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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A total of 165 cognitively normal participants of the Baltimore Longitudinal Study of Aging (BLSA) Neuroimaging substudy, aged 55-92 years (mean baseline age = 76.4 years, 85 participants were male), received an average of 2.5 PET-PiB scans over an average interval of 2.6 (3.08 SD) years between first and last visits.
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In subjects with biomarker-confirmed Alzheimer's pathology, high CSF ferritin (>6.2 ng/mL) was associated with accelerated depreciation of CSF Aβ1-42 (reporting increased plaque formation; p=0.0001).
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Identifying which neuropsychological measures detect early cognitive changes associated with Alzheimer disease (AD), brain pathology would be helpful clinically for the diagnosis of early AD and for the design of clinical trials.
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We detected an increased concordance in the visual and quantitative (standardized uptake value ratio (SUVR) and total volume of distribution (VT)) [18F]AV45 PET measures when the CSF Aβ1-42/Aβ1-40 was applied compared to Aβ1-42 alone.
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Intra- and inter-laboratory variability of cerebrospinal fluid (CSF) biomarker analyses remains an important issue.
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Increased serum proinflammatory cytokines are associated with the presence of symptoms characteristic of sickness behavior, which are common neuropsychiatric features found in AD.
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High homocysteine levels were not associated with AD and were not related to a decrease in memory scores over time.
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Immunization against amyloid-beta has been suggested as a possible preventive or therapeutic treatment for Alzheimer's disease.
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Multiple proteinopathies commonly coexist in neurodegenerative diseases, making it essential to evaluate plasma biomarker performance in these complex diseases.
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63/100
In multivariable analyses, none of the plasma biomarkers were significantly associated with cognitive impairment.
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Plasma phosphorylated tau (p-tau) biomarkers offer a minimally invasive alternative for detecting Alzheimer’s disease (AD) pathology.
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Serum p-tau217 levels were increased in individuals with iRBD and cognitive impairment (CI) on testing defined as Montreal Cognitive Assessment <26 or subthreshold parkinsonism. p-Tau217 differentiated individuals with iRBD who developed PD with CI (PD-CI) or DLB from PD phenoconverters with normal cognition (area under curve [AUC] = 0.82; 95% confidence interval, 0.70-0.93) and from iRBD non-phenoconverters with normal cognition (AUC = 0.83; 95% confidence interval, 0.77-0.89).
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Tau positron emission tomography (PET) imaging allows in vivo detection of tau proteinopathy in Alzheimer's disease, which is associated with neurodegeneration and cognitive decline.
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E280A carriers had higher p-tau231 levels than non-carriers (9.0 ± 7.4 vs. 5.2 ± 3.4 pg/mL, P < 0.001).
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Plasma p-tau217 was associated with concurrent Aβ in most cortical regions and tau in temporo-parietal cortices.
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Compared to non-carriers, APOE ε4 carriers had lower Aβ42/Aβ40 and greater longitudinal increases in p-tau181 and GFAP; in contrast, the AD-PRS (excluding the APOE region) was associated with greater declines in Aβ42/Aβ40 among APOE ε4 non-carriers.
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63/100
NfL demonstrated fair to excellent accuracy in differentiating non-ACS from CU groups (area under the curve [AUC], 0.79 to 0.94). p-tau217 had the highest accuracy for identifying Aβ (AUC 0.94) and tau positron emission tomography status (AUC 0.91).
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There were no associations among steps or TRIMP with plasma biomarkers or cognition.
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HIGHLIGHTS: We demonstrated the diagnostic performance of qLRP in Alzheimer's disease.
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Blood-based biomarkers of Alzheimer disease (AD) may facilitate testing of historically under-represented groups.
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We detected a significant correlation between AßX-42/X-40 in plasma and CSF (r = 0.473).
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Nineteen participants developed AD after a median of 60 months (interquartile range 30).
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GFAP was lower in NB compared to prodromal AD (p = 0.003, d = 1.463) and AD-D (p = 0.002, d = 1.695).
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Diagnosis of dementia with Lewy bodies (DLB) is challenging and specific biofluid biomarkers are highly needed.
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Plasma Aβ42/Aβ40 demonstrated the highest association for Aβ accumulation in the brain with an AUC 0.76 (95%CI = 0.69, 0.82) at C2 N and 0.80 (95%CI = 0.75, 0.86) at Shimadzu.
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.
- Plasma Aβ biomarker for early diagnosis and prognosis of Alzheimer's disease - a systematic review
- Optical Coherence Tomography in Patients with Alzheimer's Disease: What Can It Tell Us?
- Neuroimaging in dementia. Clinical-radiological correlation
- Blood-brain barrier opening in Alzheimer's disease using MR-guided focused ultrasound
- Inflammation Disrupts Cognitive Integrity via Plasma Neurofilament Light Chain Coupling Brain Networks in Alzheimer's Disease
- Glial and neuronal cell-free DNA in plasma of sporadic bvFTD and late onset primary psychiatric disease patients
- Agreement of amyloid PET and CSF biomarkers for Alzheimer's disease on Lumipulse
- Reduced Plasma Aβ Peptides but Stable NfL and GFAP in Major Depressive Disorder
- Too early for LATE? Age at onset is associated with the clinical and neuroimaging expression of limbic-predominant age- related TDP-43 pathology in Alzheimer’s disease
- Blood-based biomarkers for dementia with Lewy bodies