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
- 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
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) (9–11), or lacunes (9–11), 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 (16–18)]
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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