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.

Monday, December 10, 2018

Neurofilament Light Protein Tied to Cognitive Decline

Don't just lazily describe a problem and not give any solution. 

Neurofilament Light Protein Tied to Cognitive Decline


  • by Contributing Writer, MedPage Today
Neurofilament light protein levels in cerebrospinal fluid (CSF) were tied to cognitive impairment in dementia patients and neurodegeneration intensity in other disorders, researchers reported.
And adding it to a three-biomarker panel -- consisting of 42-residue amyloid beta protein (AB-42), total tau, and phosphorylated tau -- improved its ability to discriminate among certain neurodegenerative disorders for which the differential diagnosis is often difficult, according to Bob Olsson, MD, PhD, of the University of Gothenburg in Sweden, and co-authors, in JAMA Neurology.
"Neurofilament light levels reflect cognitive dysfunction in patients with Alzheimer's disease and frontotemporal dementia (FTD)," Olsson told MedPage Today. "It may help to separate different forms of neurodegenerative diseases from each other and cognitive decline from other causes than neurodegeneration, such as depression or drug-related side effects."
Neurofilament light protein previously has been shown to be elevated in different forms of dementia and amyotrophic lateral sclerosis (ALS). Although other studies have shown similar findings, "this study is the most exhaustive to date and includes a much larger sample size and a wider range of neurodegenerative diseases to compare CSF neurofilament light levels," noted Michelle Mielke, PhD, of the Mayo Clinic in Rochester, Minnesota, who was not involved with the study.
"It is notable that the addition of CSF neurofilament light to CSF amyloid-beta, total tau, and phosphorylated tau greatly increased the accuracy of distinguishing ALS or FTD patients compared to controls," Mielke told MedPage Today. "However, it is not yet clear how much the addition of CSF neurofilament light to the other CSF biomarkers will help with differentially diagnosing the specific type of neurodegenerative disease."
In this study, Olsson and co-authors analyzed neurofilament light levels in CSF samples from 913 people with an average age of about 69. The group included 75 healthy controls and 845 patients with clinical diagnoses of neurodegenerative disorders including mild cognitive impairment (n=114), Alzheimer's disease (n=397), FTD (n=96), ALS (n=68), Parkinson's disease (n=41), Parkinson's disease with mild cognitive impairment (n=19), Parkinson's disease with dementia (n=29), dementia with Lewy bodies (n=33), corticobasal syndrome (n=21), and progressive supranuclear palsy (n=20).
Mini-Mental State Examination (MMSE) scores were analyzed every 6 months for most patients, and autopsy-verified diagnoses were available for 120 of the 845 patients with diseases.
Neurofilament light levels were elevated in a stepwise manner, with the lowest levels in control participants, significantly higher levels in patients with mild cognitive impairment, and even higher levels in Alzheimer's disease. Although the highest levels were observed in patients with ALS and the second-highest levels in those with FTD, neurofilament light concentrations were elevated in Parkinson's disease with dementia, dementia with Lewy bodies, corticobasal syndrome, and progressive supranuclear palsy patients, compared with controls.
Neurofilament light levels rose with increasing cognitive impairment, with higher levels in Alzheimer's patients, intermediary levels in patients with mild cognitive impairment, and lowest levels in controls. They correlated significantly with annual worsening in cognitive performance on MMSE in patients with Alzheimer's or FTD, but not in patients with mild cognitive impairment. They also were tied to the severity of transactive response DNA-binding protein-43 in 13 of 17 brain regions.
Adding neurofilament light to the three-biomarker panel of AB-42, total tau, and phosphorylated tau led to:
  • 29% (95% CI 25.0%-33.3%) increase in accuracy in distinguishing between controls and ALS, from 62% to 91%
  • 17% (95% CI 14.9%-19.5%) increase between controls and the behavioral variant of FTD, from 63% to 81%
  • 14% (95% CI 8.7%-19.1%) increase between Parkinson's disease and progressive supranuclear palsy, from 62% to 76%
"Future studies with serially-collected samples across the neurodegenerative diseases will be useful for understanding how CSF neurofilament light tracks with the progression of each disease," noted Mielke.
The study has a number of limitations: some subgroups have small sample sizes, and the risk of false-positive statistical test results warrants replication of the findings, the authors noted. While the MMSE is not a strong indicator of disease severity for FTD, it was the only measure of cognition available for all FTD patients.
The study was supported by grants from the Swedish and European Research Councils, the Torsten Söderberg Foundation, the Swedish Brain Foundation, the Knut and Alice Wallenberg Foundation, Frimurarestiftelsen, Stiftelsen för Gamla Tjänarinnor, Foundation for Research on Alzheimer, the Swedish Alzheimer Foundation, and Swedish State Support for Clinical Research in addition to the National Institutes of Health.
Researchers reported relationships with Merck, Biogen, Avid Radiopharmaceuticals, Eli Lilly, GE Healthcare, Janssen, Brain Biomarker Solutions, Roche Diagnostics, Teva, Alzheon, BioArctic, Fujirebio Europe, IBL International, and Pfizer.
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