Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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We included 201 individuals (mean age 73.5 years, mean BMI 27.4 kg/m2).
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CRM-adjusted Aβ42 calibrator concentrations were calculated using the regression equation Y (CRM-adjusted) = 0.89X (calibrators) + 32.6.
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52/100
We found significant group-wise differences in 11C-PK-11195 binding between each patient group and controls in frontotemporal regions, in both a regions-of-interest analysis and in the comparison of principal spatial components of binding. 18F-AV-1451 binding was increased in semantic variant primary progressive aphasia compared to controls in the temporal regions, and both semantic variant primary progressive aphasia and behavioural variant frontotemporal dementia differed from controls in the expression of principal spatial components of binding, across temporal and frontotemporal cortex, respectively.
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Numerous imaging variables differed by clinical diagnosis, including hippocampal, amygdalar and inferior lateral ventricular volumes and entorhinal, lingual, inferior parietal and isthmus cingulate cortical thicknesses, at a false discovery rate (FDR)-corrected threshold for significance (analysis of covariance; p < 0.005).
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Plasma TP42/40 ratio showed a relevant and significant potential as a screening tool to identify brain Aβ positivity in preclinical and prodromal stages of Alzheimer's disease.
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Frontotemporal lobar degeneration, the neuropathological substrate of frontotemporal dementia (FTD), is characterized by the deposition of protein aggregates, including tau.
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All Centiloid cut-offs fell within the range of 25-35, except for CSF Aβ42 that rendered an optimal cut-off value of 12 CL.
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52/100
The cerebrospinal fluid (CSF) signature of Alzheimer's disease (AD) includes abnormal levels of amyloid-β 1-42 (Aβ42), total tau (t-Tau) and phosphorylated tau (p-Tau).
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Reimbursement of amyloid-positron emission tomography (PET) is lagging due to the lack of definitive evidence on its clinical utility and cost-effectiveness.
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Up to four freeze-thaw cycles do not influence single molecule array blood biomarkers of neurofilament light chain, total tau, or Aβ 42 , with at most minor reductions in Aβ 40 .
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Alzheimer's disease (AD) is currently incurable, but there is general agreement that a minimally invasive blood biomarker for screening in preclinical stages would be crucial for future therapy.
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52/100
Age-related hippocampal sclerosis may account for a significant proportion of elderly participants with amnestic dementia.
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Amyloid positron emission tomography ([18F] florbetaben (FBB) PET) can be used to determine concomitant Alzheimer's disease (AD) in idiopathic normal pressure hydrocephalus (iNPH) patients.
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52/100
More specifically, 18F-AV-1451 binding was significantly increased in patients with Alzheimer's disease, relative to patients with progressive supranuclear palsy and with control subjects, in the hippocampus and in occipital, parietal, temporal, and frontal cortices (t's > 2.2, P's < 0.04).
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See Vandenberghe and Schaeverbeke (doi:10.1093/awx065) for a scientific commentary on this article.
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Studies on markers of inflammation in subjects with mild cognitive impairment or AD dementia provided inconsistent results.
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Based on retrospective data, we develop personalized risk estimates for MCI patients.
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Increasingly, clinical trials for Alzheimer's disease (AD) are being conducted earlier in the disease phase and with biomarker confirmation using in vivo amyloid PET imaging or CSF tau and Aβ measures to quantify pathology.
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Cerebral microbleeds (CMBs) are hypothesised to have an important yet unknown role in the dementia disease pathology.
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In patients with a discrepancy between CSF p-tau181 and CSF Aβ42, the assessment of Aβ 42/40 ratio led to a reliable biological conclusion in over 50% of cases that agreed with a clinician's diagnosis.
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In HC and MCI subjects, FBP PET anterior and posterior cingulate and composite standard uptake value ratios correlated with CSF amyloid beta (Aβ1-42) and tau/Aβ1-42 ratios.
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Plasma DES/CHO was significantly reduced in Japanese AD patients and significantly correlated with Mini-Mental State Examination (MMSE) score.
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In several neurodegenerative diseases that are collectively called tauopathies, progressive accumulation of tau in the brain is closely associated with neurodegeneration and cognitive impairment.
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52/100
Total intracranial volume (TIV/ICV) is an important covariate for volumetric analyses of the brain and brain regions, especially in the study of neurodegenerative diseases, where it can provide a proxy of maximum pre-morbid brain volume.
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Major imaging biomarkers of Alzheimer's disease include amyloid deposition [imaged with [(11)C]Pittsburgh compound B (PiB) PET], altered glucose metabolism (imaged with [(18)F]fluro-deoxyglucose PET), and structural atrophy (imaged by MRI).
From across this topic
10 of the 1,573 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- β-Synuclein as a candidate blood biomarker for synaptic degeneration in Alzheimer's disease
- Feasibility of in vivo 18F-florbetaben PET/MR imaging of human carotid amyloid-β
- Prognostic value of plasma %p-tau217 in cognitively unimpaired older adults
- Cerebrospinal Fluid Biomarkers in iNPH: A Narrative Review
- Transport pathways for clearance of human Alzheimer's amyloid beta-peptide and apolipoproteins E and J in the mouse central nervous system
- Cerebrospinal fluid profile in frontotemporal dementia and Alzheimer's disease
- Plasma lipocalin-2 levels in the preclinical stage of Alzheimer's disease
- Amyloid and Tau Neuropathologic Stage, Coexisting Brain Disease, and Cognitive Status in a Population-Based Autopsy Cohort
- Cerebrospinal fluid dynamics and discordant amyloid biomarkers
- Association between plasma neurofilament light chain levels and cognitive function in patients with Parkinson's disease