It looks like you're using an Ad Blocker.
Please white-list or disable AboveTopSecret.com in your ad-blocking tool.
Some features of ATS will be disabled while you continue to use an ad-blocker.
Family hopes for miracle after young mom struck by disease
After months of debilitating symptoms with no diagnosis, doctors this week say Sandi Tucker Kennedy, a 38-year-old wife and mom of four young children ages 2 to 9, is believed to have a prion disease, a family of rare progressive neurodegenerative disorders that take over the neurological system.
“She's actually very young for it,” …
“The neurological condition is going to continue. It's a rapid-moving disease,” Tucker said. “The prognosis is four to 12 months from the onset of symptoms and she's had symptoms for four months now.”
Aguzzi and colleagues in Britain and the United States inoculated specially bred mice with prions and checked to see if the prions spread in their bodies when the mice had an inflammatory condition. This is because other studies had suggested that prions might be attracted to immune system inflammatory cells.
“In all cases, chronic lymphocytic inflammation enabled prion accumulation in otherwise prion-free organs,” the researchers wrote.
10. Central Nervous System Inflammation and Prion Disease Pathogenesis
The study of inflammation in the prion diseases is relatively new. Indeed, for a number of years the accepted dogma was that the prion diseases lacked an inflammatory response in the brain (1–3). This persists in spite of a number of studies showing that the pathological hallmarks of the prion diseases (PrPSc deposition, astrocytosis, vacuolation, and neuronal loss) are associated with the presence of activated microglia (4–7). At the heart of this discrepancy is a simple matter of what is meant by inflammation. The innate inflammatory response is the tissue’s response to injury or infection, and, as so succinctly put by Metchnikoff in the late ninetenth century, “The essential and primary element in typical inflammation consists in a reaction of the phagocytes against a harmful agent” (8). Given that the microglia are the brain’s resident macrophages (i.e., phagocytic cells), we believe that the presence of activated microglia in prion-affected brains represents an inflammatory response (9–11).
Affiliation(s): (1) CNS Inflammation Group, School of Biological Sciences, University of Southampton, Southampton, UK
Book Title: Molecular Pathology of the Prions
Brain Inflammation Likely Key Initiator to Prion and Parkinson's Disease
…researchers of the Computational Biology group at the Luxembourg Centre for Systems Biomedicine showed that neuro-inflammation plays a crucial role in initiating prion disease.
Prion diseases represent a family of neurodegenerative disorders associated with the loss of brain cells and caused by proteins called prions (derived from ‘protein’ and ‘infection’). The diseases are found in both humans and animals, such as Creutzfeld-Jakob disease and mad cow disease respectively. Although mostly harmless, prions can transform into infectious agents, which accumulate in the brain and destroy the nervous tissue.
But how exactly does the accumulation of prions cause destruction of the brain? “Understanding the process by which prions destroy neurons is critical for finding a cure for prion disease”, says Isaac Crespo, first author of the publication. He and his colleagues tackled this question with a computational approach: They ran their own computer programmes on experimental data generated by other research groups, and identified a set of 16 proteins that seems to control the onset of the disease. Interestingly, almost all of these proteins have known functions in neuro-inflammation.
...They may be newly discovered but they were not much of a problem to humans before while they have always been around. I think something is causing us to be more susceptible to them now. ...
...individuals incubating prion disease may be highly susceptible to CNS inflammation. ...During the years or decades of prion disease incubation, especially with low or subclinical prion titers, at-risk individuals are certain to encounter diverse pathological insults, such as viral and bacterial infections, autoimmune disease, or neoplastic processes, all of which may have an inflammatory component. These individuals may develop severe neurological diseases not immediately associated with prion infections due to the dissociation of the putative clinical findings from the accumulation of PrPSc. If so, then the effects of the bovine spongiform encephalopathy epidemic on the population should be looked upon differently.
A lot of the information on Prions is old yet there seems to be little research on these over the years...almost as if they want to avoid the issue.
...Prion disease seems more like a symptom to me of a misfunctioning body, we should identify and destroy these misfolded proteins continuously.
It could just be a diet that has changed too fast and includes foods and food chemistry that the body cannot properly identify.
I don't think we can successfully evolve that much in a generation though.
Viruses can stimulate evolution without killing us but I doubt if prions could successfully succeed at that.
Many organisms live symbiotically with us but I don't think a misfolded protein would be one of them.
I could be wrong, but we interact with life that is made right a lot better than life that is misformed.
I think this misfolding is a flaw in the structure myself, something that shouldn't be.
We have been messing with things for many centuries. Even consuming a protein that the body does not recognize because we changed our diet is like consuming a misfolded protein. They assumed that we would not absorb these proteins but that has been proven false in the last twenty years. Adding new foods and preparation techniques for the food should be done slowly so we can adapt.
Sooner or later the misfolded proteins will no longer be harmful to us. Maybe this is what you are thinking, it is true, humans will evolve to be able to consume these eventually, killing a lot of people along the way.
Community creates fundraisers for young mom struck by rare, fatal disease
Sandi Tucker Kennedy, a 38-year-old wife and mom of four young children ages 2 to 9, has been diagnosed with a prion disease, a family of rare progressive neurodegenerative disorders that take over the neurological system.
The disease is rapidly progressing and Kennedy, who is now at her Kennebunk home surrounded by family, has been given a short time to live.
It took months of debilitating symptoms for doctors to reach the diagnosis, including many hospital visits and stays, and the fundraisers that have been set up are helping to defray those medical costs.
…A fundraising page has also been set up at youcaring.com where 100 percent of the funds raised will benefit the Kennedy family. To donate, visit www.youcaring.com and search for "Hope for Sandi."
Alzheimer’s disease: an evolutionary approach
Summary - Alzheimer’s disease (AD) is a complex disease associated with advanced age whose causes are still not fully known. Approaching the disease from an evolutionary standpoint may help in understanding the root cause of human vulnerability to the disease. AD is very common in humans and extremely uncommon in other mammals, which suggests that the genetic changes underlying the alterations in cerebral structure or function that have taken place over the course of the evolution of the genus Homo have left specific neurons in the human brain particularly vulnerable to factors which trigger the disease. Most of the genes whose mutation leads to AD are involved in synaptic plasticity. Evidence has also been found relating AD to neuronal oxidative stress. Neurons in certain association areas of the human brain retain juvenile characteristics into adulthood, such as the increased expression of genes related to synaptic activity and plasticity, incomplete myelination and elevated aerobic metabolism, which can cause an increase in oxidative stress in these neurons. Oxidative stress can cause myelin breakdown and epigenetic changes in the promoter region of genes related to synaptic plasticity, reducing their expression. These changes may in some cases induce hyperphosphorylation of tau and β-amyloid deposits, which are characteristic of AD. The adaptation of humans to the cognitive niche probably required an increase in synaptic plasticity and activity and neuronal metabolism in neurons in areas related to certain cognitive functions such as autobiographical memory, social interaction and planning. The cost of these changes may have been the brain’s increased vulnerability to factors which can trigger AD. This vulnerability may have resulted from the evolutionary legacies that have occurred over the course of the evolution of the human brain, making AD a possible example of antagonistic pleiotropy. The evolutionary approach allows apparently unrelated data from different disciplines to be combined in a manner that may lead to an improved understanding of complex diseases such as Alzheimer’s.
....they literally would stoop to scrape the dross off the floor and feed it to their fellow man?
originally posted by: CJCrawley
I think the problem lies in red meat.