WELCOME TO OUR PARKINSON'S PLACE!

I HAVE PARKINSON'S DISEASES AND THOUGHT IT WOULD BE NICE TO HAVE A PLACE WHERE THE CONTENTS OF UPDATED NEWS IS FOUND IN ONE PLACE. THAT IS WHY I BEGAN THIS BLOG.

I COPY NEWS ARTICLES PERTAINING TO RESEARCH, NEWS AND INFORMATION FOR PARKINSON'S DISEASE, DEMENTIA, THE BRAIN, DEPRESSION AND PARKINSON'S WITH DYSTONIA. I ALSO POST ABOUT FUNDRAISING FOR PARKINSON'S DISEASE AND EVENTS. I TRY TO BE UP-TO-DATE AS POSSIBLE.

I AM NOT RESPONSIBLE FOR IT'S CONTENTS. I AM JUST A COPIER OF INFORMATION SEARCHED ON THE COMPUTER. PLEASE UNDERSTAND THE COPIES ARE JUST THAT, COPIES AND AT TIMES, I AM UNABLE TO ENLARGE THE WORDING OR KEEP IT UNIFORMED AS I WISH. IT IS IMPORTANT TO UNDERSTAND I AM A PERSON WITH PARKINSON'S DISEASE. I HAVE NO MEDICAL EDUCATION,

I JUST WANT TO SHARE WITH YOU WHAT I READ ON THE INTERNET. IT IS UP TO YOU TO DECIDE WHETHER TO READ IT AND TALK IT OVER WITH YOUR DOCTOR. I AM JUST THE COPIER OF DOCUMENTS FROM THE COMPUTER. I DO NOT HAVE PROOF OF FACT OR FICTION OF THE ARTICLE. I ALSO TRY TO PLACE A LINK AT THE BOTTOM OF EACH ARTICLE TO SHOW WHERE I RECEIVED THE INFORMATION SO THAT YOU MAY WANT TO VISIT THEIR SITE.

THIS IS FOR YOU TO READ AND TO ALWAYS KEEP AN OPEN MIND.

PLEASE DISCUSS THIS WITH YOUR DOCTOR, SHOULD YOU HAVE ANY QUESTIONS, OR CONCERNS. NEVER DO ANYTHING WITHOUT TALKING TO YOUR DOCTOR FIRST..

I DO NOT MAKE ANY MONEY FROM THIS WEBSITE. I VOLUNTEER MY TIME TO HELP ALL OF US TO BE INFORMED.

I WILL NOT ACCEPT ANY ADVERTISEMENT OR HEALING POWERS, HEALING FROM HERBS AND ETC. UNLESS IT HAS GONE THROUGH TRIALS AND APPROVED BY FDA. IT WILL GO INTO SPAM.

THIS IS A FREE SITE FOR ALL WITH NO ADVERTISEMENTS

THANK YOU FOR VISITING! TOGETHER WE CAN MAKE A DIFFERENCE!

TRANSLATE

Thursday, February 7, 2019

Blood-clotting protein contributes to Alzheimer's

February 7, 2019     By 

According to a new study, a blood protein leaked into the brain contributes to cognitive decline.


It is still unclear exactly what causes Alzheimer's disease, which is a neurodegenerative condition chiefly characterized by memory loss and other forms of cognitive impairment. However, new research is uncovering more of the factors that contribute to its pathology.

According to existing guidelines, the main mechanism associated with cognitive problems in the brains of people with Alzheimer's diseaseis the formation of beta-amyloid plaques.
These are buildups of toxic proteins that disrupt the normal functioning of synapses. Synapses are the connections formed between brain cells that allow information to circulate within and to and from the brain.
However, in a new study from the Gladstone Institutes in San Francisco, CA, a team of researchers has identified another mechanism that affects how synapses work, contributing to Alzheimer's pathology.
The researchers began by investigating problems that appear in the blood vessel network in the brain, which is another biological characteristic of this form of dementia.
Senior investigator Prof. Katerina Akassoglou and her team have for the first time identified a blood-derived protein that leaks into the brain disrupting cell-to-cell communication.
The findings, which appear in the journal Neuron, indicate that in Alzheimer's, fibrinogen, a protein that usually contributes to blood clotting, plays a vital role in cognitive dysfunction.

New factor: 'Blood leaks in the brain'

In this study, the investigators used sophisticated imaging technology to scan both the brains of mice simulating a form of dementia and those of people with an Alzheimer's diagnosis.
Through their analyses, the researchers found that fibrinogen passes from blood vessels into the brain, triggering immune cell activity, which in turn leads to the breakdown of synapses.
To confirm the protein's role in synaptic breakdown, the team tried blocking fibrinogen's action on the brain's immune cells in a mouse model of Alzheimer's. This strategy protected the rodents from experiencing the type of memory loss typically associated with this condition.
"
We found that blood leaks in the brain can cause elimination of neuronal connections that are important for memory functions. This could change the way we think about the cause and possible cure of cognitive decline in Alzheimer's disease and other neurological diseases."

Prof. Katerina Akassoglou
Moreover, Prof. Akassoglou and her team found that leaked fibrinogen can lead to synaptic breakdown even in the absence of beta-amyloid plaques.
When the researchers injected even the smallest of quantities of fibrinogen into healthy brains, they saw that the protein triggered the same mechanism that caused the loss of synapses as it did in brains affected by Alzheimer's disease.
"Traditionally, the buildup of amyloid plaques in the brain has been seen as the root of memory loss and cognitive decline in Alzheimer's disease," explains the study's first author, Mario Merlini.
"Our work identifies an alternative culprit that could be responsible for the destruction of synapses," he notes.

'Far-reaching therapeutic implications'

The team that conducted the current study explains that existing research has shown that cerebrovascular problems, as well as the formation of beta-amyloid plaques, each contribute to cognitive decline.
Moreover, both of these pathologies contribute to the cognitive decline at similar rates. However, the researchers add that people who present both pathologies at the same time experience much quicker neurodegeneration.
Prof. Akassoglou and colleagues believe that their current findings finally offer an explanation for these phenomena.
"Given the human data showing that vascular changes are early and additive to amyloid, a conclusion from those studies is that vascular changes may have to be targeted with separate therapies if we want to ensure maximum protection against the destruction of neuronal connections that leads to cognitive decline," notes the senior researcher.
So far, researchers have been developing therapies targeting beta-amyloid, but these new findings suggest that other therapeutic targets may also be valuable.
"These exciting findings greatly advance our understanding of the contributions that vascular pathology and brain inflammation make to the progression of Alzheimer's disease," says study co-author Dr. Lennart Mucke.
"The mechanisms our study identified may also be at work in a range of other diseases that combine leaks in the blood-brain barrier with neurological decline, including multiple sclerosis, traumatic brain injury, and chronic traumatic encephalopathy. It has far-reaching therapeutic implications," he adds.
https://www.medicalnewstoday.com/articles/324390.php?utm_source=newsletter&utm_medium=email&utm_country=US&utm_hcp=no&utm_campaign=MNT%20Daily%20Full%20%28non-HCP%20US%29%20-%20OLD%20STYLE%202019-02-07&utm_term=MNT%20Daily%20News%20%28non-HCP%20US%29

No comments:

Post a Comment