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plasma-p-tau181
7 studies tagged plasma-p-tau181, dated 2021-06-14 to 2024-11-19. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- Plasma p-tau181 and GFAP reflect 7T MR-derived changes in Alzheimer's disease: A longitudinal study of structural and functional MRI and MRS 2024-11-19
- Plasma p-tau181 and amyloid markers in Alzheimer's disease: A comparison between Lumipulse and SIMOA 2024-08-22
- Plasma p-tau181 as a promising non-invasive biomarker of Alzheimer's Disease pathology in Subjective Cognitive Decline and Mild Cognitive Impairment 2023-09-12
Studies
7 studies carry this tag.
Date range
2021 to 2024
Top journals
- Alzheimer's & dementia : the journal of the Alzheimer's Association 2
- Brain communications 1
- Journal of Alzheimer's disease : JAD 1
- Journal of neurology, neurosurgery, and psychiatry 1
- Journal of the neurological sciences 1
6 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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Both plasma p-tau181 and GFAP appear to reflect disease progression, as indicated by 7T MR-derived brain changes which are not limited to areas known to be affected by tau pathology and neuroinflammation measured by MRS myo-inositol, respectively.
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47/100
One-hundred-thirthy-three participants, namely 55 A+T+N+ AD, 28 Neurodegenerative disorders (NDD) and 50 controls were enrolled for the study.
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Plasma p-tau181 levels were influenced by the presence of underlying AD pathology, independently from the cognitive status and were highly accurate in differentiating SCD-MCI patients who were carriers of AD pathology from non-carriers.
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Plasma p-tau181 is elevated in patients with ALS, independently from CSF levels, and is firmly associated with LMN dysfunction.
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Clinical trials testing tau-targeting therapies may benefit from using fluid biomarkers to recruit individuals at risk of tau aggregation.
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Our findings support an association of APOE ɛ4 and p-tau181 with preclinical AD and hippocampus functioning.
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Mixed-effect models assessed rates of memory decline in relation to baseline plasma p-tau181, and whether plasma p-tau181 significantly predicted memory decline beyond widely available clinical and genetic data (age, sex, years of education, cardiovascular and metabolic conditions, and APOE ε 4 status).