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.

Sunday, October 11, 2026

Amyloid, p-tau, neurofilament light, and α-synuclein cerebrospinal fluid biomarkers across Alzheimer's disease, dementia with Lewy bodies, and Parkinson's disease

 With your risk of Parkinsons and dementia post stroke, what will your competent? doctor do with this to prevent those problems? 

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 

Oh, sorry; NOTHING AT ALL! In my opinion your doctor is completely incompetent in not using research to get you recovered!

Amyloid, p-tau, neurofilament light, and α-synuclein cerebrospinal fluid biomarkers across Alzheimer's disease, dementia with Lewy bodies, and Parkinson's disease


Abstract

Introduction: Mounting evidence suggests overlapping pathology across Alzheimer's disease (AD), dementia with Lewy bodies (DLB), and Parkinson's disease (PD), yet its extent and clinical implications remain unclear.

Methods: Cerebrospinal fluid (CSF) amyloid beta (Aβ)42/40, phosphorylated tau 181 (p-tau181), neurofilament light chain (NfL), and total α-synuclein were centrally measured using fully-automated Elecsys immunoassays in 347 participants (European Platform for Neurodegenerative Diseases [EPND] cohort) and compared between groups. Associations of amyloid and tau positivity with cognitive and motor function were evaluated.

Results: Compared to controls, amyloid and tau levels were abnormal in DLB, but not in PD. Amyloid and tau positivity in DLB were associated with worse global cognitive outcomes, but not with motor performance. NfL levels were elevated across diseases, and total α-synuclein levels were associated with tau positivity.

Discussion: AD pathology is observed in DLB, and related to worse cognition, but it is less observed in PD. CSF NfL captures non-disease-specific processes, whereas CSF total α-synuclein likely reflects CSF tau positivity. Results can help patient management in clinical practice and trials.

Keywords: Alzheimer's disease; Elecsys; Parkinson's disease; amyloid; cerebrospinal fluid; cognition; dementia with Lewy bodies; longitudinal; motor function; neurodegenerative diseases; neurofilament light; risk factors; tau; α‐synuclein.

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