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, February 13, 2021

Blood Biomarker Predicts Dementia in Cerebral Small Vessel Disease

 Describes a problem, OFFERS NO SOLUTION. USELESS.

But then your doctor should have already been doing something about this for 2.5 years already.

Serum neurofilament light - A biomarker of neuroaxonal injury after ischemic stroke October 2018 

I'd suggest firing the board of directors since they are obviously not setting the correct goals for your stroke hospital. 100% recovery for all is the only goal in stroke, the status quo is a complete failure and only YOU can change that trajectory.

 

The latest here:

Blood Biomarker Predicts Dementia in Cerebral Small Vessel Disease

Baseline neurofilament light predicted cognitive decline in SVD over 5 years

A computer rendering of neurofilaments

Serum neurofilament light chain (NfL), a marker of axonal damage, predicted future dementia risk in cerebral small vessel disease (SVD), a small longitudinal study suggested.

Baseline NfL predicted cognitive decline (global cognition β = -0.335 ± 0.094, P=0.001) and risk of converting to dementia (HR 1.676, 95% CI 1.183-2.373, P=0.004) over up to 5 years, reported Marco Egle, MSc, and Hugh Markus, MD, of the University of Cambridge in England, and co-authors in the Journal of Neurology, Neurosurgery, and Psychiatry.

"Our results demonstrate that NfL may be a useful marker to predict dementia risk in patients with lacunar stroke and SVD, and our analyses showed that it added extra prediction to simple clinical and demographic markers," Egle told MedPage Today.

While some patients with cerebral small vessel disease will develop dementia, others remain dementia-free, Egle noted. "Magnetic imaging resonance techniques provide radiological markers of SVD, which do allow some prediction. However, this is an expensive technique and is not available to all patients with this small vessel disease," he said.

Increased levels of NfL occur in neurodegenerative disorders, including Alzheimer's disease. NfL has been linked to cognition and disability in a cross-sectional study of SVD, but few studies have looked at whether it can predict cognitive changes over time. "The novelty of our study was its prospective design," Egle said.

The researchers used baseline and follow-up data from 121 patients with moderate-to-severe SVD in the St. George's Cognition and Neuroimaging in Stroke (SCANS) study. Participants were followed annually for 5 years.

Average baseline age was 70, and 74% of participants were men. MRI was performed at baseline and after 1, 2, and 3 years; blood samples also were collected then. Cognition was evaluated annually. Disability was assessed using the modified Rankin score (mRS). The study began in January 2008 and ended in October 2013; all assays were performed in 2019-2020. Six incidences of strokes were recorded over the 5-year follow-up period, four lacunar strokes and two intracerebral haemorrhages.

Baseline serum NfL levels averaged 36.51 pg/mL. Cross-sectional analyses showed NfL levels were inversely associated with global cognitive function, executive function, and processing speed. They also were negatively correlated with disability. Higher NfL levels were positively associated with lacune count, cerebral microbleed count, white matter hyperintensities, and diffusion tensor imaging (DTI) measures, and were negatively associated with normalized brain volume.

Over 5 years, both global cognition and processing speed declined significantly. Higher NfL at baseline predicted lower function in global cognition independently of clinical markers and baseline cognition.

A total of 107 participants had complete baseline DTI and NfL data; 19 of them converted to dementia over time. Higher baseline NfL predicted not only dementia, but changes in lacune count, microbleed count, and brain volume, independently of initial MRI baseline values and patient age.

In contrast to imaging, there was no change in NfL values during follow-up. A potential application of NfL might be in clinical trials of SVD where it could be used to assess treatment effect, Egle noted. "We assessed this use by measuring NfL levels on repeated blood testing over a 3-year period to see if changes in levels predicted dementia," he said. "However, we were unable to detect any significant changes in NfL levels over this time, demonstrating that they are unlikely to be a useful marker in a clinical trial in SVD."

The study had several limitations, the researchers noted. Sample sizes were small and NfL levels at more than one time point were not available for all participants. Other research showed that participants who dropped out of the SCANS study had worse cognitive function than those who remained, which may have led to cognitive, MRI, and NfL changes over time being underestimated. Larger studies are needed to confirm the findings.

Last Updated February 12, 2021
  • Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Follow

Disclosures

This study was supported by the European Union's Horizon 2020 research and innovation program. The SCANS study was supported by a Wellcome Trust grant.

Egle is supported by a grant from the Stroke Association. Markus is supported by an NIHR Senior Investigator award and his work receives support from the Cambridge University Hospitals NIHR Biomedical Research Centre.

 

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