripheral and the central nervous system immune components in response to inflammation and inflammatory episodes. As a result, the researchers suggest: (1) inflammation initiates an immune response; (2) the presence of continuing and increasing pro-inflammatory mechanisms results in a process whereby cellular protective mechanisms are overcome and the more susceptible cells, such as the dopaminergic neurons, enter into cell death pathways; and (3) this leads to a series of events that are a key part of the progression of PD...

http://www.eurekalert.org/pub_releas...-nre041813.php

reverett123 04-24-2013 05:11 AM

yes indeedy. if they keep on they will get to where we were several years ago
 
I don't want to be bitter, but it does seem reasonable to expect the researchers to know at least as much as the patients. Go back to http://neurotalk.psychcentral.com/thread101685.html



Quote:

Originally Posted by olsen (Post 977864)
New research examines connection between inflammatory stimulus and Parkinson's disease

University of Texas Health Science Center study suggests inflammation's role in the development of the disease...


The precise cause or causes of PD is unknown, but there is a consensus that an inflammatory event or episode is involved in the initiation of neurodegeneration, and that chronic neuroinflammation is a sustaining and exacerbating reason for the loss of the dopaminergic neurons. A new study conducted by a team of Texas researchers brings the understanding of inflammation's role a step further. They have found that a single, high-dose exposure of an experimental inflammatory agent in an animal model causes changes in brain tissue that are similar to those associated with the development of the disease...


In the study, the researchers examined inflammatory cell and cytokine production in brain tissue from a lipopolysaccharide (LPS)-treated rat model that mimics many of the neuropathologic changes associated with PD. Concurrently, they monitored the appearance of glial cell line-derived neurotrophic factor (GDNF), a neuronal protective agent, and circulating nitric oxide (NO) levels. They also examined the immune system associated cells in the olfactory bulb of the brain...

In general, the researchers found that a single injection of LPS elicited a systemic inflammatory response in the rats, as indicated by an elevation in certain circulatory cytokines. Tissue taken from the olfactory bulb showed the presence of immune associated cells. Individual cytokines within the olfactory bulb showed an increase in certain types of cytokines. Taken together, the complete analysis indicated that the single dose of LPS stimulated an inflammatory response that closely resembled the hallmarks of the development of the disease.

The results suggest an involvement of both the peripheral and the central nervous system immune components in response to inflammation and inflammatory episodes. As a result, the researchers suggest: (1) inflammation initiates an immune response; (2) the presence of continuing and increasing pro-inflammatory mechanisms results in a process whereby cellular protective mechanisms are overcome and the more susceptible cells, such as the dopaminergic neurons, enter into cell death pathways; and (3) this leads to a series of events that are a key part of the progression of PD...

http://www.eurekalert.org/pub_releas...-nre041813.php


Conductor71 04-25-2013 11:20 PM

They know nothing and everything...
 
Quote:

Originally Posted by reverett123 (Post 977883)
I don't want to be bitter, but it does seem reasonable to expect the researchers to know at least as much as the patients. Go back to http://neurotalk.psychcentral.com/thread101685.html

Funny, imagine applying this same scenario with Apple. Customers knowing more than the engineers, designers, and administrators. Academic researchers are not motivated to lead the pack or innovate, they are in fact, discouraged by their peers to do so. One rogue lab coat makes the others all look bad. Our synaptic shortcomings not only support a large number of careers, but they underlie the whole notion of the professional as expert. This is why lawyers, doctors, etc. have jargon with the professional degree functioning as the Rosetta Stone. This is one of the key reasons journals and databases are only accessible by subscription at institutional rates. We are not supposed to be intelligent enough to analyze data or statistics or learn some Latin. If we are, we certainly should never challenge or question.

Academic medical research is different in that you need a pedigree up front but then get paid handsomely to run in place your entire career. Imagine if researchers produced knowledge or treatments that had a 3-5 year product life cycle. If in every so many years you had to wow your profession or customers with the research equivalent of an iPhone or Google Sight, we would have far more progress. The reality is no one questions what you churn out over and over so long as you churn it and believe that it is most noble to do so. That is just good enough. The few who do innovate waste years and millions only to die in clinical trial, pack up their patents, and move on to another Milk Bar. Lather. Rinse. Repeat.


All times are GMT -5. The time now is 03:57 PM.

Powered by vBulletin • Copyright ©2000 - 2025, Jelsoft Enterprises Ltd.

vBulletin Optimisation provided by vB Optimise (Lite) - vBulletin Mods & Addons Copyright © 2025 DragonByte Technologies Ltd.