Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Saturday, January 27, 2018

A new therapeutic avenue for Parkinson's disease

You may need this due to your risk of Parkinsons after stroke. Better file this away so you can remember this when you need it. Maybe when you need it an intervention will be available.

Parkinson’s Disease May Have Link to Stroke

A new therapeutic avenue for Parkinson's disease

Buck Institute for Research on Aging News

Systemic clearing of senescent astrocytes prevents Parkinson’s neuropathology and associated symptoms in a mouse model of sporadic disease, the type implicated in 95% of human cases. Publishing in Cell Reports, researchers in the Andersen lab at the Buck Institute provide a new potential therapeutic avenue for the incurable, progressive neurological disorder that affects up to one million Americans, robbing them of the ability to control movement.
Senescent cells, which stop dividing in response to stress, secrete deleterious factors that cause tissue damage and lead to chronic inflammation. In this study, senescence was triggered by exposure to the pesticide paraquat, a neurotoxin formally linked to the development of Parkinson’s disease in farmworkers in 2011.
“While senescence has been implicated in Parkinson’s and other neurodegenerative disease, we believe this is the first time that clearing the inflammatory cells prevented symptoms from developing in a live mammal,” said Julie K. Andersen, PhD, Buck professor and senior author on the paper. “We hope that the fact that we were able to do this in a sporadic, rather than genetic, model of Parkinson’s, highlights its relevance as a potential new way to tackle the most prevalent form of the disease.”
This research is unusual given that it focuses on senescence in astrocytes, so-called “helper” cells that perform a variety of tasks, from axon guidance and synaptic support to control of the blood brain barrier and blood flow. Even though astrocytes are the most numerous cell type within the central nervous system, Andersen says they have been underappreciated “stepchildren” in most basic neuroscience research. She says the vast majority of Parkinson’s research has focused on toxicity that directly affects specific neurons implicated in the disease, “but no one has come up with an effective treatment based on that approach. This research suggests that senescent astrocytes may contribute to the development of the disease and we’re excited to explore this avenue.”
The research, led by adjunct faculty Shankar Chinta, PhD, and postdoctoral fellow Georgia Woods, PhD, showed that postmortem tissue from patients with Parkinson’s displays increased astrocytic senescence, and that cultured human astrocytes exposed to paraquat become senescent as well.
The mice used in this research were 6 months old, the human equivalent of about 34 years of age. Andersen’s lab hopes to study the impact of astrocytic senescence in mice at varying stages of lifespan to see if Parkinson’s can be reversed in addition to being prevented. “Chronic inflammation fueled by senescence drives many age-related diseases, and it’s quite possible that Parkinson’s is among them,” says Andersen, who adds that astrocytic inflammation may play a role in other neurodegenerative diseases such as Alzheimer’s. “This model gives us a way to expand how we look at and potentially treat a range of maladies,” she says.
There is a desperate need for treatments for Parkinson’s. An estimated 7 to 10 million people are living with the disease worldwide. In addition to resting tremor and difficulty with walking and balance, Parkinson’s also leads to cognitive decline and depression with symptoms becoming more severe as the disease progresses. About 5% of cases are caused by genetics. The remainder are believed to be caused by a combination of both genetic and environmental factors, such as family history, genetic mutations, drinking well water, and exposure to pesticides or metal.

1 comment:

  1. "Atlanta Center for Medical Research is currently seeking qualified individuals to participate in a clinical research trial for Parkinson's Disease

    For more details please visit Study Scavenger Atlanta

    ReplyDelete