FAQ/Help |
Calendar |
Search |
Today's Posts |
![]() |
#1 | |||
|
||||
Senior Member
|
Proteinopathy-induced neuronal senescence: a hypothesis for brain failure in Alzheimer's and other neurodegenerative diseases
Todd E Golde, Victor M Miller Alzheimer's Research & Therapy 2009, 1:5 (12 October 2009) http://alzres.com/content/1/2/5/abstract Alzheimer's disease (AD) and a host of other neurodegenerative central nervous system (CNS) proteinopathies are characterized by the accumulation of misfolded protein aggregates. Simplistically, these aggregates can be divided into smaller, soluble, oligomeric and larger, less-soluble or insoluble, fibrillar forms. Perhaps the major ongoing debate in the neurodegenerative disease field is whether the smaller oligomeric or larger fibrillar aggregates are the primary neurotoxin. Herein, we propose an integrative hypothesis that provides new insights into how a variety of misfolded protein aggregates can result in neurodegeneration. Results: We introduce the concept that a wide range of highly stable misfolded protein aggregates in AD and other neurodegenerative proteinopathies are recognized as non-self and chronically activate the innate immune system. This pro-inflammatory state leads to physiological senescence of CNS cells. Once CNS cells undergo physiological senescence, they secrete a variety of pro-inflammatory molecules. Thus, the senescence of cells, which wasinitially triggered by inflammatory stimuli, becomes a self-reinforcing stimulus for further inflammation and senescence. Ultimately, senescent CNS cells become functionally impaired and eventually die, and this neurodegeneration leads to brain organ failure...
__________________
In the last analysis, we see only what we are ready to see, what we have been taught to see. We eliminate and ignore everything that is not a part of our prejudices. ~ Jean-Martin Charcot The future is already here — it's just not very evenly distributed. William Gibson |
|||
![]() |
![]() |
![]() |
#2 | ||
|
|||
Senior Member
|
Additional support for PD's interaction/relationship to immune function. Thanks for finding and sharing this.
|
||
![]() |
![]() |
![]() |
#3 | |||
|
||||
Senior Member
|
though just a hypothesis, would make a case for use of immune stimulating agents such as LDN or anti inflammatory agents.
__________________
In the last analysis, we see only what we are ready to see, what we have been taught to see. We eliminate and ignore everything that is not a part of our prejudices. ~ Jean-Martin Charcot The future is already here — it's just not very evenly distributed. William Gibson |
|||
![]() |
![]() |
![]() |
#4 | ||
|
|||
Member
|
Quote:
Olsen, please check your im! Thanks'Girija |
||
![]() |
![]() |
![]() |
#5 | ||
|
|||
Senior Member
|
this is one of those theories that seem to have a kind of plausible logic......
my personal feeling is that inflammation and immune response are part of my condition..... whether this could be a sole cause of PD is another matter, especially when you read of all the drugs and chemicals that are likely suspects.... and the genetic causes - we are both more fragile and tougher than we seem....... |
||
![]() |
![]() |
Reply |
|
|
![]() |
||||
Thread | Forum | |||
Damaged Brain Can Be Repaired And Cerebral Functions Restored, Neuronal Study Suggest | Traumatic Brain Injury and Post Concussion Syndrome | |||
Damaged Brain Can Be Repaired And Cerebral Functions Restored, Neuronal Study Suggest | Reflex Sympathetic Dystrophy (RSD and CRPS) | |||
ion channel function and neuronal firing | Parkinson's Disease | |||
Discussion of Vicc's Hypothesis on RSD | Reflex Sympathetic Dystrophy (RSD and CRPS) | |||
Serotonin hypothesis debunked yet again.... | Bipolar Disorder |