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, May 11, 2019

A Post-hoc Study of D-Amino Acid Oxidase in Blood as an Indicator of Post-stroke Dementia

With your very likely chance of getting dementia your doctor, if any good at all, will be following this closely. OR, you could train them. Ask for the protocol that will prevent such dementia if this biomarker exists. Scream at your doctor if they have no protocol. Maybe suing them might get them to do their job.

Your chances of getting dementia.

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

 

A Post-hoc Study of D-Amino Acid Oxidase in Blood as an Indicator of Post-stroke Dementia

Yi-Chun Chen1,2, Wen-Hai Chou3, Hsiao-Hui Tsou4,5, Chiu-Ping Fang3, Tung-Hsia Liu3, Hsien-Hao Tsao6, Wen-Chuin Hsu1,2, Yi-Chinn Weng3, Yun Wang3 and Yu-Li Liu3*
  • 1Department of Neurology, Chang Gung Memorial Hospital Linkou Medical Center and College of Medicine, Chang Gung University, Taoyuan, Taiwan
  • 2Dementia Center, Chang Gung Memorial Hospital, Taoyuan, Taiwan
  • 3Center for Neuropsychiatric Research, National Health Research Institutes, Miaoli, Taiwan
  • 4Division of Biostatistics and Bioinformatics, Institute of Population Health Sciences, National Health Research Institutes, Miaoli, Taiwan
  • 5Graduate Institute of Biostatistics, China Medical University, Taichung, Taiwan
  • 6Department of Medicine, Chang Gung University, Taoyuan, Taiwan
Stroke is an important risk factor for dementia. Epidemiological studies have indicated a high incidence of dementia in stroke patients. There is currently no effective biomarker for the diagnosis of post-stroke dementia (PSD). D-amino acid oxidase (DAO) is a flavin-dependent enzyme widely distributed in the central nervous system. DAO oxidizes D-amino acids, a process which generates neurotoxic hydrogen peroxide and leads to neurodegeneration. This study aimed to examine post-stroke plasma DAO levels as a biomarker for PSD. In total, 53 patients with PSD, 20 post-stroke patients without dementia (PSNoD), and 71 age- and gender-matched normal controls were recruited. Cognitive function was evaluated at more than 30 days post-stroke. Plasma DAO was measured using the enzyme-linked immunosorbent assay. White matter hyperintensity (WMH), a neuroimaging biomarker of cerebral small vessel diseases, was determined by magnetic resonance imaging. We found that plasma DAO levels were independently higher in PSD subjects than in PSNoD subjects or the controls and were correlated with the WMH load in stroke patients. Using an area under the curve (AUC)/receiver operating characteristic analysis, plasma DAO levels were significantly reliable for the diagnosis of PSD. The sensitivity and specificity of the optimal cut-off value of 321 ng/ml of plasma DAO for the diagnosis of PSD were 75 and 88.7%, respectively. In conclusion, our data support that plasma DAO levels were increased in PSD patients and correlated with brain WMH, independent of age, gender, hypertension, and renal function. Plasma DAO levels may therefore aid in PSD diagnosis.

Introduction

Stroke is a risk factor for both vascular dementia and Alzheimer's disease (1, 2). Functional recovery develops over the course of 26 weeks after a stroke (3), but the survivors are often left with disabilities. In addition to the sequelae of acute neuronal damage, the 1-year post-stroke dementia (PSD) rates after first-ever and recurrent stroke are ~10 and 30%, respectively (4). Although there is a high risk of PSD in chronic stroke patients, no effective biomarker has been established for PSD (5). Limited studies have indicated that PSD involves secondary degeneration (6), including neuronal death, axonal degeneration, inflammation, and gliosis (7, 8). These secondary neurodegenerative changes result in Wallerian degeneration (9), cortical atrophy (9), white matter hyperintensities (WMHs) (911), or lacunes (911), and have been used as neuroimaging biomarkers for vascular brain injury (12) and cognitive impairment (13). The value of these indicators in predicting PSD is, however, still uncertain (11). A few blood biomarkers [e.g., β-secretase (14), homocysteine (15), and inflammation markers (1618)] for predicting PSD have been examined. However, the use of these biomarkers for clinical PSD patients is limited by their specificity and sensitivity. Currently, there are no effective blood biomarkers for PSD (2).
D-amino acid oxidase (DAO), a peroxisome flavin-dependent oxidase, catalyzes the stereospecific oxidative deamination of D-serine to imino-serine, hydrogen peroxide, and ammonia, which lead to oxidative stress (19). DAO expression and D-serine catabolism is widespread in different brain regions (20). Areas enriched in D-serine include the cerebral cortex, hippocampus, thalamus, hypothalamus, and amygdala (21). Since ischemic injury induces peroxisome biogenesis in neurons (22), DAO expression may also be regulated after stroke. This study aimed to examine post-stroke plasma DAO levels and determine whether they can be used as a biomarker for PSD.


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