You'll want your competent? doctor to make sure followup research occurs because of your increased risk of dementia post stroke. Do you even have a competent doctor?My definition of competence is having EXACT 100% RECOVERY PROTOCOLS. None of this guideline shit!
Your risk of dementia, has your doctor told you of this?
1. A documented 33% dementia chance post-stroke from an Australian study? May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.`
3. A 20% chance in this research. July 2013.
4. Dementia Risk Doubled in Patients Following Stroke September 2018
The latest here:
New Alzheimer’s Breakthrough Targets Plexin-B1 Protein
Summary: Researchers identified a novel way to potentially slow or halt Alzheimer’s progression by targeting the plexin-B1 protein. Their study shows how reactive astrocytes and plexin-B1 play crucial roles in clearing amyloid plaques. This discovery opens new pathways for Alzheimer’s treatments and emphasizes the importance of cellular interactions.
Key Facts:
- Key Protein: Targeting plexin-B1 protein can enhance the brain’s ability to clear amyloid plaques.
- Cellular Interactions: Reactive astrocytes help control the clearance of harmful deposits in the brain.
- Innovative Treatments: The study opens new pathways for developing treatments for Alzheimer’s disease.
Source: Mount Sinai Hospital
Researchers at the Icahn School of Medicine at Mount Sinai have made a significant breakthrough in Alzheimer’s disease research by identifying a novel way to potentially slow down or even halt disease progression.
The study, which focuses on the role of reactive astrocytes and the plexin-B1 protein in Alzheimer’s pathophysiology, provides crucial insights into brain cell communication and opens the door to innovative treatment strategies.
It was published in Nature Neuroscience on May 27.
This groundbreaking work is centered on the manipulation of the plexin-B1 protein to enhance the brain’s ability to clear amyloid plaques, a hallmark of Alzheimer’s disease. Reactive astrocytes, a type of brain cell that becomes activated in response to injury or disease, were found to play a crucial role in this process.
They help control the spacing around amyloid plaques, affecting how other brain cells can access and clear these harmful deposits.
“Our findings offer a promising path for developing new treatments by improving how cells interact with these harmful plaques,” said Roland Friedel, PhD, Associate Professor of Neuroscience, and Neurosurgery, at Icahn Mount Sinai and a senior author of the study.
The research was driven by the analysis of complex data comparing healthy individuals to those with Alzheimer’s, aiming to understand the disease’s molecular and cellular foundations.
Hongyan Zou, PhD, Professor of Neurosurgery, and Neuroscience, at Icahn Mount Sinai and one of the study’s lead authors, highlighted the broader implications of their findings: “Our study opens new pathways for Alzheimer’s research, emphasizing the importance of cellular interactions in developing neurodegenerative disease treatments.”
One of the study’s most significant achievements is its validation of multiscale gene network models of Alzheimer’s disease.
“This study not only confirms one of the most important predictions from our gene network models but also significantly advances our understanding of Alzheimer’s. It lays a solid foundation for developing novel therapeutics targeting such highly predictive network models,” said Bin Zhang, PhD, Willard T.C. Johnson Research Professor of Neurogenetics at Icahn Mount Sinai and one of the study’s lead authors.
By demonstrating the critical role of plexin-B1 in Alzheimer’s disease, the research underscores the potential of targeted therapies to disrupt the disease’s progression.
The research team emphasizes that while their findings mark a significant advance in the fight against Alzheimer’s, more research is needed to translate these discoveries into treatments for human patients.
“Our ultimate goal is to develop treatments that can prevent or slow down Alzheimer’s progression,” Dr. Zhang added, outlining the team’s commitment to further exploring the therapeutic potential of plexin-B1.
Funding: This study is supported by the NIH National Institute on Aging (NIA) grants U01AG046170 and RF1AG057440 and is part of the NIA-led Accelerating Medicines Partnership – Alzheimer’s Disease (AMP-AD) Target Discovery and Preclinical Validation program.
This public private partnership aims to shorten the time between the discovery of potential drug targets and the development of new drugs for Alzheimer’s disease treatment and prevention.
About this Alzheimer’s disease research news
Author: Jennifer Gutierrez
Source: Mount Sinai Hospital
Contact: Jennifer Gutierrez – Mount Sinai Hospital
Image: The image is credited to Neuroscience News
No comments:
Post a Comment