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lobar-degeneration
7 studies tagged lobar-degeneration, dated 2003-04-01 to 2025-01-08. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- Plasma p-tau217 and neurofilament/p-tau217 ratio in differentiating Alzheimer's disease from syndromes associated with frontotemporal lobar degeneration 2025-01-08
- Diagnostic and prognostic value of serum NfL and p-Tau181 in frontotemporal lobar degeneration 2020-07-01
- Serum Glial Fibrillary Acidic Protein (GFAP) Is a Marker of Disease Severity in Frontotemporal Lobar Degeneration 2020-01-01
Studies
7 studies carry this tag.
Date range
2003 to 2025
Top journals
- Acta neuropathologica 1
- Alzheimer's & dementia : the journal of the Alzheimer's Association 1
- Brain : a journal of neurology 1
- Journal of Alzheimer's disease : JAD 1
- Journal of neurology 1
7 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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Plasma p-tau 217 and the NfL/p-tau 217 ratio are promising non-invasive biomarkers for differentiating AD from FTLD, suggesting their use as a potential alternative to traditional diagnostic methods.
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62/100
The assessment of serum NfL and p-Tau 181 may provide a comprehensive view of FTLD, aiding in the differential diagnosis, in staging disease severity and in defining survival probability.
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Serum GFAP is increased in FTLD, correlates with cognition and GABAergic deficits, and thus shows promise as a biomarker of disease severity in FTLD.
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Due to the significant clinical overlap between frontotemporal lobar degeneration (FTLD) spectrum disorders and late-onset primary psychiatric disorders (PPD), diagnostic biomarkers reflecting the different underlying pathophysiologies are urgently needed.
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The effect of genome-wide significant variants at the GFRA2 locus on expression of GFRA2 was assessed using mRNA expression studies in cerebellar tissue samples from the Mayo Clinic brain bank.
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Mutations in the gene coding for Sequestosome 1 (SQSTM1) have been genetically associated with amyotrophic lateral sclerosis (ALS) and Paget disease of bone.
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Formalin-fixed brain specimens from sporadic cases with frontotemporal dementia (eight with tau-positive Pick bodies, five with frontotemporal lobar degeneration without inclusions) were compared with those from non-diseased controls (n = 5).